PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27191787-2 2016 There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes. Thiamine 119-127 solute carrier family 19 member 2 Homo sapiens 38-45 27191787-2 2016 There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes. Thiamine 119-127 solute carrier family 19 member 3 Homo sapiens 47-54 27191787-2 2016 There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes. Thiamine 119-127 solute carrier family 25 member 19 Homo sapiens 56-64 27191787-2 2016 There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes. Thiamine 119-127 thiamin pyrophosphokinase 1 Homo sapiens 69-73 27191787-6 2016 Expert commentary: Doses of thiamine vary according to the genetic defect: for SLC19A2, the usual dose is 25-200 mg/day (1-4 mg/kg per day), for SLC19A3, 10-40 mg/kg per day, and for TPK1, 30 mg/kg per day. Thiamine 28-36 solute carrier family 19 member 2 Homo sapiens 79-86 27191787-6 2016 Expert commentary: Doses of thiamine vary according to the genetic defect: for SLC19A2, the usual dose is 25-200 mg/day (1-4 mg/kg per day), for SLC19A3, 10-40 mg/kg per day, and for TPK1, 30 mg/kg per day. Thiamine 28-36 solute carrier family 19 member 3 Homo sapiens 145-152 27191787-6 2016 Expert commentary: Doses of thiamine vary according to the genetic defect: for SLC19A2, the usual dose is 25-200 mg/day (1-4 mg/kg per day), for SLC19A3, 10-40 mg/kg per day, and for TPK1, 30 mg/kg per day. Thiamine 28-36 thiamin pyrophosphokinase 1 Homo sapiens 183-187 27191787-7 2016 Thiamine supplementation in SLC19A3-mutated patients restores CSF and intracellular thiamine levels, resulting in successful clinical benefits. Thiamine 0-8 solute carrier family 19 member 3 Homo sapiens 28-35 27191787-7 2016 Thiamine supplementation in SLC19A3-mutated patients restores CSF and intracellular thiamine levels, resulting in successful clinical benefits. Thiamine 84-92 solute carrier family 19 member 3 Homo sapiens 28-35 27191787-8 2016 In conclusion, evidence collected so far suggests that the administration of thiamine improves outcome in SLC19A-2, SLC19A3- and TPK1-mutated patients, so most efforts should be aimed at early diagnosis of these disorders. Thiamine 77-85 solute carrier family 19 member 2 Homo sapiens 106-114 27191787-8 2016 In conclusion, evidence collected so far suggests that the administration of thiamine improves outcome in SLC19A-2, SLC19A3- and TPK1-mutated patients, so most efforts should be aimed at early diagnosis of these disorders. Thiamine 77-85 solute carrier family 19 member 3 Homo sapiens 116-123 27191787-8 2016 In conclusion, evidence collected so far suggests that the administration of thiamine improves outcome in SLC19A-2, SLC19A3- and TPK1-mutated patients, so most efforts should be aimed at early diagnosis of these disorders. Thiamine 77-85 thiamin pyrophosphokinase 1 Homo sapiens 129-133 15546879-1 2005 The thymidylate synthase inhibitor 5-fluorouracil (5-FU) is used widely for chemotherapy of colorectal carcinoma. Fluorouracil 51-55 thymidylate synthetase Homo sapiens 4-24 15770397-0 2005 Expression level of thymidylate synthase is a good predictor of chemosensitivity to 5-fluorouracil in colorectal cancer. Fluorouracil 84-98 thymidylate synthetase Homo sapiens 20-40 15770397-5 2005 RESULTS: A significant increase in the TS expression score was observed in 5-FU-sensitive colorectal cancers (0.57 +/- 0.19) compared to 5-FU-resistant ones (1.16 +/- 0.98; P = 0.029), whereas no significant differences in DPD expression scores were observed in 5-FU-sensitive colorectal cancers (0.86 +/- 1.19) compared to 5-FU-resistant ones (0.56 +/- 1.05; P = 0.603). Fluorouracil 75-79 thymidylate synthetase Homo sapiens 5-7 15655543-6 2005 Quantitative expression levels of drug pathway genes were determined using TaqMan RT-PCR (5-fluorouracil (5-FU): TYMS, DPYD, ECGF1; oxaliplatin: GSTP1 (glutathione S-transferase pi), ERCC1 and 2; irinotecan: ABCB1, ABCG2, CYP3A4, UGT1A1, CES2, TOP1). Fluorouracil 90-104 thymidylate synthetase Homo sapiens 113-117 15655543-6 2005 Quantitative expression levels of drug pathway genes were determined using TaqMan RT-PCR (5-fluorouracil (5-FU): TYMS, DPYD, ECGF1; oxaliplatin: GSTP1 (glutathione S-transferase pi), ERCC1 and 2; irinotecan: ABCB1, ABCG2, CYP3A4, UGT1A1, CES2, TOP1). Fluorouracil 106-110 thymidylate synthetase Homo sapiens 113-117 15727486-8 2005 Although fewer studies are available regarding therapy of hepatic metastases, the same relationship between thymidylate synthase activity and outcome of fluorouracil therapy observed for primary colorectal cancer was found. Fluorouracil 153-165 thymidylate synthetase Homo sapiens 108-128 15638735-2 2005 TS was established as the principal target of the widely used anticancer drug 5-fluorouracil (5FU). Fluorouracil 78-92 thymidylate synthetase Homo sapiens 0-2 15638735-2 2005 TS was established as the principal target of the widely used anticancer drug 5-fluorouracil (5FU). Fluorouracil 94-97 thymidylate synthetase Homo sapiens 0-2 15638735-5 2005 5FU is non-ideal as a TS-inhibitory drug because it is only inefficiently converted to FdUMP, while the remainder of the administered dose is converted to toxic metabolites. Fluorouracil 0-3 thymidylate synthetase Homo sapiens 22-24 15386371-0 2004 Single nucleotide polymorphism in the 5" tandem repeat sequences of thymidylate synthase gene predicts for response to fluorouracil-based chemotherapy in advanced colorectal cancer patients. Fluorouracil 119-131 thymidylate synthetase Homo sapiens 68-88 16178783-4 2005 Thymidylate synthase (TS or ThyA) has long been considered as one of the best-known drug targets in the anti-cancer area, after which old and new drugs, such as 5-fluoro uracil and the anti-folate ZD1694, have been introduced into chemotherapy to treat solid tumours. Fluorouracil 161-176 thymidylate synthetase Homo sapiens 0-20 15999119-1 2005 The enzymes thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP), and orotate phosphoribosyl transferase (OPRT) are involved in the metabolism of the anticancer drug 5-fluorouracil. Fluorouracil 208-222 thymidylate synthetase Homo sapiens 12-32 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 0-20 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 51-65 thymidylate synthetase Homo sapiens 22-24 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 0-20 15386371-1 2004 Thymidylate synthase (TS) is the primary target of 5-fluorouracil (5-FU). Fluorouracil 67-71 thymidylate synthetase Homo sapiens 22-24 15386371-2 2004 A VNTR polymorphism in the TS promoter region is associated with the efficacy of 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 81-85 thymidylate synthetase Homo sapiens 27-29 15386371-14 2004 The selection of patients who are likely to respond to 5-FU therapy may be considerably improved if the TS genotype were to include both the VNTR and the SNP located within the promoter region of the gene. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 104-106 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 91-105 thymidylate synthetase Homo sapiens 0-20 15359285-3 2004 Mutants of two of these enzymes, dihydrofolate reductase (DHFR F/S) and thymidylate synthase (TS G52S), were previously shown to confer resistance to methotrexate and 5-FU, respectively, and recently a fusion cDNA of both mutant enzymes (DHFR F/S-TS G52S) was shown to confer dual resistance to both antimetabolites. Fluorouracil 167-171 thymidylate synthetase Homo sapiens 58-92 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 91-105 thymidylate synthetase Homo sapiens 22-24 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 107-110 thymidylate synthetase Homo sapiens 0-20 15571969-1 2004 Thymidylate Synthase (TS) is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU). Fluorouracil 107-110 thymidylate synthetase Homo sapiens 22-24 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 71-85 thymidylate synthetase Homo sapiens 3-5 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 71-85 thymidylate synthetase Homo sapiens 117-119 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 87-90 thymidylate synthetase Homo sapiens 3-5 15571969-7 2004 As TS is the key enzyme for DNA synthesis pathways and is inhibited by 5-fluorouracil (5FU), we can hypothesise that TS expression levels in the different histotypes of CRC could affect the potential responsiveness of these tumours to fluoropyrimidine chemotherapy, with a low efficacy being expected in signet ring cell areas. Fluorouracil 87-90 thymidylate synthetase Homo sapiens 117-119 15640503-0 2004 Prognostic implications of the expression of erbB2, topoisomerase II alpha and thymidylate synthase in metastatic gastric cancer after fluorouracil-based therapy. Fluorouracil 135-147 thymidylate synthetase Homo sapiens 79-99 15538739-3 2004 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are thought to be important predictors for the efficiency of 5-FU-based treatment. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 0-20 15538739-3 2004 Thymidylate synthase (TS), thymidine phosphorylase (TP), and dihydropyrimidine dehydrogenase (DPD) are thought to be important predictors for the efficiency of 5-FU-based treatment. Fluorouracil 160-164 thymidylate synthetase Homo sapiens 22-24 15538739-4 2004 The aim of this study was to determine the correlation between TS-, TP-, and DPD-gene expression and the response to 5-FU-based long-term pre-operative chemoradiotherapy assessed by histopathological tumour regression. Fluorouracil 117-121 thymidylate synthetase Homo sapiens 63-65 15538739-12 2004 In conclusion, this study shows that TS gene expression in a pretreatment biopsy predicts the response of local rectal cancer to neo-adjuvant 5-FU-based chemoradiotherapy in a high percentage. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 37-39 15205195-0 2004 5-Fluorouracil incorporation into RNA and DNA in relation to thymidylate synthase inhibition of human colorectal cancers. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 61-81 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-97 thymidylate synthetase Homo sapiens 186-206 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 83-97 thymidylate synthetase Homo sapiens 208-210 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 99-102 thymidylate synthetase Homo sapiens 186-206 15688605-2 2004 An example of a drug for which clear predictive parameters have been identified is 5-fluorouracil (5FU): its antitumor activity is limited by either a high activity of the target enzyme thymidylate synthase (TS) and/or a high activity of its degrading enzyme, dihydropyrimidine dehydrogenase (DPD). Fluorouracil 99-102 thymidylate synthetase Homo sapiens 208-210 15549590-0 2004 Prognostic significance of thymidylate synthase in patients with metastatic colorectal cancer who receive protracted venous infusions of 5-fluorouracil. Fluorouracil 137-151 thymidylate synthetase Homo sapiens 27-47 15549590-1 2004 BACKGROUND: This study was conducted to evaluate the prognostic significance of thymidylate synthase (TS) expression in the tumor tissue of patients with metastatic colorectal cancer (CRC) who received protracted venous infusions of 5-fluorouracil (5-FU). Fluorouracil 233-247 thymidylate synthetase Homo sapiens 80-100 15549590-1 2004 BACKGROUND: This study was conducted to evaluate the prognostic significance of thymidylate synthase (TS) expression in the tumor tissue of patients with metastatic colorectal cancer (CRC) who received protracted venous infusions of 5-fluorouracil (5-FU). Fluorouracil 233-247 thymidylate synthetase Homo sapiens 102-104 15549590-1 2004 BACKGROUND: This study was conducted to evaluate the prognostic significance of thymidylate synthase (TS) expression in the tumor tissue of patients with metastatic colorectal cancer (CRC) who received protracted venous infusions of 5-fluorouracil (5-FU). Fluorouracil 249-253 thymidylate synthetase Homo sapiens 102-104 15549590-5 2004 CONCLUSION: In patients with metastatic CRC who received protracted venous infusions of 5-FU, TS expression was related to survival independently of other established clinical prognostic factors. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 94-96 15591457-0 2004 Immunohistochemical evaluation of thymidylate synthase (TS) and p16INK4a in advanced colorectal cancer: implication of TS expression in 5-FU-based adjuvant chemotherapy. Fluorouracil 136-140 thymidylate synthetase Homo sapiens 119-121 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 55-75 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 77-79 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 139-153 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 55-75 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 77-79 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 155-159 thymidylate synthetase Homo sapiens 211-213 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 244-248 thymidylate synthetase Homo sapiens 55-75 15591457-1 2004 BACKGROUND: Our previous analyses on the expression of thymidylate synthase (TS) and p16(INK4a) in colorectal cancer patients administered 5-fluorouracil (5-FU) pre-operatively demonstrated that a high level of TS expression was a predictor of 5-FU resistance, and that the combination of a low level of TS expression and induction of p16(INK4a) after chemotherapy implicated chemosensitivity. Fluorouracil 244-248 thymidylate synthetase Homo sapiens 77-79 15591457-2 2004 The present study aimed to assess the relationship between the biological behavior of advanced colorectal cancer treated post-operatively by 5-FU-based chemotherapy and the expression of TS and p16(INK4a) in primary tumors. Fluorouracil 141-145 thymidylate synthetase Homo sapiens 187-189 15591457-10 2004 We suggest that, in the Dukes" C group, a 5-FU-based regimen can be chosen as a first-line chemotherapy for low TS expressors. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 112-114 15571286-1 2004 The action of 5-Fluorouracil (5-FU) is mediated by inhibition of thymidylate synthase (TS), which is regulated by cell cycle proteins controlled by protein phosphorylation. Fluorouracil 14-28 thymidylate synthetase Homo sapiens 65-85 15571286-1 2004 The action of 5-Fluorouracil (5-FU) is mediated by inhibition of thymidylate synthase (TS), which is regulated by cell cycle proteins controlled by protein phosphorylation. Fluorouracil 30-34 thymidylate synthetase Homo sapiens 65-85 15500737-1 2004 OBJECTIVE: To study the relationship between the expression of thymidylate synthase (TS) gene and the prognosis of colorectal carcinoma and between the TS expression and the effect of 5-fluorouracil (5-Fu) on advanced colorectal carcinoma. Fluorouracil 184-198 thymidylate synthetase Homo sapiens 152-154 15500737-1 2004 OBJECTIVE: To study the relationship between the expression of thymidylate synthase (TS) gene and the prognosis of colorectal carcinoma and between the TS expression and the effect of 5-fluorouracil (5-Fu) on advanced colorectal carcinoma. Fluorouracil 200-204 thymidylate synthetase Homo sapiens 152-154 15355913-5 2004 RESULTS: We identified the following three genes coding for proliferation-related proteins: thymidylate synthase (TYMS), which is involved in chemoresistance (5-fluorouracil); 5"-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide transfolmylase/inosinicase (AICRT/I); and phosphoglycerate kinase 1 (PKG1), which was secreted by tumor cells and involved in the angiogenic process. Fluorouracil 161-173 thymidylate synthetase Homo sapiens 92-112 15355913-5 2004 RESULTS: We identified the following three genes coding for proliferation-related proteins: thymidylate synthase (TYMS), which is involved in chemoresistance (5-fluorouracil); 5"-aminoimidazole-4-carboxamide-1-beta-d-ribonucleotide transfolmylase/inosinicase (AICRT/I); and phosphoglycerate kinase 1 (PKG1), which was secreted by tumor cells and involved in the angiogenic process. Fluorouracil 161-173 thymidylate synthetase Homo sapiens 114-118 15355913-9 2004 CONCLUSIONS: TYMS and PGK1, as well as their epitope peptides, might be appropriate target molecules for specific immunotherapy of HLA-A2(+) colon cancer patients because of the positive role of TYMS and PGK1 in chemoresistance (5-fluorouracil) and angiogenesis of tumor cells, respectively. Fluorouracil 229-243 thymidylate synthetase Homo sapiens 13-17 15355920-0 2004 Thymidylate synthase gene polymorphism predicts toxicity in colorectal cancer patients receiving 5-fluorouracil-based chemotherapy. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 0-20 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 31-45 thymidylate synthetase Homo sapiens 56-76 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 31-45 thymidylate synthetase Homo sapiens 78-80 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 47-51 thymidylate synthetase Homo sapiens 56-76 15355920-1 2004 PURPOSE: The target enzyme for 5-fluorouracil (5-FU) is thymidylate synthase (TS). Fluorouracil 47-51 thymidylate synthetase Homo sapiens 78-80 15355920-3 2004 TS expression predicts response to 5-FU-based chemotherapy, and the expression seems to be determined by the TYMS gene promoter. Fluorouracil 35-39 thymidylate synthetase Homo sapiens 0-2 15355920-4 2004 The aim of this study was to investigate the utility of determining these two TYMS gene polymorphisms to predict the toxicity and efficacy of 5-FU treatment in patients with colorectal cancer. Fluorouracil 142-146 thymidylate synthetase Homo sapiens 78-82 15355920-5 2004 EXPERIMENTAL DESIGN: The determination of TYMS genotypes was performed in tumor and normal tissues by PCR amplification from 90 patients with colorectal cancer who were treated with adjuvant or palliative 5-FU-based chemotherapy. Fluorouracil 205-209 thymidylate synthetase Homo sapiens 42-46 15355920-8 2004 RESULTS: Individuals who were homozygous for the double repeat in the TYMS promoter region had more severe side effects to 5-FU. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 70-74 15355920-10 2004 The TYMS promoter and TYMS 3"-UTR polymorphisms were in linkage disequilibrium, and the haplotype 2R/ins 6-bp was significantly associated with a high risk of severe side effects to 5-FU. Fluorouracil 182-186 thymidylate synthetase Homo sapiens 4-8 15355920-10 2004 The TYMS promoter and TYMS 3"-UTR polymorphisms were in linkage disequilibrium, and the haplotype 2R/ins 6-bp was significantly associated with a high risk of severe side effects to 5-FU. Fluorouracil 182-186 thymidylate synthetase Homo sapiens 22-26 15355920-12 2004 CONCLUSIONS: This study demonstrated that TYMS genotyping could be of help in predicting toxicity to 5-FU-based chemotherapy. Fluorouracil 101-105 thymidylate synthetase Homo sapiens 42-46 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 0-20 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 22-24 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 0-20 15353299-6 2004 Thymidylate synthase (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of 2-deoxythymidine-5-monophosphate, a precursor for DNA synthesis. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 22-24 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 21-35 thymidylate synthetase Homo sapiens 66-86 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 21-35 thymidylate synthetase Homo sapiens 88-90 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 66-86 15353301-1 2004 Cancer drugs such as 5-fluorouracil (5-FU) that target the enzyme thymidylate synthase (TS) have been and are still being widely used in cancer treatment, but as with other anti-cancer drugs, the majority of tumors do not respond to the treatment, whereas the patients still suffer drug-related toxicity. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 88-90 15353301-5 2004 Thus, considerable interest was generated by data suggesting that the variable number of a 28 base-pair (bp) segment in the promoter region of the TS gene was associated with TS gene expression and/or protein expression, as well as with tumor response to 5-FU therapy, toxicity and patient survival. Fluorouracil 255-259 thymidylate synthetase Homo sapiens 147-149 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 0-20 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 79-81 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 0-20 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 64-68 thymidylate synthetase Homo sapiens 79-81 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 0-20 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 22-24 15446554-1 2004 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU), and the TS expression level of cancer tissues is a potential predictor of the response to 5-FU-based chemotherapy. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 79-81 15446554-3 2004 Therefore, the TS polymorphism may also be a predictor of the response to 5-FU-based chemotherapy. Fluorouracil 74-78 thymidylate synthetase Homo sapiens 15-17 15446554-11 2004 These results suggest that the TS gene polymorphism and TS protein level may be independent predictors for 5-FU-based chemotherapy. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 31-33 15446554-11 2004 These results suggest that the TS gene polymorphism and TS protein level may be independent predictors for 5-FU-based chemotherapy. Fluorouracil 107-111 thymidylate synthetase Homo sapiens 56-58 15197779-0 2004 Topoisomerase-I, thymidylate synthase primary tumour expression and clinical efficacy of 5-FU/CPT-11 chemotherapy in advanced colorectal cancer patients. Fluorouracil 89-93 thymidylate synthetase Homo sapiens 17-37 15197779-1 2004 While several studies have reported that thymidylate synthase (TS) tumour expression can be a reliable predictive marker of clinical response to 5-Fluorouracil (5-FU) for advanced colorectal cancer patients, only a few studies that searched for predictive factors of irinotecan (CPT-11) clinical response are available. Fluorouracil 145-159 thymidylate synthetase Homo sapiens 41-61 15197779-1 2004 While several studies have reported that thymidylate synthase (TS) tumour expression can be a reliable predictive marker of clinical response to 5-Fluorouracil (5-FU) for advanced colorectal cancer patients, only a few studies that searched for predictive factors of irinotecan (CPT-11) clinical response are available. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 41-61 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 19-39 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 41-43 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 19-39 15260847-1 2004 High expression of thymidylate synthase (TS) is allegedly associated with the chemoresistance to 5-fluorouracil (5-FU) in colorectal cancers. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 41-43 15260847-4 2004 We immunohistochemically evaluated the relationship between the expression of TS, p16(INK4a), CDK4 and cyclin D1 and the effect of 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 131-135 thymidylate synthetase Homo sapiens 78-80 15260847-12 2004 In conclusion, the combination of low expression of TS and induction of p16(INK4a) after chemotherapy can be important indicators of the sensitivity to 5-FU-based chemotherapy in colorectal cancers. Fluorouracil 152-156 thymidylate synthetase Homo sapiens 52-54 15213713-2 2004 Functional polymorphisms in DNA-repair genes XPD, ERCC1, XRCC1, XPA, and metabolising genes glutathione S-transferase GSTP1, GSTT1, GSTM1, and thymidylate synthase (TS) were assessed retrospectively in 106 patients with refractory stage IV disease who received 5-FU/oxaliplatin combination chemotherapy, using a polymerase chain reaction-based RFLP technique. Fluorouracil 261-265 thymidylate synthetase Homo sapiens 143-163 15330198-0 2004 Thymidylate synthetase (TS) genotype and TS/dihydropyrimidine dehydrogenase mRNA level as an indicator in determining chemosensitivity to 5-fluorouracil in advanced gastric carcinoma. Fluorouracil 138-152 thymidylate synthetase Homo sapiens 0-22 15330198-1 2004 BACKGROUND: One of the target enzymes of 5-fluorouracil (5-FU) is thymidylate synthetase (TS). Fluorouracil 41-55 thymidylate synthetase Homo sapiens 66-88 15330198-1 2004 BACKGROUND: One of the target enzymes of 5-fluorouracil (5-FU) is thymidylate synthetase (TS). Fluorouracil 57-61 thymidylate synthetase Homo sapiens 66-88 15492820-9 2004 Vinorelbine suppressed the 5-FU-induced increase in TS protein in A549 cells. Fluorouracil 27-31 thymidylate synthetase Homo sapiens 52-54 15375535-0 2004 Thymidylate synthase expression pattern is a prognostic factor in patients of colorectal cancer treated with 5-fluorouracil. Fluorouracil 109-123 thymidylate synthetase Homo sapiens 0-20 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 100-120 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 122-124 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 100-120 15205195-1 2004 BACKGROUND: The mechanism of action of 5-fluorouracil (5-FU) has been associated with inhibition of thymidylate synthase (TS) and incorporation of 5-FU into RNA and DNA, but limited data are available in human tumor tissue for the latter. Fluorouracil 55-59 thymidylate synthetase Homo sapiens 122-124 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 311-315 thymidylate synthetase Homo sapiens 23-43 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 119-133 thymidylate synthetase Homo sapiens 0-20 15222106-1 2004 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been identified as a predictor of response to 5-fluorouracil (5-FU). Fluorouracil 135-139 thymidylate synthetase Homo sapiens 0-20 15060742-1 2004 PURPOSE: Expression of thymidylate synthase (TS) and the 5-fluorouracil (5-FU) metabolic enzymes, including dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyl transferase (OPRT), thymidine phosphorylase (TP), and uridine phosphorylase (UP), has been reported to be associated with the sensitivity to 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 311-315 thymidylate synthetase Homo sapiens 45-47 15132128-2 2004 5-FU interferes with DNA synthesis by blocking thymidylate synthase (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 47-67 15132128-2 2004 5-FU interferes with DNA synthesis by blocking thymidylate synthase (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD). Fluorouracil 0-4 thymidylate synthetase Homo sapiens 69-71 15132128-3 2004 Favorable enzyme profiles (high TP and low DPD) generate high intratumor levels of 5-FU that are effective against many tumors, especially those with low TS. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 154-156 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 54-68 thymidylate synthetase Homo sapiens 161-181 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 40-44 15067352-9 2004 5-FU metabolism-associated genes (e.g., TYMS, DTYMK, UP) and DNA repair genes (e.g., FEN1, FANCG, RAD23B) were also up-regulated in one or both resistant derivatives, suggesting that the resistant derivatives might be able to overcome both 5-FU inhibition of thymidylate synthase and the DNA damage caused by 5-FU, respectively. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 259-279 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 0-20 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 48-52 thymidylate synthetase Homo sapiens 22-24 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 208-212 thymidylate synthetase Homo sapiens 0-20 14689231-2 2004 Thymidylate synthase (TS), the target enzyme of FUra, and dihydropyrimidine dehydrogenase (DPD), the rate-limiting catabolic enzyme of pyrimidines, have both been reported to be predictors of the response to FUra-based chemotherapies. Fluorouracil 208-212 thymidylate synthetase Homo sapiens 22-24 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 54-68 thymidylate synthetase Homo sapiens 183-185 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 70-74 thymidylate synthetase Homo sapiens 161-181 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 70-74 thymidylate synthetase Homo sapiens 183-185 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 161-181 15114696-2 2004 Dihydropyrimidine dehydrogenase (DPD) which catalyzes 5-fluorouracil (5-FU), thymidine phosphorylase (TP), responsible for catalyzing doxifluridine to 5-FU, and thymidylate synthase (TS) were estimated for breast cancer. Fluorouracil 151-155 thymidylate synthetase Homo sapiens 183-185 14735204-0 2004 Thymidylate synthase and methylenetetrahydrofolate reductase gene polymorphisms: relationships with 5-fluorouracil sensitivity. Fluorouracil 100-114 thymidylate synthetase Homo sapiens 0-20 14962716-2 2004 In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU. Fluorouracil 154-158 thymidylate synthetase Homo sapiens 58-78 14962716-2 2004 In vitro studies have shown that irinotecan downregulates thymidylate synthase (TS) expression in tumour cells, leading to synergy between irinotecan and 5-FU that is maximal when irinotecan is given 24 h prior to 5-FU. Fluorouracil 214-218 thymidylate synthetase Homo sapiens 58-78 15025795-0 2004 Dihydropyrimidine dehydrogenase and thymidylate synthase polymorphisms and their association with 5-fluorouracil/leucovorin chemotherapy in colorectal cancer. Fluorouracil 98-112 thymidylate synthetase Homo sapiens 36-56 15010882-2 2004 In this study we have investigated the association between the MSI status and the mRNA expression as well as the polymorphisms of the cellular target of 5-FU therapy, thymidylate synthase. Fluorouracil 153-157 thymidylate synthetase Homo sapiens 167-187 14970324-0 2004 Digital karyotyping identifies thymidylate synthase amplification as a mechanism of resistance to 5-fluorouracil in metastatic colorectal cancer patients. Fluorouracil 98-112 thymidylate synthetase Homo sapiens 31-51 14970324-4 2004 Analysis of TYMS by fluorescence in situ hybridization identified TYMS gene amplification in 23% of 31 5-FU-treated cancers, whereas no amplification was observed in metastases of patients that had not been treated with 5-FU. Fluorouracil 103-107 thymidylate synthetase Homo sapiens 66-70 14970324-6 2004 These data suggest that genetic amplification of TYMS is a major mechanism of 5-FU resistance in vivo and have important implications for the management of colorectal cancer patients with recurrent disease. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 49-53 14760062-1 2004 Thymidylate synthase (TS), the target enzyme of the fluoropyrimidine class of drugs, has a 28-bp repeat polymorphism in the promoter region that has been associated with response of tumors to 5-fluorouracil-based therapy. Fluorouracil 192-206 thymidylate synthetase Homo sapiens 0-20 14760062-1 2004 Thymidylate synthase (TS), the target enzyme of the fluoropyrimidine class of drugs, has a 28-bp repeat polymorphism in the promoter region that has been associated with response of tumors to 5-fluorouracil-based therapy. Fluorouracil 192-206 thymidylate synthetase Homo sapiens 22-24 14716816-0 2004 Correlation of thymidylate synthase, thymidine phosphorylase and dihydropyrimidine dehydrogenase with sensitivity of gastrointestinal cancer cells to 5-fluorouracil and 5-fluoro-2"-deoxyuridine. Fluorouracil 150-164 thymidylate synthetase Homo sapiens 15-35 14716816-1 2004 AIM: To determine the expression levels of three metabolic enzymes of fluoropyrimidines: thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) in seven human gastrointestinal cancer cell lines, and to compare the enzyme levels with the sensitivity to 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FdUrd). Fluorouracil 295-309 thymidylate synthetase Homo sapiens 89-109 14726200-1 2004 Thymidylate synthase (TS) is the target in colon cancer therapeutic protocols utilizing such drugs as 5-fluorouracil and raltitrexed. Fluorouracil 102-116 thymidylate synthetase Homo sapiens 0-20 14679120-1 2004 BACKGROUND: The level of the enzyme thymidylate synthase (TS) is known to inversely correlate with the clinical activity of 5-fluorouracil (FU) in advanced colorectal cancer patients. Fluorouracil 124-138 thymidylate synthetase Homo sapiens 36-56 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 21-35 thymidylate synthetase Homo sapiens 233-253 15224198-1 2004 BACKGROUND: Although 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum (cisplatin) in combination have synergistic cytotoxicity against both murine and human neoplasms, the precise mechanism of the synergism, and the effects on thymidylate synthase and its percent inhibition, and the effects on dihydropyrimidine dehydrogenase (DPD) remained to be elucidated. Fluorouracil 37-41 thymidylate synthetase Homo sapiens 233-253 14654960-0 2004 The transfection of thymidylate synthase antisense suppresses oncogenic properties of a human colon cancer cell line and augments the antitumor effect of fluorouracil. Fluorouracil 154-166 thymidylate synthetase Homo sapiens 20-40 14654960-3 2004 The aim of this study was to determine if antisense TS technology could augment the chemosensitivity of human cancer cells to 5-FU. Fluorouracil 126-130 thymidylate synthetase Homo sapiens 52-54 14654960-8 2004 The 50% inhibition values of 5-FU on DLD-1/anti-TS were approximately one forth that on parental cells. Fluorouracil 29-33 thymidylate synthetase Homo sapiens 48-50 14654960-10 2004 The tumor growth of DLD-1/anti-TS cells was suppressed significantly more than that of DLD-1 cells by the 5-FU. Fluorouracil 106-110 thymidylate synthetase Homo sapiens 31-33 14654960-11 2004 The expression and activity of TS in human colon cancer cells were effectively inhibited by TS antisense treatment and the effect of 5-FU to cancer cells can be augmented. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 31-33 15043163-3 2004 The magnitude and duration of TS inhibition following exposure of HT29 cells to FdUMP[10] at 1 x 10(-8) M was greater than that which occurred following exposure of these cells to 5FU at 1 x 10(-6) M. FdUMP[10] exposure also resulted in much more extensive DNA damage to HT29 cells than occurred following exposure to 100-fold higher concentrations of 5FU. Fluorouracil 180-183 thymidylate synthetase Homo sapiens 30-32 15539918-0 2004 Thymidylate synthase expression in normal colonic mucosa: a predictive marker of toxicity in colorectal cancer patients receiving 5-fluorouracil-based adjuvant chemotherapy. Fluorouracil 130-144 thymidylate synthetase Homo sapiens 0-20 15539918-1 2004 OBJECTIVES: We retrospectively evaluated the relevance of thymidylate synthase (TS) expression in normal colonic mucosa as a predictive factor of toxicity in colorectal cancer patients receiving adjuvant fluorouracil (5-FU)-based chemotherapy. Fluorouracil 204-216 thymidylate synthetase Homo sapiens 58-78 15539918-1 2004 OBJECTIVES: We retrospectively evaluated the relevance of thymidylate synthase (TS) expression in normal colonic mucosa as a predictive factor of toxicity in colorectal cancer patients receiving adjuvant fluorouracil (5-FU)-based chemotherapy. Fluorouracil 204-216 thymidylate synthetase Homo sapiens 80-82 15539918-2 2004 METHODS: TS expression was immunohistochemically assessed on normal colonic mucosa from 50 patients with colorectal cancer Dukes" stages B (15 patients) and C (35 patients) treated with 5-FU-based adjuvant chemotherapy. Fluorouracil 186-190 thymidylate synthetase Homo sapiens 9-11 15539918-6 2004 CONCLUSIONS: Immunohistochemical TS expression in normal colonic mucosa may represent an important predictive parameter for identifying a subset of patients with a high risk of developing severe 5-FU-related toxicities. Fluorouracil 195-199 thymidylate synthetase Homo sapiens 33-35 14716816-1 2004 AIM: To determine the expression levels of three metabolic enzymes of fluoropyrimidines: thymidylate synthase (TS), thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) in seven human gastrointestinal cancer cell lines, and to compare the enzyme levels with the sensitivity to 5-fluorouracil (5-FU) and 5-fluoro-2"-deoxyuridine (FdUrd). Fluorouracil 311-315 thymidylate synthetase Homo sapiens 89-109 14612954-1 2003 Thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) has been suggested to be sensitivity-limiting factors of 5-fluorouracil therapy in cancer patients. Fluorouracil 125-139 thymidylate synthetase Homo sapiens 0-20 13680162-1 2003 BACKGROUND/PURPOSE: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes for predicting the efficacy of 5-FU in the treatment of malignant tumors. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 62-82 13680162-1 2003 BACKGROUND/PURPOSE: Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) are key enzymes for predicting the efficacy of 5-FU in the treatment of malignant tumors. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 84-86 13680162-14 2003 Some HCC patients may be good candidates for 5-FU-based chemotherapy based on measurements of tumor levels of DPD and TS. Fluorouracil 45-49 thymidylate synthetase Homo sapiens 118-120 14576935-2 2003 In the present study, the associations among phenotypic marker expression of gastric carcinomas, tumor thymidylate synthase (TS) expression, and the chemotherapeutic response to 5-fluorouracil (5-FU) were examined. Fluorouracil 178-192 thymidylate synthetase Homo sapiens 125-127 14576935-2 2003 In the present study, the associations among phenotypic marker expression of gastric carcinomas, tumor thymidylate synthase (TS) expression, and the chemotherapeutic response to 5-fluorouracil (5-FU) were examined. Fluorouracil 194-198 thymidylate synthetase Homo sapiens 103-123 14576935-2 2003 In the present study, the associations among phenotypic marker expression of gastric carcinomas, tumor thymidylate synthase (TS) expression, and the chemotherapeutic response to 5-fluorouracil (5-FU) were examined. Fluorouracil 194-198 thymidylate synthetase Homo sapiens 125-127 14576935-12 2003 CONCLUSIONS: These results indicate that postoperative chemotherapy with 5-FU could be effective for patients with the G-phenotype tumor, since the incidence of intratumoral expression of TS, the target enzyme of 5-FU, is significantly low in G-phenotype tumors. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 188-190 14576935-12 2003 CONCLUSIONS: These results indicate that postoperative chemotherapy with 5-FU could be effective for patients with the G-phenotype tumor, since the incidence of intratumoral expression of TS, the target enzyme of 5-FU, is significantly low in G-phenotype tumors. Fluorouracil 213-217 thymidylate synthetase Homo sapiens 188-190 14519634-0 2003 Thymidylate synthase and dihydropyrimidine dehydrogenase mRNA expression levels: predictors for survival in colorectal cancer patients receiving adjuvant 5-fluorouracil. Fluorouracil 154-168 thymidylate synthetase Homo sapiens 0-20 14570375-1 2003 Although the expression of thymidylate synthase (TS) in metastatic colorectal cancer (CRC) may be a better predictor of response to 5-fluorouracil chemotherapy than TS expression in primary CRC, this enzyme has not been well studied in tumor-draining regional lymph nodes. Fluorouracil 132-146 thymidylate synthetase Homo sapiens 27-47 14570375-1 2003 Although the expression of thymidylate synthase (TS) in metastatic colorectal cancer (CRC) may be a better predictor of response to 5-fluorouracil chemotherapy than TS expression in primary CRC, this enzyme has not been well studied in tumor-draining regional lymph nodes. Fluorouracil 132-146 thymidylate synthetase Homo sapiens 49-51 14570375-9 2003 Nodal expression of TS may be important in predicting response to 5-fluorouracil when a primary CRC is TS-negative. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 20-22 14570375-9 2003 Nodal expression of TS may be important in predicting response to 5-fluorouracil when a primary CRC is TS-negative. Fluorouracil 66-80 thymidylate synthetase Homo sapiens 103-105 14522928-1 2003 The variable number of tandem repeat (VNTR) of thymidylate synthase (TS) gene, mainly 2 repeat (2R) and 3 repeat (3R), is one of the genetic variations that can potentially predict the effectiveness of 5-fluorouracil-based chemotherapy. Fluorouracil 202-216 thymidylate synthetase Homo sapiens 47-67 14522928-1 2003 The variable number of tandem repeat (VNTR) of thymidylate synthase (TS) gene, mainly 2 repeat (2R) and 3 repeat (3R), is one of the genetic variations that can potentially predict the effectiveness of 5-fluorouracil-based chemotherapy. Fluorouracil 202-216 thymidylate synthetase Homo sapiens 69-71 14522928-12 2003 These results suggest that the double polymorphism in the TS tandem repeat sequence, the SNP and the VNTR, may provide a potential for more effective prediction of the clinical outcome of 5-fluorouracil-based chemotherapy. Fluorouracil 188-202 thymidylate synthetase Homo sapiens 58-60 12948860-4 2003 5-Fluorouracil is known to inhibit thymidylate synthase (TS), a key enzyme that transfers a methyl group from 5,10-methylene-tetrahydrofolate to dUMP during nucleotide biosynthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 35-55 12948860-4 2003 5-Fluorouracil is known to inhibit thymidylate synthase (TS), a key enzyme that transfers a methyl group from 5,10-methylene-tetrahydrofolate to dUMP during nucleotide biosynthesis. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 57-59 12948860-7 2003 In contrast, 5-fluorouracil inhibited TS activity by >90% but increased TS protein levels. Fluorouracil 13-27 thymidylate synthetase Homo sapiens 38-40 12948860-7 2003 In contrast, 5-fluorouracil inhibited TS activity by >90% but increased TS protein levels. Fluorouracil 13-27 thymidylate synthetase Homo sapiens 75-77 12948860-11 2003 These results suggest that synergy between methionine restriction and 5-fluorouracil is attributable to multiple factors, including depletion of reduced folates, selective inhibition of TS, and creation of an imbalanced nucleotide pool. Fluorouracil 70-84 thymidylate synthetase Homo sapiens 186-188 12845668-0 2003 Overexpression of thymidylate synthase mediates desensitization for 5-fluorouracil of tumor cells. Fluorouracil 68-82 thymidylate synthetase Homo sapiens 18-38 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 125-139 thymidylate synthetase Homo sapiens 84-86 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 125-139 thymidylate synthetase Homo sapiens 112-114 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 141-145 thymidylate synthetase Homo sapiens 84-86 12845668-2 2003 It has been suggested that the poor prognosis is partly due to a low sensitivity of TS-overexpressing tumors to TS-targeting 5-fluorouracil (5-FU). Fluorouracil 141-145 thymidylate synthetase Homo sapiens 112-114 12845668-3 2003 To investigate the relationship between TS expression and sensitivity to 5-FU, we used the TS-overexpressing cervical cancer cell line SKG-II/TS and SKG-I/TS that had been established by TS gene transfer. Fluorouracil 73-77 thymidylate synthetase Homo sapiens 40-42 12845668-4 2003 The 50% growth inhibitory concentration (IC(50)) of 5-FU for SKG-II/TS was 24 +/- 6.0 microM, which was 6 times as high as that for the control (4.0 +/- 1.1 microM), showing significantly decreased sensitivity to 5-FU (p < 0.01). Fluorouracil 52-56 thymidylate synthetase Homo sapiens 68-70 12845668-5 2003 The IC(50) of 5-FU for SKG-I/TS was 90 +/- 15 microM, which was over 2 times as high as that for the control (40 +/- 0.6 microM), showing significantly decreased sensitivity to 5-FU (p < 0.05). Fluorouracil 14-18 thymidylate synthetase Homo sapiens 29-31 12845668-5 2003 The IC(50) of 5-FU for SKG-I/TS was 90 +/- 15 microM, which was over 2 times as high as that for the control (40 +/- 0.6 microM), showing significantly decreased sensitivity to 5-FU (p < 0.05). Fluorouracil 177-181 thymidylate synthetase Homo sapiens 29-31 12845668-6 2003 Thus, TS-overexpressing tumors have decreased sensitivity to 5-FU, which may be one of the factors that determine the prognosis of these tumors. Fluorouracil 61-65 thymidylate synthetase Homo sapiens 6-8 12707718-11 2003 Thymidylate synthase ternary complex formation was demonstrated in bone marrow mononuclear cells isolated 24 h after the first oral 5-FU dose; the average was 66.5% bound. Fluorouracil 132-136 thymidylate synthetase Homo sapiens 0-20 12819937-3 2003 5-Fluorouracil (5-FU) was synthesized in 1957 and represents the first class of antineoplastic agents to be developed as inhibitors of TS. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 135-137 12819937-3 2003 5-Fluorouracil (5-FU) was synthesized in 1957 and represents the first class of antineoplastic agents to be developed as inhibitors of TS. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 135-137 14519641-10 2003 This difference in survival among patients with low- and high-TS-expressing tumors became more significant when the analysis was restricted to the 73 patients receiving 5-FU-based adjuvant therapy (RR = 0.37; 95% CI = 0.16-0.86; P = 0.0006). Fluorouracil 169-173 thymidylate synthetase Homo sapiens 62-64 12883718-2 2003 Thymidylate synthase (TS) is inhibited to form an inactive ternary complex by 5-fluoro-dUMP and is considered to be a target enzyme of 5-FU treatment. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 0-20 12883718-2 2003 Thymidylate synthase (TS) is inhibited to form an inactive ternary complex by 5-fluoro-dUMP and is considered to be a target enzyme of 5-FU treatment. Fluorouracil 135-139 thymidylate synthetase Homo sapiens 22-24 12883718-3 2003 Two enzymes, DPD and TS, have been reported to be major determinants of individual sensitivity to 5-FU, and it has been reported that TS mRNA levels are modified by 5-FU treatment. Fluorouracil 98-102 thymidylate synthetase Homo sapiens 21-23 12883718-3 2003 Two enzymes, DPD and TS, have been reported to be major determinants of individual sensitivity to 5-FU, and it has been reported that TS mRNA levels are modified by 5-FU treatment. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 134-136 12883718-6 2003 Furthermore inter-individual variations of TS mRNA levels after 5-FU treatment were found, and the individual TS induction varied between patients (0.2-2.4). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 43-45 12883718-12 2003 These findings suggest that TS mRNA was induced by 5-FU treatment, and the overall induction level varied between individuals. Fluorouracil 51-55 thymidylate synthetase Homo sapiens 28-30 12883718-13 2003 Therefore, the estimation of TS mRNA induction may be useful to predict the efficacy of 5-FU treatment. Fluorouracil 88-92 thymidylate synthetase Homo sapiens 29-31 14519634-2 2003 In this study, we determined the prognostic value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression in colorectal cancer patients treated with adjuvant 5-FU. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 53-73 14519634-2 2003 In this study, we determined the prognostic value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) expression in colorectal cancer patients treated with adjuvant 5-FU. Fluorouracil 184-188 thymidylate synthetase Homo sapiens 75-77 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 68-70 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 107-109 14519634-7 2003 Among the patients receiving adjuvant 5-FU therapy, those with high TS survived longer than those with low TS, and in each TS subgroup, the ones with low DPD survived longer than the ones with high DPD levels. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 107-109 14519634-9 2003 CONCLUSIONS: This suggests that TS and DPD quantitation may be helpful to evaluate prognosis of patients receiving adjuvant 5-FU and that patients with high TS and low DPD may benefit from adjuvant 5-FU chemotherapy. Fluorouracil 198-202 thymidylate synthetase Homo sapiens 157-159 14519641-0 2003 Thymidylate synthase expression predicts the response to 5-fluorouracil-based adjuvant therapy in pancreatic cancer. Fluorouracil 57-71 thymidylate synthetase Homo sapiens 0-20 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 60-74 thymidylate synthetase Homo sapiens 9-29 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 60-74 thymidylate synthetase Homo sapiens 31-33 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 76-80 thymidylate synthetase Homo sapiens 9-29 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 76-80 thymidylate synthetase Homo sapiens 31-33 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 9-29 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 31-33 14519641-1 2003 PURPOSE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and TS expression may determine clinical response and survival after therapy with 5-FU in colorectal cancer. Fluorouracil 165-169 thymidylate synthetase Homo sapiens 87-89 12802789-1 2003 Thymidylate synthase (TS) is a chemotherapeutic target for the fluoropyrimidine 5-fluorouracil (5-FU) and antifolate tomudex (TDX). Fluorouracil 96-100 thymidylate synthetase Homo sapiens 0-20 12870370-0 2003 Intratumoural thymidylate synthase and dihydropyrimidine dehydrogenase activities are good predictors of 5-fluorouracil sensitivity in colorectal cancer. Fluorouracil 105-119 thymidylate synthetase Homo sapiens 14-34 12684658-2 2003 Overexpression of TS has been correlated to 5-fluorouracil (5FU)-resistance. Fluorouracil 44-58 thymidylate synthetase Homo sapiens 18-20 12684658-2 2003 Overexpression of TS has been correlated to 5-fluorouracil (5FU)-resistance. Fluorouracil 60-63 thymidylate synthetase Homo sapiens 18-20 12870370-3 2003 The activities of TS and DPD were significantly lower in the tumours sensitive to 5-FU compared with those that were not sensitive to 5-FU. Fluorouracil 82-86 thymidylate synthetase Homo sapiens 18-20 12870370-3 2003 The activities of TS and DPD were significantly lower in the tumours sensitive to 5-FU compared with those that were not sensitive to 5-FU. Fluorouracil 134-138 thymidylate synthetase Homo sapiens 18-20 12870370-6 2003 Tumour sensitivity to 5-FU can be more precisely predicted by taking the activities of both TS and DPD into consideration than by using either alone. Fluorouracil 22-26 thymidylate synthetase Homo sapiens 92-94 12720098-8 2003 RESULTS: 5-FU sensitivity was high in the low-TS-activity group and in the high-OPRT-activity group. Fluorouracil 9-13 thymidylate synthetase Homo sapiens 5-7 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 78-98 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 100-102 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 78-98 12649104-2 2003 Phase II trials have shown that gemcitabine can be successfully combined with thymidylate synthase (TS) inhibitors such as continuous-infusion 5-fluorouracil (5-FU). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 100-102 12684419-2 2003 5-FU inhibits thymidylate synthase (TS) and blocks DNA synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 14-34 12684419-2 2003 5-FU inhibits thymidylate synthase (TS) and blocks DNA synthesis. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 36-38 12684419-5 2003 We investigated the activity of TS in 68 RCCs and the association with dihydropyrimidine dehydrogenase (DPD) activities, which is a principal enzyme in the degradation of 5-FU and pyrimidine nucleotides. Fluorouracil 171-175 thymidylate synthetase Homo sapiens 32-34 12684419-7 2003 EXPERIMENTAL DESIGN: The levels of TS and DPD activities in nonfixed fresh-frozen RCC and normal kidney were determined biochemically by the 5-fluoro-2"-deoxyuridine 5"-monophosphate binding assay and the 5-FU degradation assay, respectively. Fluorouracil 205-209 thymidylate synthetase Homo sapiens 35-37 12684419-17 2003 TS activity in primary cultured RCC cells was positively correlated with their sensitivity to 5-FU. Fluorouracil 94-98 thymidylate synthetase Homo sapiens 0-2 12684419-18 2003 Furthermore, RCC cells with both high TS activity and low DPD activity were more sensitive to 5-FU, compared with those with either low TS activity or high DPD activity. Fluorouracil 94-98 thymidylate synthetase Homo sapiens 38-40 12684419-19 2003 CONCLUSIONS: The present study is the first study to demonstrate that the level of TS activity was correlated with both the progression of the stage and the increase of the grade of RCC, and that higher TS activity in primary cultured RCC predicted higher sensitivity to 5-FU. Fluorouracil 271-275 thymidylate synthetase Homo sapiens 203-205 12684419-20 2003 These results suggest that high TS activity may be associated with malignant potential of RCC, and that it may be possible to use 5-FU for RCC with high TS activity. Fluorouracil 130-134 thymidylate synthetase Homo sapiens 153-155 12720098-0 2003 Relationships between the expression of thymidylate synthase, dihydropyrimidine dehydrogenase, and orotate phosphoribosyltransferase and cell proliferative activity and 5-fluorouracil sensitivity in colorectal carcinoma. Fluorouracil 169-183 thymidylate synthetase Homo sapiens 40-60 12569298-2 2003 The cytotoxic activity of the metabolized 5-FU depends on thymidylate synthase (TS) inhibition, leading to defective DNA synthesis. Fluorouracil 42-46 thymidylate synthetase Homo sapiens 58-78 12488549-8 2003 Treatment of H630-C6 cells with 5-FU, FUrd, FUdR, TFT, AG331, AG337, ZD1694, and methotrexate up-regulated TS levels as determined by Western blot analysis, although TS mRNA levels remained unchanged as determined by reverse transcription-polymerase chain reaction. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 107-109 12488549-8 2003 Treatment of H630-C6 cells with 5-FU, FUrd, FUdR, TFT, AG331, AG337, ZD1694, and methotrexate up-regulated TS levels as determined by Western blot analysis, although TS mRNA levels remained unchanged as determined by reverse transcription-polymerase chain reaction. Fluorouracil 32-36 thymidylate synthetase Homo sapiens 166-168 12739060-10 2003 In a biopsy of an esophageal adenocarcinoma metastasis that had regressed, thymidylate synthase, the target of 5-FU, was inhibited 50%, but increased four- to tenfold after relapse in subsequent biopsies. Fluorouracil 111-115 thymidylate synthetase Homo sapiens 75-95 12610179-1 2003 PURPOSE: The aim of this study was to investigate the utility of quantitating thymidylate synthase (TS) in the primary tumor as a surrogate for metastatic disease sites to predict the likelihood of response and outcome to fluorouracil (FU) treatment in patients with metastatic colorectal cancer. Fluorouracil 222-234 thymidylate synthetase Homo sapiens 78-98 12610179-1 2003 PURPOSE: The aim of this study was to investigate the utility of quantitating thymidylate synthase (TS) in the primary tumor as a surrogate for metastatic disease sites to predict the likelihood of response and outcome to fluorouracil (FU) treatment in patients with metastatic colorectal cancer. Fluorouracil 222-234 thymidylate synthetase Homo sapiens 100-102 12536082-3 2003 Both dThdPase and TS levels seemed to be related to response to 5-fluorouracil (5-FU) therapy in different types of human solid tumors. Fluorouracil 64-78 thymidylate synthetase Homo sapiens 18-20 12536082-3 2003 Both dThdPase and TS levels seemed to be related to response to 5-fluorouracil (5-FU) therapy in different types of human solid tumors. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 18-20 12536082-7 2003 These imply that immunohistochemical analysis of dThdPase and TS is available for selection of patients who will be received 5-FU based chemotherapy. Fluorouracil 125-129 thymidylate synthetase Homo sapiens 62-64 12469154-2 2003 On the other hand, variability of 5-FU sensitivity of the tumors is also presumed to depend on the enzymes of 5-FU metabolism (e.g. dihydropyrimidine dehydrogenase; DPD, rate limiting enzyme of catabolism) and action target (e.g. thymidylate synthase; TS). Fluorouracil 34-38 thymidylate synthetase Homo sapiens 230-250 12469154-2 2003 On the other hand, variability of 5-FU sensitivity of the tumors is also presumed to depend on the enzymes of 5-FU metabolism (e.g. dihydropyrimidine dehydrogenase; DPD, rate limiting enzyme of catabolism) and action target (e.g. thymidylate synthase; TS). Fluorouracil 110-114 thymidylate synthetase Homo sapiens 230-250 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 41-55 thymidylate synthetase Homo sapiens 132-134 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 57-61 thymidylate synthetase Homo sapiens 132-134 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 132-134 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 110-130 12616366-3 2003 METHODS: To predict tumor sensitivity to 5-fluorouracil (5-FU) in thymoma, we investigated the mRNA levels of thymidylate synthase (TS), the key enzyme that catalyzes the methylation of deoxyuridine monophosphate, and correlates with the resistance of 5-FU and dihydropyrimidine dehydrogenase (DPD), which degrades 5-FU in thymoma. Fluorouracil 252-256 thymidylate synthetase Homo sapiens 132-134 12616366-8 2003 CONCLUSIONS: The combined use of measurements of TS and DPD mRNA levels using real-time RT-PCR analyses may provide an indication of the selective cytoxicity of 5-FU on thymoma. Fluorouracil 161-165 thymidylate synthetase Homo sapiens 49-51 12482336-0 2002 Combination of 5-fluorouracil and irinotecan on modulation of thymidylate synthase and topoisomerase I expression and cell cycle regulation in human colon cancer LoVo cells: clinical relevance. Fluorouracil 15-29 thymidylate synthetase Homo sapiens 62-82 12453856-0 2002 Thymidylate synthase protein expression in colorectal cancer metastases predicts for clinical outcome to leucovorin-modulated bolus or infusional 5-fluorouracil but not methotrexate-modulated bolus 5-fluorouracil. Fluorouracil 146-160 thymidylate synthetase Homo sapiens 0-20 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 22-36 thymidylate synthetase Homo sapiens 182-202 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 22-36 thymidylate synthetase Homo sapiens 204-206 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 182-202 12453856-1 2002 BACKGROUND: Different 5-fluorouracil (5-FU) schedules and/or biochemical modulators may result in different mechanisms of cytotoxicity, potentially affecting the correlation between thymidylate synthase (TS) expression and the clinical response to the fluoropyrimidine. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 204-206 12453856-6 2002 CONCLUSIONS: The correlation between intratumoral TS levels and the clinical response to 5-FU depends strongly on the schedule of administration/biochemical modulators that are used in different 5-FU regimens. Fluorouracil 89-93 thymidylate synthetase Homo sapiens 50-52 12453856-6 2002 CONCLUSIONS: The correlation between intratumoral TS levels and the clinical response to 5-FU depends strongly on the schedule of administration/biochemical modulators that are used in different 5-FU regimens. Fluorouracil 195-199 thymidylate synthetase Homo sapiens 50-52 12451472-1 2002 PURPOSE: Combinations of vinorelbine (VRB) and drugs targeting thymidylate synthase (TS) such as 5-fluorouracil (5-FU) have proven clinical efficacy in the management of advanced breast cancer. Fluorouracil 97-111 thymidylate synthetase Homo sapiens 63-83 12451472-1 2002 PURPOSE: Combinations of vinorelbine (VRB) and drugs targeting thymidylate synthase (TS) such as 5-fluorouracil (5-FU) have proven clinical efficacy in the management of advanced breast cancer. Fluorouracil 113-117 thymidylate synthetase Homo sapiens 63-83 12457437-13 2002 Future advances in the effective use of TS inhibitors may be forthcoming in the form of improved dosing, fewer untoward effects and increased tumour selectivity with novel fluorouracil prodrug formulations. Fluorouracil 172-184 thymidylate synthetase Homo sapiens 40-42 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 62-76 thymidylate synthetase Homo sapiens 11-31 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 62-76 thymidylate synthetase Homo sapiens 33-35 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 11-31 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 78-82 thymidylate synthetase Homo sapiens 33-35 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 164-178 thymidylate synthetase Homo sapiens 11-31 12464897-1 2002 OBJECTIVE: Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU), and dihydropyrimidine dehydrogenase (DPD) is the first enzyme that metabolizes 5-fluorouracil. Fluorouracil 164-178 thymidylate synthetase Homo sapiens 33-35 12439919-15 2002 CONCLUSION: The continuous exposure of Bel(7402) cells to 5-FU led to overexpression of TS and MRP, as well as increased intracellular GSH content and total GST activity. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 88-90 12482336-7 2002 The TS expression was decreased following 24 hours of 5-FU and it remained at reduced levels for > 24 hours after removal of 5-FU. Fluorouracil 54-58 thymidylate synthetase Homo sapiens 4-6 12482336-7 2002 The TS expression was decreased following 24 hours of 5-FU and it remained at reduced levels for > 24 hours after removal of 5-FU. Fluorouracil 128-132 thymidylate synthetase Homo sapiens 4-6 12437479-3 2002 There is compelling evidence that TS gene transcripts and TS polymorphisms could be used to decide which patients can best benefit from adjuvant chemotherapy approaches, especially in colorectal cancer, and not less importantly, to tailor chemotherapy in metastatic NSCLC when using drugs akin to fluorouracil, such as pemetrexed. Fluorouracil 297-309 thymidylate synthetase Homo sapiens 34-36 12353234-4 2002 The antitumor effect of 5FU is enhanced by augmenting 5-fluorodeoxyuridine monophosphate (FdUMP) converted from FUMP, which inhibits thymidylate synthetase (TS). Fluorouracil 24-27 thymidylate synthetase Homo sapiens 133-155 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 122-136 thymidylate synthetase Homo sapiens 37-39 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 122-136 thymidylate synthetase Homo sapiens 180-182 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 138-142 thymidylate synthetase Homo sapiens 37-39 12460463-2 2002 The repeat length is associated with TS protein expression, which suggests that we may be able to predict the efficacy of 5-fluorouracil (5-FU)-based chemotherapy from a patient"s TS genotype determined through analysis of normal tissue obtained non-invasively. Fluorouracil 138-142 thymidylate synthetase Homo sapiens 180-182 12422306-1 2002 In the last 50 years, 5-fluorouracil-based therapy has been the mainstay of adjuvant and palliative treatment for colorectal cancer but response rates and median survival have been dismal despite the introduction of thymidylate synthase modulators such as leucovorin. Fluorouracil 22-36 thymidylate synthetase Homo sapiens 216-236 12487851-1 2002 OBJECTIVE: To study target killing of 5-FU drug-fast cancer cells with thymidylate synthase (TS) and p16 gene promoters inducting TK gene expression. Fluorouracil 38-42 thymidylate synthetase Homo sapiens 71-91 12116375-2 2002 Thymidylate synthase expression was tested in vitro, in vivo, and clinically as a prognostic factor for 5-fluorouracil (5FU) sensitivity. Fluorouracil 104-118 thymidylate synthetase Homo sapiens 0-20 12147691-1 2002 Thymidylate synthase (TS) catalyzes methylation of dUMP to dTMP and is the target of cancer chemotherapeutic agents (e.g. 5-fluorouracil). Fluorouracil 122-136 thymidylate synthetase Homo sapiens 0-20 12147691-1 2002 Thymidylate synthase (TS) catalyzes methylation of dUMP to dTMP and is the target of cancer chemotherapeutic agents (e.g. 5-fluorouracil). Fluorouracil 122-136 thymidylate synthetase Homo sapiens 22-24 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 0-20 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 48-62 thymidylate synthetase Homo sapiens 22-24 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 0-20 12530000-1 2002 Thymidylate synthase (TS) is a target enzyme of 5-fluorouracil (5-FU). Fluorouracil 64-68 thymidylate synthetase Homo sapiens 22-24 12530000-3 2002 TS polymorphism has been reported to link with the efficacy of 5-FU-based chemotherapy in colorectal cancer. Fluorouracil 63-67 thymidylate synthetase Homo sapiens 0-2 12530000-12 2002 These results warrant further large-scale clinical study of the role of the TS genotyping for the prediction of efficacy using 5-FU-based chemotherapy and prognosis in gastric cancer. Fluorouracil 127-131 thymidylate synthetase Homo sapiens 76-78 12703544-13 2002 The antitumor effect of 5FU is enhanced by augmenting 5-fluorodeoxyuridine monophosphate (FdUMP) converted from FUMP, which inhibits Thymidylate Synthetase (TS). Fluorouracil 24-27 thymidylate synthetase Homo sapiens 133-155 12183426-10 2002 We hypothesize that potentiation of FUra cytotoxicity by rMETase may result from increased inhibition of thymidylate synthase, together with DNA hypomethylation and enhanced DNA repair that could be involved in cell responses to drug-induced damage. Fluorouracil 36-40 thymidylate synthetase Homo sapiens 105-125 12102601-2 2002 As a consequence, TS is a target for anticancer chemotherapy by several drugs, including 5-fluorouracil (5-FU) and raltitrexed (Tomudex), in treatment of colorectal and other tumors. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 18-20 12102601-2 2002 As a consequence, TS is a target for anticancer chemotherapy by several drugs, including 5-fluorouracil (5-FU) and raltitrexed (Tomudex), in treatment of colorectal and other tumors. Fluorouracil 105-109 thymidylate synthetase Homo sapiens 18-20 12102601-7 2002 These studies have revealed that targeting the 3" end of human TS mRNA downregulates TS mRNA and protein, inhibits cell proliferation, and sensitizes HeLa cells to raltitrexed, 5-FU, and 5-fluorodeoxyuridine (5-FUdR) in vitro (Ferguson et al., Br. Fluorouracil 177-181 thymidylate synthetase Homo sapiens 63-65 12118326-3 2002 In vitro studies have demonstrated that the resistance to 5-FU is correlated with increased activity of thymidylate synthase (TS), whose gene has a E2F binding site in its promoter region. Fluorouracil 58-62 thymidylate synthetase Homo sapiens 104-124 12084458-14 2002 We have also generated mutants of both DHFR and TS that confer resistance to MTX as well as 5-FU by random as well as site-directed mutagenesis. Fluorouracil 92-96 thymidylate synthetase Homo sapiens 48-50 12084461-0 2002 Induction of thymidylate synthase as a 5-fluorouracil resistance mechanism. Fluorouracil 39-53 thymidylate synthetase Homo sapiens 13-33 12084461-2 2002 TS is an important target for chemotherapy; it is inhibited by folate and nucleotide analogs, such as by 5-fluoro-dUMP (FdUMP), the active metabolite of 5-fluorouracil (5FU). Fluorouracil 153-167 thymidylate synthetase Homo sapiens 0-2 12084461-2 2002 TS is an important target for chemotherapy; it is inhibited by folate and nucleotide analogs, such as by 5-fluoro-dUMP (FdUMP), the active metabolite of 5-fluorouracil (5FU). Fluorouracil 169-172 thymidylate synthetase Homo sapiens 0-2 12084461-13 2002 Treatment with 5FU or RTX rapidly induced TS levels two- to five-fold. Fluorouracil 15-18 thymidylate synthetase Homo sapiens 42-44 12090040-1 2002 Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) in cancer are considered to play key roles in the sensitivity to 5-FU-based chemotherapy. Fluorouracil 133-137 thymidylate synthetase Homo sapiens 42-62 12085207-0 2002 Expression of multidrug resistance-associated protein1,P-glycoprotein, and thymidylate synthase in gastric cancer patients treated with 5-fluorouracil and doxorubicin-based adjuvant chemotherapy after curative resection. Fluorouracil 136-150 thymidylate synthetase Homo sapiens 75-95 12085207-2 2002 In a variety of malignancies, high expression of multidrug resistance-associated protein1 and P-glycoprotein has been associated with resistance to doxorubicin, whereas 5-fluorouracil resistance has correlated with the level of thymidylate synthase expression. Fluorouracil 169-183 thymidylate synthetase Homo sapiens 228-248 11980662-0 2002 The role of thymidylate synthase induction in modulating p53-regulated gene expression in response to 5-fluorouracil and antifolates. Fluorouracil 102-116 thymidylate synthetase Homo sapiens 12-32 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 0-20 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 83-97 thymidylate synthetase Homo sapiens 22-24 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 0-20 11980662-1 2002 Thymidylate synthase (TS) is a critical target for chemotherapeutic agents such as 5-fluorouracil (5-FU) and antifolates such as tomudex (TDX),multitargeted antifolate, and ZD9331. Fluorouracil 99-103 thymidylate synthetase Homo sapiens 22-24 12084458-7 2002 Studies thus far involving colorectal tumors obtained from patients have focused predominantly on the predictive value of levels of TS expression and p53 mutations in determining response to 5-FU. Fluorouracil 191-195 thymidylate synthetase Homo sapiens 132-134 12067974-1 2002 Thymidylate synthase (TS) is a key enzyme in folate metabolism and the primary target of 5-fluorouracil. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 0-20 12067974-1 2002 Thymidylate synthase (TS) is a key enzyme in folate metabolism and the primary target of 5-fluorouracil. Fluorouracil 89-103 thymidylate synthetase Homo sapiens 22-24 12116375-2 2002 Thymidylate synthase expression was tested in vitro, in vivo, and clinically as a prognostic factor for 5-fluorouracil (5FU) sensitivity. Fluorouracil 120-123 thymidylate synthetase Homo sapiens 0-20 11953901-0 2002 Thymidylate synthase polymorphism and survival of colorectal cancer patients treated with 5-fluorouracil. Fluorouracil 90-104 thymidylate synthetase Homo sapiens 0-20 12022983-2 2002 High levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been associated with resistance to 5-FU in advanced colorectal cancer. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 15-35 12022983-2 2002 High levels of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) have been associated with resistance to 5-FU in advanced colorectal cancer. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 37-39 12022983-3 2002 The aim of this study was to investigate the association of TS and DPD mRNA levels with recurrence-free survival in patients with colorectal cancer who are receiving adjuvant 5-FU-based chemotherapy. Fluorouracil 175-179 thymidylate synthetase Homo sapiens 60-62 12022983-8 2002 The TS mRNA level may be a useful marker to predict the time to recurrence in patients with colorectal cancer who are receiving adjuvant 5-FU treatment. Fluorouracil 137-141 thymidylate synthetase Homo sapiens 4-6 12052139-1 2002 Folate metabolism is the target of two major drug groups: folate antagonists (e.g., methotrexate) and thymidylate synthase inhibitors (for example, 5-fluorouracil). Fluorouracil 148-162 thymidylate synthetase Homo sapiens 102-122 11919227-0 2002 Thymidylate synthase expression in colorectal cancer: a prognostic and predictive marker of benefit from adjuvant fluorouracil-based chemotherapy. Fluorouracil 114-126 thymidylate synthetase Homo sapiens 0-20 11919227-8 2002 The study indicates that patients with high TS levels may benefit from adjuvant 5-FU-based chemotherapy. Fluorouracil 80-84 thymidylate synthetase Homo sapiens 44-46 12014648-0 2002 Roles of thymidylate synthase and dihydropyrimidine dehydrogenase in tumor progression and sensitivity to 5-fluorouracil in human gastric cancer. Fluorouracil 106-120 thymidylate synthetase Homo sapiens 9-29 12023789-6 2002 5-FU is equally interesting because it permits investigation of thymidylate synthase (TS) levels as a genetic target for predicting response and survival. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 64-84 12023789-6 2002 5-FU is equally interesting because it permits investigation of thymidylate synthase (TS) levels as a genetic target for predicting response and survival. Fluorouracil 0-4 thymidylate synthetase Homo sapiens 86-88 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 150-164 thymidylate synthetase Homo sapiens 46-48 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 166-170 thymidylate synthetase Homo sapiens 24-44 12014648-1 2002 BACKGROUND: The role of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) enzyme activities in tumor progression and sensitivity to 5-fluorouracil (5-FU) were evaluated. Fluorouracil 166-170 thymidylate synthetase Homo sapiens 46-48 11872345-13 2002 These results suggest that high TS levels in resected metastases of colorectal cancer are associated with a poor outcome after surgery and 5-FU adjuvant therapy; therefore, a prospective assessment of TS levels in resected colorectal metastases could be useful to define which patients will most likely benefit from 5-FU adjuvant therapy after metastasectomy. Fluorouracil 139-143 thymidylate synthetase Homo sapiens 32-34 12017314-6 2002 Furthermore, neoadjuvant chemotherapy using the 5-fluorouracil derivative UFT demonstrates a stronger suppression of increased activities of thymidylate synthase in the tumorous tissues than in the non-tumorous mucosa. Fluorouracil 48-62 thymidylate synthetase Homo sapiens 141-161 11836594-5 2002 The levels of TS and DPD activities in non-fixed fresh frozen bladder cancer specimens were determined biochemically by the 5-fluoro-2"-deoxyuridine 5"-monophosphate binding assay and the 5-fluorouracil degradation assay, respectively. Fluorouracil 188-202 thymidylate synthetase Homo sapiens 14-16 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 0-20 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 143-157 thymidylate synthetase Homo sapiens 22-24 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 0-20 12027413-1 2002 Thymidylate Synthase (TS) is a rate-limiting enzyme in the DNA synthetic pathway and represents the cellular target of the antimetabolite drug 5-fluorouracil (FUra). Fluorouracil 159-163 thymidylate synthetase Homo sapiens 22-24 12027413-3 2002 In particular, five recent studies have consistently demonstrated an inverse correlation between the level of TS gene or protein expression measured in colorectal cancer metastases and the clinical response to either FUra or 5-fluorodeoxyuridine (FUdR). Fluorouracil 217-221 thymidylate synthetase Homo sapiens 110-112 12027413-7 2002 In this review preclinical and clinical data supporting the use of TS quantitation to predict for the clinical response to FUra will be described and unresolved problems including assays standardization, response prediction based on TS levels measured in primary tumors, intrapatient variations in TS levels and biological/biochemical limitations of this strategy will be discussed. Fluorouracil 123-127 thymidylate synthetase Homo sapiens 67-69 11862424-9 2002 The cytotoxicity of FUra alone or in combination with MCLR, but not that of PPIs alone, was abrogated almost completely by exogenous thymidine (dThd), suggesting that inhibition of thymidylate synthetase (TS) is the growth-limiting event in the cytotoxic action of FUra even in combination with MCLR. Fluorouracil 20-24 thymidylate synthetase Homo sapiens 181-203 12450420-3 2002 As the first TS inhibitor in clinical use, 5-fluorouracil (5-FU) remains widely used for the treatment of colorectal, pancreatic, breast, head and neck, gastric, and ovarian cancers. Fluorouracil 43-57 thymidylate synthetase Homo sapiens 13-15 12450420-3 2002 As the first TS inhibitor in clinical use, 5-fluorouracil (5-FU) remains widely used for the treatment of colorectal, pancreatic, breast, head and neck, gastric, and ovarian cancers. Fluorouracil 59-63 thymidylate synthetase Homo sapiens 13-15 11914638-8 2002 Dipyridamole and p-nitrobenzylthioinosine (NBMPR), potent inhibitors of equilibrative nucleoside transport, synergized with NB1011 selectively against 5-fluorouracil (5-FU)-resistant H630R10 colon carcinoma cells [combination index (CI)=0.75 and 0.35] and Tomudex-resistant MCF7TDX breast carcinoma cells (CI=0.51 and 0.57), both TS overexpressing cell lines. Fluorouracil 151-165 thymidylate synthetase Homo sapiens 330-332 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 69-89 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 0-14 thymidylate synthetase Homo sapiens 91-93 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 69-89 11801545-1 2002 5-Fluorouracil (5-FU) exerts cytotoxic effects through inhibition of thymidylate synthase (TS) and incorporation of metabolites into RNA. Fluorouracil 16-20 thymidylate synthetase Homo sapiens 91-93 11801545-2 2002 TS inhibition may be greater for infusional 5-FU, with bolus regimens more likely to cause RNA effects. Fluorouracil 44-48 thymidylate synthetase Homo sapiens 0-2 11801545-11 2002 Thus, both 5-FU regimens inhibit TS, and prolonged TS inhibition is achieved by CI 5-FU without significant toxicity. Fluorouracil 83-87 thymidylate synthetase Homo sapiens 51-53 12018454-1 2002 Thymidylate synthase is a target enzyme for chemotherapeutic agents such as 5-fluorouracil and capecitabine, its oral prodrug. Fluorouracil 76-90 thymidylate synthetase Homo sapiens 0-20