S-1 as a core anticancer fluoropyrimidine agent.
Sendai, Japan. In Expert Opin Drug Deliv, 2012
AREAS COVERED: S-1 is an FT-based oral 5-FU prodrug in combination with a DPD inhibitor (CDHP) and an OPRT inhibitor (Oxo), which exerts the following effects: i) maintaining normal gut immunity, Oxo can decrease GI toxicities of 5-FU; ii) sustaining high plasma 5-FU concentrations, Cmax of FBAL after S-1 administration is extremely low, which dramatically decreases adverse reactions such as HFS, neurotoxicities and cardiotoxicities; iii) plasma 5-FU concentrations vary less extensively after S-1 administration and iv) S-1 can be safely administered to patients with DPD deficiency.
Pharmacogenetic analyses of a phase III trial in metastatic gastroesophageal adenocarcinoma with fluorouracil and leucovorin plus either oxaliplatin or cisplatin: a study of the arbeitsgemeinschaft internistische onkologie.
Dresden, Germany. In J Clin Oncol, 2009
Polymorphisms within genes of TS, MTHFR, MTR, OPRT, XPD, ERCC1, XRCC1, XPA, GSTP1, GSTT1, and GSTM1 were genotyped using polymerase chain reaction-based techniques.
Challenges in predicting the clinical outcome in S-1-based chemotherapy for gastric cancer patients.
Saitama, Japan. In Int J Clin Oncol, 2008
In this review, the role of the "candidate" genetic factors affecting the therapeutic efficacy of S-1 is discussed with a special emphasis on polymorphism and gene expressions involved in the S-1 metabolic pathway, including CYP2A6, thymidylate synthase, thymidine phosphorylase, and orotate phosphoribosyltransferase. The predictive values of these candidates might be overcome with drugs combined with S-1.
Molecular-based choice of cancer therapy: realities and expectations.
Saint Petersburg, Russia. In Clin Chim Acta, 2007
Other predictive markers have been identified both for cytotoxic and for targeted therapies, and include, for example, expression of TS, TP, DPD, OPRT, ERCC1, MGMT, TOP2A, class III beta-tubulin molecules as well as genomic alterations of EGFR, KIT, ABL oncogenes.
Genetic factors influencing pyrimidine-antagonist chemotherapy.
Meppel, Netherlands. In Pharmacogenomics J, 2004
Germline polymorphisms of uridine monophosphate kinase (UMPK), orotate phosphoribosyl transferase (OPRT), thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD) and methylene tetrahydrofolate reductase (MTHFR) and gene expression levels of OPRT, UMPK, TS, DPD, uridine phosphorylase, uridine kinase, thymidine phosphorylase, thymidine kinase, deoxyuridine triphosphate nucleotide hydrolase are discussed in relation to 5-FU efficacy.