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• W7208726 startingPage "37" @default.
• W7208726 abstract "The sensitivity of many, but not all, human carcinoma cell lines to 5-fluorouracil (5-FU) is substantially increased by exposure of cells to 0.3–10 µM concentrations of reduced folates. The synergism is due to an enhanced kinetic trapping of thymidylate synthase (TS) in an inactive ternary complex, which, although covalent, is in dynamic equilibrium with unbound, active enzyme. Several factors interact to prevent or reverse complete inhibition of TS by fluoropyrimidines. Yet, cellular TS must be maintained completely inactive for a length of time equivalent to one cell generation before any appreciable cell kill ensues. Successful blockade for longer periods yields extensive commitment to cell death, and antitumor kill has been faithfully mirrored by the duration of complete inhibition of TS in those few studies that allow assessment of the time course of enzyme inhibition. In spite of the potency of 5-FU as an inhibitor of TS, maintenance of such a prolonged complete blockade of tumor TS is quite difficult under clinical conditions. These counterintuitive concepts are borne out by abundant preclinical information, and may lie behind the limited clinical activity of the drug. However, the current literature would support the conclusions that the therapeutic objective of fluoropyrimidine therapy is a sustained complete inhibition of TS for periods of 48 h or more, that such inhibition should permit substantial therapeutic effects against human colon carcinomas, and that this objective is probably seldom met." @default.
• W7208726 created "2016-06-24" @default.
• W7208726 creator A5032651935 @default.
• W7208726 date "2003-01-01" @default.
• W7208726 modified "2023-09-23" @default.
• W7208726 title "Biochemical Bases of the 5-Fluorouracil—Folinic Acid Interaction and of its Limitations" @default.
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