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- W2439969221 abstract "The uracil analog 5-fluorouracil (5-FU) is used as part of combination therapy for the treatment of breast, head/neck, and gastrointestinal malignancies, and has single-agent activity in colorectal cancer. 5-FU itself is inactive and requires intracellular conversion to form cytotoxic nucleotides (1). Several cellular targets for fluoropyrimidines have been well-characterized, including inhibition of thymidylate synthase (TS) by fluorodeoxyuridine monophosphate (FdUMP) and false base incorporation into RNA or DNA. Most investigations into cellular resistance factors regulating 5-FU activity have focused on alterations in (TS) levels and reduced folate pools, the required cofactor for binding dUMP to thymidylate synthase (1). However, the majority of an administered 5-FU dose undergoes metabolism to inactive species through a three-enzyme process, which is initiated and rate-limited by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2). Following a bolus injection of 5-FU, 80% is degraded via DPD after 24 h after administration (2). Studies of (19)F nuclear magnetic resonance (NMR) spectroscopy in mice bearing colon tumors found catabolites made up 51% of labeled drug in the tumor, compared with 26% for the anabolic products (3)." @default.
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- W2439969221 date "2003-11-21" @default.
- W2439969221 modified "2023-09-23" @default.
- W2439969221 title "5-Fluorouracil Metabolizing Enzymes" @default.
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- W2439969221 doi "https://doi.org/10.1385/1-59259-687-8:111" @default.
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