About this Biochemistry, Genetics and Molecular Biology article
5-Fluorouracil: mechanisms of action and clinical strategies by Daniel B. Longley; D. Paul Harkin; Patrick G. Johnston is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.
Antimetabolite drugs work by inhibiting essential biosynthetic processes, or by being incorporated into macromolecules, such as DNA and RNA, and inhibiting their normal function. The fluoropyrimidine 5-fluorouracil (5-FU) does both. FLUOROPYRIMIDINES were developed in the 1950s following the observation that rat hepatomas used the pyrimidine uracil -one of the four bases found in RNA -more rapidly than normal tissues, indicating that uracil metabolism was a potential target for antimetabolite chemotherapy 1 . The mechanism of cytotoxicity of 5-FU has been ascribed to the misincorporation of fluoronucleotides into RNA and DNA and to the inhibition of the nucleotide synthetic enzyme thymidylate synthase (TS).5-FU is widely used in the treatment of a range of cancers, including colorectal and breast cancers, and cancers of the aerodigestive tract. Although 5-FU in combination with other chemotherapeutic agents improves response rates and survival in breast and head and neck cancers, it is in colorectal cancer that 5-FU has had the greatest impact. 5-FU-based chemotherapy improves overall and disease-free survival of patients with resected stage III colorectal cancer 2 . Nonetheless, r
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- Author
- Daniel B. Longley; D. Paul Harkin; Patrick G. Johnston
- Publisher
- Springer Science and Business Media LLC
- Published
- 2003
- Language
- EN
- Field
- Biochemistry, Genetics and Molecular Biology (Life Sciences)