Abstract
NSAIDs inhibit prostaglandin synthesis. In 1983, Waddell et al first reported that sulindac, a NSAID (Clinoril), caused regression of rectal adenomatous polyps in several patients with familial adenomatous polyposis, an inherited form of colorectal cancer. Subsequently, NSAIDs have been used as chemopreventive agents in animal carcinogenesis models and adenoma regression had been confirmed in human trials with sulindac. This article summarizes these developments and describes possible mechanisms of colorectal neoplasia chemoprevention.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Adenomatous Polyposis Coli / genetics
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Adenomatous Polyposis Coli / metabolism
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Adenomatous Polyposis Coli / prevention & control*
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
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Chromosome Aberrations
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Chromosome Disorders
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Chromosomes, Human, Pair 17 / genetics
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Chromosomes, Human, Pair 5 / genetics
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DNA, Neoplasm / drug effects
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DNA, Neoplasm / metabolism
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Humans
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Pedigree
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Prostaglandin Antagonists / therapeutic use
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Prostaglandins / biosynthesis
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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DNA, Neoplasm
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Prostaglandin Antagonists
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Prostaglandins