NSAID-induced polyp regression in familial adenomatous polyposis patients.
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.
Giardiello
F M
FM
Deparment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
D011125:Adenomatous Polyposis Coli / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics; D002895:Chromosomes, Human, Pair 5 / Q000235:genetics; D004273:DNA, Neoplasm / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D010375:Pedigree; D011448:Prostaglandin Antagonists / Q000627:therapeutic use; D011453:Prostaglandins / Q000096:biosynthesis
D000894:Anti-Inflammatory Agents, Non-Steroidal; D004273:DNA, Neoplasm; D011448:Prostaglandin Antagonists; D011453:Prostaglandins