Intestinal Tumor Load in the Min/+ Mouse Model is not Correlated with Eicosanoid Biosynthesis
Several lines of evidence demonstrate an inverse relationship between the use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and aspirin-like drugs, and intestinal cancer. NSAIDs have been shown to reduce the risk of intestinal cancer in humans by 50%.1–4 It is well known that the anti-inflammatory properties of NSAIDs are related to their ability to inhibit prostaglandin biosynthesis. Cyclooxygenase (COX) catalyzes the committed step in prostaglandin formation. Two isoforms of cyclooxygenase exist, COX-1 and COX-2. NSAIDs can inhibit both. COX-1 is the constitutively expressed isoform, and COX-2 is the inducible form of the enzyme involved in inflammation.5–7
KeywordsArachidonic Acid Familial Adenomatous Polyposis Adenomatous Polyposis Coli Tumor Number Tumor Load
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