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Shortly after the discovery of prostaglandins being involved in vertebrate carcinogenesis (during the 1970s), trials in patients with familial adenomatous polyposis (FAP) had shown that nonsteroidal anti-inflammatory drugs (NSAIDs) could reduce the number and size of these precancerous lesions. In the late 1980s epidemiological evidence was provided that long term use of aminosalicylic acid (ASA) for various indications seemed to be protective against colonic cancer and malignancies of other sites. Controlled intervention studies with nonselective cyclooxygenase (COX) inhibitors (i.e. traditional NSAIDs) were hampered by the risks of gastrointestinal and renal side effects. Recently, selective COX-2 receptor antagonists have been developed, improving pain and inflammation without the above mentioned adverse effects. In animal models it has been shown that COX-2 inhibitors are able to reduce colonic neoplasia and/or its proxy markers. This is the rationale for the presently ongoing testing of those drugs in hereditary and sporadic colonic adenomas.