Several lines of evidence suggest that cyclooxygenase-2 (COX-2) is a rational target for anticancer therapy. Epidemiologic data have shown that chronic use of nonsteroidal antiinflammatory agents (NSAIDs) reduce the risk of a number of solid malignancies, including colorectal and esophageal carcinoma.1 NSAIDs inhibit cyclooxygenase, a family of enzymes critical for arachidonic acid metabolism (Figure 11.1).2 The cyclooxygenase enzymes convert arachidonic acid to prostaglandin H2 (PGH2) and subsequently thromboxane (TXA2) and prostaglandins PGE2, PGF2, PGD2, and PGI2.3 The constitutive cyclooxygenase-1 (COX-1) isozyme is present in most normal tissues to control normal physiologic functions, including maintenance of the gastrointestinal mucosa, regulation of renal blood flow, and platelet aggregation. In contrast, the COX-2 enzyme isozyme inducible by cytokines and growth factors is often present in inflammatory conditions and cancer.4.

Original languageEnglish
Title of host publicationAntiangiogenic Cancer Therapy
PublisherCRC Press
Number of pages16
ISBN (Electronic)9781420004298
ISBN (Print)9780849327995
StatePublished - Jan 1 2007


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