Journal of Clinical Oncology, Vol 23, No 12 (April 20), 2005: pp. 2840-2855
© 2005 American Society of Clinical Oncology.
DOI: 10.1200/JCO.2005.09.051
COX-2: A Molecular Target for Colorectal Cancer Prevention
Joanne R. Brown,
Raymond N. DuBois
From the Vanderbilt-Ingram Cancer Center, Nashville, TN
Address reprint requests to Raymond N. DuBois, MD, PhD, Professor of Medicine and Cancer Biology, 694 Preston Research Building, The Vanderbilt-Ingram Cancer Center, Nashville, TN 37232; e-mail: raymond.dubois{at}vanderbilt.edu
Cyclooxygenase (COX), a key enzyme in the prostanoid biosynthetic pathway, has received considerable attention due to its role in human cancers. Observational and randomized controlled studies in many different population cohorts and settings have demonstrated protective effects of nonsteroidal anti-inflammatory drugs (NSAIDs; the inhibitors of COX activity) for colorectal cancers (CRCs). COX-2, the inducible isoform of cyclooxygenase, is overexpressed in early and advanced CRC tissues, which portends a poor prognosis. Experimental studies have thus identified important mechanisms and pathways by which COX-2 plays an important role in carcinogenesis. Selective COX-2 inhibitors have been approved for use as adjunctive therapy for patients with familial polyposis. The role of COX-2 inhibitors is currently being evaluated for use in wider populations.
Authors' disclosures of potential conflicts of interest are found at the end of this article.
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