© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 8, 545-546,
April 17, 2002
© 2002 Oxford University Press
EDITORIAL |
COX-2 in Cancer—A Player That's Defining the Rules
Affiliations of authors: E. T. Hawk, J. L. Viner, Gastrointestinal and Other Cancers Research Group, National Cancer Institute, Division of Cancer Prevention, National Institutes of Health, Bethesda, MD; A. Dannenberg, Weill Medical College of Cornell University and Strang Cancer Prevention Center, New York, NY; R. N. DuBois, Division of Gastroenterology, Vanderbilt University, Nashville, TN.
Correspondence to: Ernest T. Hawk, M.D., M.P.H., Chief, Gastrointestinal and Other Cancers Research Group, National Cancer Institute, Division of Cancer Prevention, EPN, Suite 2141, 6130 Executive Blvd., Bethesda, MD 20892–7317 (e-mail: eh51p@nih.gov).
Cyclooxygenase (COX) inhibitors are being developed as potential agents for the prevention and treatment of cancer after a century of widespread use for inflammation, fever, and pain. Beginning in the late 1970s, researchers noted elevated concentrations of prostaglandins in neoplastic lesions, which suggested a role for arachidonic acid metabolites in tumorigenesis. Multiple lines of evidence—in vitro, in vivo, observational, and clinical—now confirm that COX inhibitors reduce prostaglandin production and the risk of colorectal, skin, and other neoplasias (1). Owing to gastrointestinal safety concerns with traditional nonselective COX inhibitors, derivatives that selectively target COX-2 have been developed for applications in arthritis, analgesia, and the treatment of neoplasia.
COX-2 selective inhibitors serve as a paradigm of molecularly targeted, cytostatic, antineoplastic agents (2)
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