COX-2 Inhibitors and Cancer Therapeutics: Potential Roles for Inhibitors of COX-2 in Combination With Cytotoxic Therapy Reports From a Symposium Held in Conjunction With the Radiation Therapy Oncology Group June 2001 MeetingDicker, Adam P., M.D., Ph.D.American Journal of Clinical Oncology: August 2003 - Volume 26 - Issue 4 - p S46-S47 doi: 10.1097/01.COC.0000074180.16144.B3 Article Buy Abstract Author InformationAuthors Article MetricsMetrics Tumor growth and angiogenesis are interdependent. Cyclooxygenase (COX) catalyzes the synthesis of prostaglandins (PGs) from arachidonic acid. Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit COX-mediated synthesis of PGs. Although COX-1 is constitutively expressed in a wide range of tissues, COX-2 is cytokine inducible. Enhanced COX-2 expression has been attributed a key role in the development of inflammation and related processes observed in pathologically altered disease states. Two specific COX-2 inhibitors, namely, rofecoxib (Vioxx) and celecoxib (Celebrex), both oral agents and FDA approved, have been shown preclinically and clinically to have efficacy comparable to that of NSAIDs for relief of pain and inflammation in osteoarthritis, with decreased risk of gastrointestinal damage. Significant preclinical evidence strongly supports the potential role for these inhibitors for the treatment of cancer. On June 29, 2001, the Radiation Therapy Oncology Group (http://www.rtog.org), a National Cancer Institute–sponsored cooperative group, held a 1-day symposium focusing on the potential role of inhibitors of COX-2 in the treatment of cancer. This issue of the American Journal of Clinical Oncology contains the summary of those presentations. From the Department of Radiation Oncology, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A. Address correspondence and reprint requests to Adam P. Dicker, Department of Radiation Oncology, Thomas Jefferson University, 111 South 11th Street, Philadelphia, PA 19107-5097, U.S.A. e-mail: firstname.lastname@example.org © 2003 Lippincott Williams & Wilkins, Inc.