Mechanisms for the Prevention of Gastrointestinal Cancer: The Role of Prostaglandin E2Backlund M.G. · Mann J.R. · DuBois R.N.
Departments of aMedicine, bCell and Developmental Biology, and cCancer Biology, Vanderbilt University Medical Center and Vanderbilt-Ingram Cancer Center, Nashville, Tenn., USA
Carcinoma of the colon or rectum represents one of the most common malignancies worldwide with a higher prevalence in industrialized regions. Epidemiologic studies of individuals taking non-steroidal anti-inflammatory drugs (NSAIDs) have shown a significant reduction in colorectal cancer (CRC) mortality compared to those individuals not receiving these agents. NSAIDs inhibit the enzymatic activity of both isoforms of cyclooxygenase (COX-1 and COX-2), while COX-2-selective inhibitors have shown some efficacy in reducing polyp formation. COX-2-derived bioactive lipids, including the primary prostaglandin (PG) generated in colorectal tumors, PGE2, are known to stimulate cell migration, proliferation and tumor-associated neovascularization while inhibiting cell death. Here we briefly review the role of NSAIDs in preventing CRC, as well as the proposed mechanism by which a COX-2-derived PG, PGE2, promotes colon cancer.
Raymond N. DuBois
Vanderbilt-Ingram Cancer Center, 691 Preston Research Building
2300 Pierce Avenue
Nashville, TN 37232-6838 (USA)
Tel. +1 615 343 0527, Fax +1 615 936 2697, E-Mail email@example.com
Published online: September 19, 2005
Number of Print Pages : 5
Number of Figures : 1, Number of Tables : 0, Number of References : 30
Oncology (International Journal of Cancer Research and Treatment)
Vol. 69, No. Suppl. 1, Year 2005 (Cover Date: Released September 2005)
Journal Editor: Trump, D.L. (Buffalo, N.Y.)
ISSN: 0030–2414 (print), 1423–0232 (Online)
For additional information: http://www.karger.com/ocl