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COX-2 Polymorphisms in Patients With Familial Adenomatous Polyposis

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Abstract:

Cyclooxygenase-2 (COX-2) is an enzyme involved in the synthesis of prostaglandins and thromboxanes, which are regulators of biologic processes such as inflammation, cell proliferation, and angiogenesis. COX-2 has been found overexpressed in (pre)malignant tissues and may be relevant to cancer development. We investigated whether functional genetic polymorphisms in COX-2 may have a risk-modifying effect on duodenal adenomatosis in patients with familial adenomatous polyposis (FAP). Blood from 85 patients with FAP and 218 age- and sex-matched healthy subjects was investigated for the presence of two functional promoter region polymorphisms (−1195G → A and −765G → C) in COX-2. Logistic regression analysis revealed an overrepresentation of the −1195GG genotype compared to the −1195AA genotype in patients with FAP (odds ratio = 2.81; 95% CI = 1.00‐7.91, p = 0.042). No associations between single COX-2 polymorphisms or COX-2 haplotype were found when patients were evaluated according to their Spigelman stage. The predicted low COX-2 expression genotype −1195GG was found overrepresented in the patients with FAP. The COX-2 genotypes showed no association with the severity of duodenal adenomatosis.

Keywords: Cyclooxygenase-2; Duodenal adenomatosis; Familial adenomatous polyposis; Genetic polymorphism

Document Type: Research Article

DOI: http://dx.doi.org/10.3727/096504009788428451

Publication date: January 1, 2009

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  • Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
    Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.
cog/or/2009/00000017/00000008/art00002
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