News Release

Is there any association between COX2 and colon cancer?

Peer-Reviewed Publication

World Journal of Gastroenterology

Non-steroidal anti-inflammatory drugs (NSAIDs), which are known to reduce the risk of colon cancer, act directly on cyclooxygenase-2 (COX2) and reduce its activity. Population studies have found an association of inherited variations in the COX2 gene with colon cancer risk, but others were unable to replicate this finding. Similarly, variations in the uridine diphosphate glucuronosyltransferase 1A6 (UGT1A6) gene, which is also known to be key in the metabolism of NSAIDs, have been shown to modify the effect of NSAIDs on developing colon polyps, a precursor of colon cancer, but these modifications of NSAID effects have not been observed in risk of colon cancer.

A research article to be published on May 14, 2009 in the World Journal of Gastroenterology addresses this question. The research team led by Dr. Li from Case Western Reserve University examined the association of variants of the COX2 and UGT1A6 genes, and their interaction with NSAID consumption, on risk of colon cancer in attempt to more fully understand the relationship between genetic variation and the protective effect of NSAIDs on colon cancer risk.

They found that no single nucleotide polymorphisms (SNPs) in either gene were individually statistically significantly associated with colon cancer, nor did they statistically significantly change the protective effect of NSAID consumption. Like others, the authors were unable to replicate the association of variants in the COX2 gene with colon cancer risk (P > 0.05), and they did not observe that these variants modify the protective effect of NSAIDs (P > 0.05). Their study does not support a role of COX2 and UGT1A6 genetic variations in the development of colon cancer.

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Reference: Thompson CL, Plummer SJ, Merkulova A, Cheng I, Tucker TC, Casey G, Li L. No association between cyclooxygenase-2 and uridine diphosphate glucuronosyltransferase 1A6 genetic polymorphisms and colon cancer risk. World J Gastroenterol 2009; 15(18): 2240-2244 http://www.wjgnet.com/1007-9327/15/2240.asp

Correspondence to: Li Li, MD, PhD, Department of Family Medicine, Research Division, Case Western Reserve University, 11001 Cedar Ave., Suite 306, Cleveland, Ohio 44106-7136, United States. li.li@case.edu

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H. pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.


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