Journal Article

Genetic variability in prostaglandin synthesis, fish intake and risk of colorectal polyps

Elizabeth M. Poole, Jeannette Bigler, John Whitton, Justin G. Sibert, Richard J. Kulmacz, John D. Potter and Cornelia M. Ulrich

in Carcinogenesis

Volume 28, issue 6, pages 1259-1263
Published in print June 2007 | ISSN: 0143-3334
Published online February 2007 | e-ISSN: 1460-2180 | DOI:
Genetic variability in prostaglandin synthesis, fish intake and risk of colorectal polyps

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Dietary polyunsaturated fatty acids (PUFAs) can be converted to prostaglandins and leukotrienes. Metabolism of omega-6 (n-6) PUFAs results in the production of pro-inflammatory mediators whereas downstream products of omega-3 (n-3) PUFAs have lower inflammatory activity. Elevated n-3 PUFA intake from dietary fish may be associated with lower risk of colorectal neoplasia among those with genetic variants resulting in higher levels of pro-inflammatory mediators. We investigated interactions between dietary fish intake and polymorphisms in cyclooxygenase (COX)-1, COX-2, ALOX5 and PGIS in a case–control study of adenomas (N = 522), hyperplastic polyps (N = 194) and polyp-free controls (N = 626). Polyp risk did not differ by fish intake. A suggested interaction with fish intake was observed for COX-1 P17L. Among those who were homozygous wild type, increasing fish intake was associated with a modestly reduced risk of adenoma, whereas among those with at least one variant allele, the reverse trend was observed (p-interaction = 0.08). The interaction was statistically significant when non-steroidal anti-inflammatory drug (NSAID) use was also taken into account: among those with COX-1 17PP genotypes, high fish intake and regular NSAID use was associated with a decreased risk compared with low fish intake and low NSAID use (odds ratio = 0.60, 95% confidence interval 0.33–1.09). The opposite association was observed among those with COX-1 17PL or LL genotypes (p-interaction = 0.04). Our results suggest that the effects of dietary n-3 PUFA intake and NSAID use may differ by genetic variation in COX-1.

Journal Article.  3847 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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