Carcinogenesis Advance Access published online on November 18, 2004
Carcinogenesis, doi:10.1093/carcin/bgh336
© 2004 by Oxford University Press
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1 Department of Toxicology, Pathology and Genetics, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands; Department of Pathology, Josephine Nefkens Institute, Erasmus University Rotterdam, Rotterdam, The Netherlands
* To whom correspondence should be addressed. Associations between polymorphisms in genes (SNPs) involved in the arachidonic acid (AA) pathway, and colorectal adenomas were investigated in a Dutch case control study including 384 cases and 403 polyp-free controls. Twenty-one polymorphisms in seven candidate genes were studied, and a potential modifying effect of fish consumption was considered. A protective effect on colorectal adenomas was found for the CT genotype of SNP H477H in PPAR These results indicate that SNPs in genes involved in the AA-pathway are associated with colorectal adenoma risk. Part of these associations is modified by fish consumption.
Revised November 2, 2004
Accepted November 7, 2004
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
Colorectal adenoma risk is modified by the interplay between polymorphisms in arachidonic acid pathway genes and fish consumption
2 Division of Human Nutrition, Wageningen University and Research Centre, Wageningen, The Netherlands
3 Department of Toxicology, Pathology and Genetics, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands
Ellen Kampman, E-mail: Ellen.Kampman{at}wur.nl
Abstract 
and the GC genotype of SNP V102V in COX-2 (OR, 0.63; 95%CI, 0.45-0.89 and OR, 0.65; 95%CI, 0.46-0.92 respectively) compared to the homozygote major genotypes. An increase in adenoma risk was observed for the TC genotype of SNP c.2242T>C in COX-2 (OR, 1.47; 95%CI, 1.07-2.00) compared to the TT genotype. Analysis with estimated haplotypes confirmed these associations and revealed three additional associations with COX-2, sPLA2 and 15LOX haplotypes. Fish consumption modified the associations with COX-2 and PPAR
genotypes. For SNP c.-789C>T in PPAR, the major genotype showed a decrease in adenoma risk for those in the highest tertile of fish consumption (T3), as compared to the lowest tertile (T1) (OR, 0.65; 95%CI, 0.41-1.02). Protective effects were also observed for SNPs V102V and c.2242T>C in COX-2 and high fish intake. The interaction between fish consumption and c.2242T>C was statistically significant, with an OR for the TT genotype and high fish consumption of 0.52 (95%CI, 0.27-1.01) as compared to low fish intake.
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