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The association between use of nonsteroidal anti-inflammatory drugs (NSAIDs) and breast cancer risk remains unclear. Inconsistencies in previously reported findings may be partly due to differences in expression of cyclooxygenase (COX)-2. We hypothesized that genetic polymorphisms ( COX-2  .926,  COX-2  .5209, and  COX-2  .8473) may reduce overall breast cancer risk or risk for subtypes of breast cancer by modulating the inflammatory response and may interact with aspirin or any NSAID use.    Methods  We conducted a population-based, case-control study in which we genotyped 1,067 breast cancer cases and 1,110 control individuals included in the Long Island Breast Cancer Study Project.    Results  No major effects of the three  COX-2  variant alleles on breast cancer risk were found. A total of eight distinct haplotypes and 18 diplotypes were observed in the population. Overall, no significant associations between  COX-2  haplotypes/diplotypes and breast cancer risk were observed. Among women who used aspirin or any NSAID there was little evidence for an interaction with the at-risk  COX-2  genotypes, with one exception. Among women with hormone receptor positive breast cancer, the reduced risk for any NSAID use was only evident among those who had at least one variant C allele of  COX-2  .8473 (odds ratio = 0.7, 95% confidence interval = 0.5 to 1.0;  P  for the interaction = 0.02). There was no corresponding interaction for aspirin use, possibly because of limited power.    Conclusion  These data provide modest evidence that the C allele of  COX-2  .8473 may interact with NSAIDs to reduce risk for hormone receptor positive breast cancer.

Genetic polymorphisms in the cyclooxygenase-2 gene, use of nonsteroidal anti-inflammatory drugs, and breast cancer risk