Cathryn H Bock1, Allison M Jay2, Gregory Dyson3, Jennifer L Beebe-Dimmer3, Michele L Cote3, Lifang Hou4, Barbara V Howard5, Pinkal Desai6, Kristen Purrington3, Ross Prentice7, Michael S Simon3. 1. Karmanos Cancer Institute, Wayne State University School of Medicine, 4100 John R, Detroit, MI, 48201, USA. bockc@karmanos.org. 2. St. John Health System, Van Elslander Cancer Center, 19229 Mack Ave, Grosse Pointe Woods, MI, 48236, USA. 3. Karmanos Cancer Institute, Wayne State University School of Medicine, 4100 John R, Detroit, MI, 48201, USA. 4. Department of Preventive Medicine and Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, 675 North St. Clair, Chicago, IL, 60611, USA. 5. Medstar Health Research Institute and Georgetown/Howard Universities Center for Clinical and Translational Science, 6525 Belcrest Road, Suite 700, Hyattsville, MD, 20782, USA. 6. Division of Hematology/Oncology, Weill Cornell Medical College, 1300 York Ave, New York, NY, 10065, USA. 7. Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N, PO Box 19024, Seattle, WA, 98109, USA.
Abstract
PURPOSE: Statins have been postulated to have chemopreventive activity against breast cancer. We evaluated whether germline genetic polymorphisms modified the relationship between statins and breast cancer risk using data from the Women's Health Initiative. We evaluated these interactions using both candidate gene and agnostic genome-wide approaches. METHODS: To identify candidate gene-statin interactions, we tested interactions between 22 SNPS in nine candidate genes implicated in the effect of statins on lipid metabolism in 1687 cases and 1687 controls. We then evaluated statin use interaction with the remaining 30,380 SNPs available in this sample from the CGEMS GWAS study. RESULTS: After adjusting for multiple comparisons, no SNP interactions with statin usage and risk of breast cancer were statistically significant in either the candidate genes or genome-wide approaches. CONCLUSIONS: We found no evidence of SNP interactions with statin usage for breast cancer risk in a population of 3374 individuals. These results suggest that genome-wide common genetic variants do not moderate the association between statin usage and breast cancer in the population of women in the Women's Health Initiative.
PURPOSE: Statins have been postulated to have chemopreventive activity against breast cancer. We evaluated whether germline genetic polymorphisms modified the relationship between statins and breast cancer risk using data from the Women's Health Initiative. We evaluated these interactions using both candidate gene and agnostic genome-wide approaches. METHODS: To identify candidate gene-statin interactions, we tested interactions between 22 SNPS in nine candidate genes implicated in the effect of statins on lipid metabolism in 1687 cases and 1687 controls. We then evaluated statin use interaction with the remaining 30,380 SNPs available in this sample from the CGEMS GWAS study. RESULTS: After adjusting for multiple comparisons, no SNP interactions with statin usage and risk of breast cancer were statistically significant in either the candidate genes or genome-wide approaches. CONCLUSIONS: We found no evidence of SNP interactions with statin usage for breast cancer risk in a population of 3374 individuals. These results suggest that genome-wide common genetic variants do not moderate the association between statin usage and breast cancer in the population of women in the Women's Health Initiative.
Entities:
Keywords:
Breast cancer; Cholesterol; GWAS; SNPS; Statins
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