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Carcinogenesis Advance Access published online on February 14, 2008
Carcinogenesis, doi:10.1093/carcin/bgn042
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Estrogen-biosynthesis Gene CYP17 and Its Interactions with Reproductive, Hormonal and Lifestyle Factors in Breast Cancer Risk: Results from the Long Island Breast Cancer Study Project*

Yu Chen1, Marilie D. Gammon2, Susan L. Teitelbaum3, Julie A. Britton3, Mary Beth Terry4, Sumitra Shantakumar2, Sybil M. Eng5, Qiao Wang6, Irina Gurvich6, Alfred I. Neugut4, Regina M. Santella6 and Habibul Ahsan4,7

1 Department of Environmental Medicine and New York University Cancer Institute, New York University School of Medicine
2 Department of Epidemiology, University of North Carolina at Chapel Hill
3 Department of Community and Preventive Medicine, Mount Sinai School of Medicine
4 Department of Epidemiology, Mailman School of Public Health, Columbia University
5 Global Epidemiology, Pfeizer, Inc
6 Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University
7 Departments of Health Studies, Medicine, and Human Genetics, and Cancer Research Center, The University of Chicago

Reprint requests and correspondence should be addressed to: Dr. Habibul Ahsan, Department of Health Studies, The University of Chicago, 5841 South Maryland Avenue, Suite N102, Chicago, IL 60637, Phone: 773-834-9956, Fax: 773-834-0139, Email: habib{at}uchicago.edu

The genes that are involved in estrogen biosynthesis, cellular binding, and metabolism may contribute to breast cancer susceptibility. We examined the effect of the CYP17 promoter T–>C polymorphism and its interactions with the reproductive history, exogenous hormone use and selected lifestyle risk factors on breast cancer risk among 1037 population-based incident cases and 1096 population-based controls in the Long Island Breast Cancer Study Project. Overall, there were no associations between the CYP17 genotype and breast cancer risk. Among postmenopausal women, the joint exposure to higher body mass index and the variant C allele was associated with an increased the risk of breast cancer (OR, 1.60; 95% CI, 1.15-2.22). The joint exposure to the variant C allele and long-term use of hormone replacement therapy (HRT) (> 51 months) was related to an increased risk of breast cancer (OR, 1.51; 95% CI, 0.99-2.31) especially estrogen receptor-positive, progesterone receptor-positive breast cancer (OR, 1.87; 95% CI, 1.08-3.25). Among the control population, the CYP17 variant C allele was inversely associated with long-term use of post-menopausal HRT and a higher BMI in postmenopausal women. In conclusion, the findings suggest that the CYP17 variant C allele may increase breast cancer risk in conjunction with long-term HRT use and high body mass index in postmenopausal women.

Received September 19, 2007; revised January 8, 2008; accepted February 2, 2008.


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