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1 Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute; 2 Ontario Breast Screening Program, Cancer Care Ontario; 3 Imaging Research, Sunnybrook and Women's College Health Sciences Center, Toronto, Ontario; and the 4 BC Cancer Agency, Vancouver, British Columbia, Canada
Requests for reprints: Norman F. Boyd, Ontario Cancer Institute, 610 University Avenue, Suite 10-415, Toronto, Ontario, Canada M5G 2K9. Phone: 416-946-2945; Fax: 416-946-2024. E-mail: boyd{at}uhnres.utoronto.ca
Background: Greater weight and body mass index (BMI) are negatively correlated with mammographic density, a strong risk factor for breast cancer, and are associated with an increased risk of breast cancer in postmenopausal women, but with a reduced risk in premenopausal women. We have examined the associations of body size and mammographic density on breast cancer risk.
Method: We examined the associations of body size and the percentage of mammographic density at baseline with subsequent risk of breast cancer among 1,114 matched case-control pairs identified from three screening programs. The effect of each factor on risk of breast cancer was examined before and after adjustment for the other, using logistic regression.
Results: In all subjects, before adjustment for mammographic density, breast cancer risk in the highest quintile of BMI, compared with the lowest, was 1.04 [95% confidence interval (CI), 0.8-1.4]. BMI was associated positively with breast cancer risk in postmenopausal women, and negatively in premenopausal women. After adjustment for density, the risk associated with BMI in all subjects increased to 1.60 (95% CI, 1.2-2.2), and was positive in both menopausal groups. Adjustment for BMI increased breast cancer risk in women with 75% or greater density, compared with 0%, increased from 4.25 (95% CI, 1.6-11.1) to 5.86 (95% CI, 2.2-15.6).
Conclusion: BMI and mammographic density are independent risk factors for breast cancer, and likely to operate through different pathways. The strong negative correlated between them will lead to underestimation of the effects on risk of either pathway if confounding is not controlled. (Cancer Epidemiol Biomarkers Prev 2006;15(11):2086–92)
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