Body weight and postmenopausal breast cancer risk defined by estrogen and progesterone receptor status among Swedish women: A prospective cohort study

Authors

  • Reiko Suzuki,

    1. Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
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  • Tove Rylander-Rudqvist,

    1. Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
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  • Weimin Ye,

    1. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
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  • Shigehira Saji,

    1. Division of Clinical Trials and Research, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital, Tokyo, Japan
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  • Alicja Wolk

    Corresponding author
    1. Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden
    • Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Nobelsväg 13, P. O. Box 210, S-171 77, Stockholm, Sweden
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    • Fax +46(8) 30 45 71.


Abstract

Although obesity is one of the established risk factors for postmenopausal breast cancer, it is not clear whether this positive association differs across estrogen receptor (ER) and progesterone receptor (PR) status of breast tumors. We evaluated the association between body weight and ER/PR defined breast cancer risk stratified by postmenopausal hormone (PMH) use and a family history of breast cancer in the population-based Swedish Mammography Screening Cohort comprising 51,823 postmenopausal women. Relative body weight was measured by body mass index (kg/m2) based on self-reported weight and height collected in 1987 and 1997. Relative risks (RRs) were estimated by hazard ratios derived from Cox proportional hazards regression models. During an average of 8.3-year follow-up, 1,188 invasive breast cancer cases with known ER and PR status were diagnosed. When comparing to normal weight group, we observed a positive association between obesity and risk for the development of ER+ PR+ tumors (RR = 1.67, 95% CI = 1.34–2.07) and an inverse association for the development of all PR− tumors (RR = 0.68, 95% CI = 0.47–0.98). Statistically significant heterogeneity was observed in the RRs between ER+ PR+ tumors and all PR− tumors (pheterogeneity < 0.0001). The positive association of obesity with the development of ER+ PR+ tumors was confined to never-users of PMHs (RR = 1.90 (CI 95%:1.38–2.61)) and to those without a family history of breast cancer (RR = 1.82 (CI 95%:1.45–2.29)). Our results support the hypothesis that excess endogenous estrogen due to obesity contributes to an increased risk of ER+ PR+ postmenopausal breast cancer. © 2006 Wiley-Liss, Inc.

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