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1 International Agency for Research on Cancer (IARC-WHO), 150 cours Albert-Thomas, 69372 Lyon cedex 08, France
2 Epidemiology Unit, Cancer Research UK, University of Oxford, Oxford, UK
3 National Cancer Institute, Milan, Italy
4 Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands
5 New York University School of Medicine, New York, USA
6 MRC Dunn Human Nutrition Unit, Welcome Trust/MRC Building, Cambridge, UK
7 Clinical Gerontology Unit, Addenbrooke’s Hospital, Cambridge, UK
8 Centre for Nutrition and Health, National Institute for Public Health and the Environment, Bilthoven, The Netherlands
9 Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany
10 Division of Clinical Epidemiology, German Cancer Research Center, Heidelberg, Germany
11 INSERM, Institut Gustave Roussy, Villejuif, France
12 Department of Epidemiology, Catalan Institute of Oncology, Barcelona, Spain
13 Sección Información Sanitaria, Consejería de Salud y Servicios Sanitarios de Asturias, Asturias, Spain
14 Epidemiology Department, Murcia Health Council, Murcia, Spain
15 Public Health Institute of Navarre, Navarre, Spain
16 Public Health Division of Gipuzkoa, Health Department of the Basque Country, Donostia-San Sebastian, Spain
17 Molecular and Nutritional Epidemiology Unit, CSPO, Scientific Institute of Tuscany, Florence, Italy
18 Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy
19 Cancer Registry, Azienda Ospedaliera ‘Civile M.P. Arezzo’, Ragusa, Italy
20 University of Turin, Turin, Italy
21 Imperial College of Science, Technology and Medicine, London, UK
22 University of Athens Medical School, Athens, Greece
(Requests for offprints should be addressed to R Kaaks; Email: kaaks{at}iarc.fr)
Considerable experimental and epidemiological evidence suggests that elevated endogenous sex steroids — notably androgens and oestrogens — promote breast tumour development. In spite of this evidence, postmenopausal androgen replacement therapy with dehydroepiandrosterone (DHEA) or testosterone has been advocated for the prevention of osteoporosis and improved sexual well-being. We have conducted a case–control study nested within the European Prospective Investigation into Cancer and Nutrition. Levels of DHEA sulphate (DHEAS), (
4-androstenedione), testosterone, oestrone, oestradiol and sex-hormone binding globulin (SHBG) were measured in prediagnostic serum samples of 677 postmenopausal women who subsequently developed breast cancer and 1309 matched control subjects. Levels of free testosterone and free oestradiol were calculated from absolute concentrations of testosterone, oestradiol and SHBG. Logistic regression models were used to estimate relative risks of breast cancer by quintiles of hormone concentrations. For all sex steroids –the androgens as well as the oestrogens – elevated serum levels were positively associated with breast cancer risk, while SHBG levels were inversely related to risk. For the androgens, relative risk estimates (95% confidence intervals) between the top and bottom quintiles of the exposure distribution were: DHEAS 1.69 (1.23–2.33), androstenedione 1.94 (1.40–2.69), testosterone 1.85 (1.33–2.57) and free testosterone 2.50 (1.76–3.55). For the oestrogens, relative risk estimates were: oestrone 2.07 (1.42–3.02), oestradiol 2.28 (1.61–3.23) and free oestradiol (odds ratios 2.13 (1.52–2.98)). Adjustments for body mass index or other potential confounding factors did not substantially alter any of these relative risk estimates. Our results have shown that, among postmenopausal women, not only elevated serum oestrogens but also serum androgens are associated with increased breast cancer risk. Since DHEAS and androstenedione are largely of adrenal origin in postmenopausal women, our results indicated that elevated adrenal androgen synthesis is a risk factor for breast cancer. The results from this study caution against the use of DHEA(S), or other androgens, for postmenopausal androgen replacement therapy.
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