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Serum Follicle-Stimulating Hormone and Risk of Epithelial Ovarian Cancer in Postmenopausal Women

¹ Departments of Obstetrics and Gynecology, and ² Environmental Medicine, New York University School of Medicine, New York, New York; ³ Departments of Medical Biosciences/Pathology, ⁵ Public Health and Clinical Medicine/Nutritional Research, and ⁶ Oncology, University of Umeå, Umeå, Sweden; ⁸ Hormones and Cancer Group, International Agency for Research on Cancer, Lyon, France; ⁴ Unit of Epidemiology, Istituto Nazionale Tumori, Milan, Italy; and ⁷ Department of Social and Preventive Medicine, State University of New York at Buffalo, Buffalo, New York

The "gonadotropin hypothesis" postulates that gonadotropin overstimulation of ovarian epithelium results in its increased proliferation and subsequent malignant transformation. To address this hypothesis, we assessed the association between prediagnostic serum levels of follicle-stimulating hormone (FSH) and the risk of epithelial ovarian cancer in postmenopausal women who were part of a case–control study nested within three prospective cohorts in New York City, Umeå, Sweden, and Milan, Italy. Case subjects were 88 women with primary invasive epithelial ovarian cancer diagnosed between 3 months and 13.1 years after the blood donation. Controls were 168 women who were free of cancer and matched the case on cohort, age, and enrollment date. Serum FSH was determined using a quantitative immunoradiometric assay. FSH concentrations were similar in women who subsequently received a diagnosis of epithelial ovarian cancer (median, 44.0 mIU/ml; range, 13.8–101.2) and in controls (median, 43.4 mIU/ml; range, 13.5–109.5; P = 0.17). Compared with women in the lowest third, women in the highest third of serum FSH were not at increased risk of epithelial ovarian cancer after an adjustment for potential confounders (odds ratio, 0.85; 95% confidence interval, 0.36–1.99). These observations provide no evidence for an association between circulating FSH and risk of epithelial ovarian cancer in postmenopausal women and do not appear to support the gonadotropin hypothesis of epithelial ovarian carcinogenesis.

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