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- Author: David C Whiteman x
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Cancer and Population Studies Group, School of Population Health, Queensland Institute of Medical Research, Brisbane, 4029, Australia
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Cancer and Population Studies Group, School of Population Health, Queensland Institute of Medical Research, Brisbane, 4029, Australia
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In 1998, Risch proposed a hypothesis for the pathogenesis of ovarian cancer relating to the role of androgens in stimulating epithelial cell proliferation. Although this hypothesis has been widely discussed, direct evidence to support it is scant. To address this issue, we have conducted a detailed analysis of factors possibly associated with high circulating levels of androgens, including polycystic ovary syndrome (PCOS), hirsutism and acne (all clinically associated with hyperandrogenism) using the data collected in an Australia-wide, population-based case-control study. Cases aged 18–79 years with a new diagnosis of invasive epithelial ovarian cancer (n=1276) or borderline malignant tumour (n=315) were identified through a network of clinics and cancer registries throughout Australia. Controls (n=1508) were selected from the National Electoral Roll. Women self-reported a history of PCOS, acne, hirsutism and also use of testosterone supplements or the androgenic medication Danazol. We found no evidence that a history of PCOS, acne or hirsutism was associated with ovarian cancer overall, or with specific subtypes, with the exception of serous borderline tumours that were positively associated with a history of PCOS (OR 2.6; 95% CI 1.0–6.1). Women who had ever used testosterone supplements had an increased risk of ovarian cancer (OR 3.7; 95% CI 1.1–12.0); however, use of the androgenic medication Danazol did not increase risk (OR 1.0; 95% CI 0.4–2.9). Overall, our results do not support the hypothesis that androgen-related disorders increase the risk of ovarian cancer.
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Queensland Institute of Medical Research, School of Public Health, Department of Preventive Medicine, Department of Epidemiology and Biostatistics, Program in Epidemiology, Obstetrics and Gynecology Epidemiology Center, Peter MacCallum Cancer Centre, Department of Epidemiology and Public Health, Cancer Epidemiology Program, Division of Cancer Epidemiology, Department of Obstetrics and Gynecology, Department of Biomedical Sciences, Department of Obstetrics and Gynecology, Roswell Park Cancer Center, Virus, Gynecologic Clinic, Department of Health Sciences Research, Department of Community and Family Medicine, Robert Wood Johnson Medical School, School of Public Health, National Cancer Institute, Division of Genetics and Epidemiology, Department of Cancer Epidemiology and Prevention, Department of Epidemiology, Department of Gynaecological Oncology, Royal Brisbane Hospital, Locked Bag 2000, Brisbane, Queensland 4029, Australia
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Queensland Institute of Medical Research, School of Public Health, Department of Preventive Medicine, Department of Epidemiology and Biostatistics, Program in Epidemiology, Obstetrics and Gynecology Epidemiology Center, Peter MacCallum Cancer Centre, Department of Epidemiology and Public Health, Cancer Epidemiology Program, Division of Cancer Epidemiology, Department of Obstetrics and Gynecology, Department of Biomedical Sciences, Department of Obstetrics and Gynecology, Roswell Park Cancer Center, Virus, Gynecologic Clinic, Department of Health Sciences Research, Department of Community and Family Medicine, Robert Wood Johnson Medical School, School of Public Health, National Cancer Institute, Division of Genetics and Epidemiology, Department of Cancer Epidemiology and Prevention, Department of Epidemiology, Department of Gynaecological Oncology, Royal Brisbane Hospital, Locked Bag 2000, Brisbane, Queensland 4029, Australia
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Queensland Institute of Medical Research, School of Public Health, Department of Preventive Medicine, Department of Epidemiology and Biostatistics, Program in Epidemiology, Obstetrics and Gynecology Epidemiology Center, Peter MacCallum Cancer Centre, Department of Epidemiology and Public Health, Cancer Epidemiology Program, Division of Cancer Epidemiology, Department of Obstetrics and Gynecology, Department of Biomedical Sciences, Department of Obstetrics and Gynecology, Roswell Park Cancer Center, Virus, Gynecologic Clinic, Department of Health Sciences Research, Department of Community and Family Medicine, Robert Wood Johnson Medical School, School of Public Health, National Cancer Institute, Division of Genetics and Epidemiology, Department of Cancer Epidemiology and Prevention, Department of Epidemiology, Department of Gynaecological Oncology, Royal Brisbane Hospital, Locked Bag 2000, Brisbane, Queensland 4029, Australia
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Whilst previous studies have reported that higher BMI increases a woman's risk of developing ovarian cancer, associations for the different histological subtypes have not been well defined. As the prevalence of obesity has increased dramatically, and classification of ovarian histology has improved in the last decade, we sought to examine the association in a pooled analysis of recent studies participating in the Ovarian Cancer Association Consortium. We evaluated the association between BMI (recent, maximum and in young adulthood) and ovarian cancer risk using original data from 15 case–control studies (13 548 cases and 17 913 controls). We combined study-specific adjusted odds ratios (ORs) using a random-effects model. We further examined the associations by histological subtype, menopausal status and post-menopausal hormone use. High BMI (all time-points) was associated with increased risk. This was most pronounced for borderline serous (recent BMI: pooled OR=1.24 per 5 kg/m2; 95% CI 1.18–1.30), invasive endometrioid (1.17; 1.11–1.23) and invasive mucinous (1.19; 1.06–1.32) tumours. There was no association with serous invasive cancer overall (0.98; 0.94–1.02), but increased risks for low-grade serous invasive tumours (1.13, 1.03–1.25) and in pre-menopausal women (1.11; 1.04–1.18). Among post-menopausal women, the associations did not differ between hormone replacement therapy users and non-users. Whilst obesity appears to increase risk of the less common histological subtypes of ovarian cancer, it does not increase risk of high-grade invasive serous cancers, and reducing BMI is therefore unlikely to prevent the majority of ovarian cancer deaths. Other modifiable factors must be identified to control this disease.