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¹ Nutrition and Hormones Unit, International Agency for Research on Cancer, Lyon, France
² School of Public Health, University of Sydney, Level 2, K25-Medical Foundation Building, Sydney, New South Wales, Australia
³ Center for Research in Human Nutrition Rhône-Alpes, Université Lyon 1, Lyon, France
⁴ Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
⁵ Division of Population Health and Information, Alberta Cancer Board, Calgary, Alberta, Canada
⁶ UMR INSERM U449/INRA 1235, Lyon, France
⁷ Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark
⁸ Department of Clinical Epidemiology, Aarhus University Hospital, Aalborg, Denmark
⁹ Inserm ERI 20, Institut Gustave Roussy, Paris-Sud University, EA4045 Villejuif, France
¹⁰ German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
¹¹ Department of Hygiene and Epidemiology, University of Athens Medical School, Athens, Greece
¹² Hellenic Health Foundation, Athens, Greece
¹³ Molecular and Nutritional Epidemiology Unit, CSPO-Scientific Institute of Tuscany, Florence, Italy
¹⁴ Nutritional Epidemiology Unit, National Cancer Institute, Milan, Italy
¹⁵ Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy
¹⁶ Cancer Registry, Azienda Ospedaliera ‘Civile M P Arezzo’, Ragusa, Italy
¹⁷ CPO-Piemonte, Torino, Italy
¹⁸ Faculty of Medicine, Institute of Community Medicine, University of Tromsø, Tromsø, Norway
¹⁹ Public Health and Health Planning Directorate, Asturias, Spain
²⁰ Department of Epidemiology and Cancer Registry, Catalan Institute of Oncology, Barcelona, Spain
²¹ Andalusian School of Public Health, Granada, Spain
²² Public Health Department of Gipuzkoa, Basque Government, San Sebastian, Spain
²³ Epidemiology Department, Murcia Health Council, Murcia, Spain
²⁴ Public Health Institute of Navarra, Pamplona, Spain
²⁵ Department of Medicine, Malmö University Hospital, Lund University, Malmö, Sweden
²⁶ Department of Medical Biosciences, Umeå University, Umeå, Sweden
²⁷ National Institute of Public Health and the Environment, Centre for Nutrition and Health, Bilthoven, The Netherlands
²⁸ Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, The Netherlands
²⁹ MRC Dunn Human Nutrition Unit, Cambridge, UK
³⁰ Department of Public Health and Primary Care, MRC Centre for Nutritional Epidemiology in Cancer Prevention and Survival, University of Cambridge, Cambridge, UK
³¹ Clinical Gerontology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
³² Cancer Research UK Epidemiology Unit, University of Oxford, Oxford, UK
³³ Department of Epidemiology and Public Health, Imperial College London, London, UK

(Correspondence should be addressed to A E Cust; Email: annec{at}health.usyd.edu.au)

To clarify the role of metabolic factors in endometrial carcinogenesis, we conducted a case–control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), and examined the relation between prediagnostic plasma lipids, lipoproteins, and glucose, the metabolic syndrome (MetS; a cluster of metabolic factors) and endometrial cancer risk. Among pre- and postmenopausal women, 284 women developed endometrial cancer during follow-up. Using risk set sampling, 546 matched control subjects were selected. From conditional logistic regression models, high-density lipoprotein cholesterol (HDL-C) levels were inversely associated with risk body mass index (BMI)-adjusted relative risk (RR) for top versus bottom quartile 0.61 (95% confidence intervals (CI) 0.38–0.97), P_trend = 0.02). Glucose levels were positively associated with risk (BMI-adjusted RR top versus bottom quartile 1.69 (95% CI 0.99–2.90), P_trend = 0.03), which appeared stronger among postmenopausal women (BMI-adjusted RR top versus bottom tertile 2.61 (95% CI 1.46–4.66), P_trend = 0.0006, P_{heterogeneity} = 0.13) and never-users of exogenous hormones (P_{heterogeneity} = 0.005 for oral contraceptive (OC) use and 0.05 for hormone replacement therapy-use). The associations of HDL-C and glucose with risk were no longer statistically significant after further adjustment for obesity-related hormones. Plasma total cholesterol, Low-density lipoprotein cholesterol (LDL-C), and triglycerides were not significantly related to overall risk. The presence of MetS was associated with risk (RR 2.12 (95% CI 1.51–2.97)), which increased with the number of MetS factors (P_trend = 0.02). An increasing number of MetS factors other than waist circumference, however, was marginally significantly associated with risk only in women with waist circumference above the median (P_interaction = 0.01). None of the associations differed significantly by fasting status. These findings suggest that metabolic abnormalities and obesity may act synergistically to increase endometrial cancer risk.

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