HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Cust, A. E Articles by Riboli, E. Search for Related Content PubMed PubMed Citation Articles by Cust, A. E Articles by Riboli, E.

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.

This article has been cited by other articles:

				T. Bjorge, T. Stocks, A. Lukanova, S. Tretli, R. Selmer, J. Manjer, K. Rapp, H. Ulmer, M. Almquist, H. Concin, et al. Metabolic Syndrome and Endometrial Carcinoma Am. J. Epidemiol., March 10, 2010; (2010) kwq006v1. [Abstract] [Full Text] [PDF]

				G. Lane Obesity and gynaecological cancer Menopause Int, March 1, 2008; 14(1): 33 - 37. [Abstract] [Full Text] [PDF]