Jennifer Ose1,2, Helena Schock1, Elizabeth M Poole3, Matti Lehtinen4, Kala Visvanathan5, Kathy Helzlsouer5, Julie E Buring6,7, I-Min Lee6,7, Anne Tjønneland8, Marie-Christine Boutron-Ruault9,10, Antonia Trichopoulou11,12, Amalia Mattiello13, N Charlotte Onland-Moret14, Elisabete Weiderpass15,16,17,18, María-José Sánchez19,20, Annika Idahl21, Ruth C Travis22, Sabina Rinaldi23, Melissa A Merritt24, Nicolas Wentzensen25, Shelley S Tworoger3,7, Rudolf Kaaks1, Renée T Fortner26. 1. Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120, Heidelberg, Baden-Württemberg, Germany. 2. Department of Population Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA. 3. Channing Division of Network Medicine, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA, USA. 4. Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden. 5. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. 6. Division of Preventive Medicine, Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA, USA. 7. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 8. Unit of Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen, Denmark. 9. Université Paris-Saclay, Université Paris-Sud, UVSQ, CESP, INSERM, Villejuif, France. 10. Gustave Roussy, 94805, Villejuif, France. 11. Hellenic Health Foundation, Athens, Greece. 12. Unit of Nutritional Epidemiology and Nutrition in Public Health, Department of Hygiene, Epidemiology and Medical Statistics, WHO Collaborating Center for Nutrition and Health, University of Athens Medical School, Athens, Greece. 13. Dipartimento di Medicina Clinica e Chirurgia, Federico II University, Naples, Italy. 14. Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. 15. Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. 16. Department of Research, Cancer Registry of Norway, Oslo, Norway. 17. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden. 18. Genetic Epidemiology Group, Folkhälsan Research Center, Helsinki, Finland. 19. Escuela Andaluza de Salud Pública, Instituto de Investigación Biosanitaria ibs.GRANADA, Hospitales Universitarios de Granada/Universidad de Granada, Granada, Spain. 20. CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, Spain. 21. Department of Clinical Sciences, Obstetrics and Gynecology, Umea University, Umea, Sweden. 22. Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK. 23. Section of Nutrition and Metabolism, International Agency for Research on Cancer (IARC), Lyon, France. 24. Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. 25. Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. 26. Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120, Heidelberg, Baden-Württemberg, Germany. r.fortner@dkfz-heidelberg.de.
Abstract
PURPOSE: Biologic evidence suggests that the Insulin-like growth factor (IGF)-family may be involved in the etiology of epithelial invasive ovarian cancer (EOC). However, prospective studies investigating the role of IGF-I in ovarian carcinogenesis have yielded conflicting results. METHODS: We pooled and harmonized data from 6 case-control studies nested within the Ovarian Cancer Cohort Consortium to investigate the association between pre-diagnosis IGF-I concentrations and subsequent risk of EOC. We evaluated IGF-I concentrations and risk of EOC overall and by tumor subtype (defined by histology, grade, stage) in 1,270 cases and 2,907 matched controls. Multivariable conditional logistic regression models were used to calculate odds ratios (OR) and 95% confidence intervals (CI). RESULTS: Doubling of IGF-I concentration was associated with significantly lower risk of overall EOC [ORlog2 = 0.82; CI 0.72-0.93]. We observed no heterogeneity by tumor characteristics (e.g., histology, p het = 0.62), menopausal status at blood collection (p het = 0.79), or age at diagnosis (p het = 0.60). CONCLUSIONS: These results suggest that IGF-I concentrations are inversely associated with EOC risk, independent of histological phenotype. Future prospective research should consider potential mechanisms for this association, including, considering other members of the IGF-family to better characterize the role of IGF-signaling in the etiology of EOC.
PURPOSE: Biologic evidence suggests that the Insulin-like growth factor (IGF)-family may be involved in the etiology of epithelial invasive ovarian cancer (EOC). However, prospective studies investigating the role of IGF-I in ovarian carcinogenesis have yielded conflicting results. METHODS: We pooled and harmonized data from 6 case-control studies nested within the Ovarian Cancer Cohort Consortium to investigate the association between pre-diagnosis IGF-I concentrations and subsequent risk of EOC. We evaluated IGF-I concentrations and risk of EOC overall and by tumor subtype (defined by histology, grade, stage) in 1,270 cases and 2,907 matched controls. Multivariable conditional logistic regression models were used to calculate odds ratios (OR) and 95% confidence intervals (CI). RESULTS: Doubling of IGF-I concentration was associated with significantly lower risk of overall EOC [ORlog2 = 0.82; CI 0.72-0.93]. We observed no heterogeneity by tumor characteristics (e.g., histology, p het = 0.62), menopausal status at blood collection (p het = 0.79), or age at diagnosis (p het = 0.60). CONCLUSIONS: These results suggest that IGF-I concentrations are inversely associated with EOC risk, independent of histological phenotype. Future prospective research should consider potential mechanisms for this association, including, considering other members of the IGF-family to better characterize the role of IGF-signaling in the etiology of EOC.
Authors: Britton Trabert; Ligia Pinto; Patricia Hartge; Troy Kemp; Amanda Black; Mark E Sherman; Louise A Brinton; Ruth M Pfeiffer; Meredith S Shiels; Anil K Chaturvedi; Allan Hildesheim; Nicolas Wentzensen Journal: Gynecol Oncol Date: 2014-08-23 Impact factor: 5.482
Authors: Meghan A McSorley; Anthony J Alberg; Diane S Allen; Naomi E Allen; Louise A Brinton; Joanne F Dorgan; Michael Pollak; Yuzhen Tao; Kathy J Helzlsouer Journal: Obstet Gynecol Date: 2007-04 Impact factor: 7.661
Authors: Annekatrin Lukanova; Eva Lundin; Paolo Toniolo; Andrea Micheli; Arslan Akhmedkhanov; Sabina Rinaldi; Paola Muti; Per Lenner; Carine Biessy; Vittorio Krogh; Anne Zeleniuch-Jacquotte; Franco Berrino; Göran Hallmans; Elio Riboli; Rudolf Kaaks Journal: Int J Cancer Date: 2002-10-20 Impact factor: 7.396