Heather M Ochs-Balcom1, Courtney Johnson2, Kristin A Guertin3, Bo Qin4, Alicia Beeghly-Fadiel5, Fabian Camacho6, Traci N Bethea7, Lauren F Dempsey2, Will Rosenow6, Charlotte E Joslin8, Evan Myers9, Patricia G Moorman10, Holly R Harris11, Lauren C Peres12, V Wendy Setiawan13, Anna H Wu13, Lynn Rosenberg14, Joellen M Schildkraut2, Elisa V Bandera4. 1. Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, The State University of New York, Buffalo, NY, USA. hmochs2@buffalo.edu. 2. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA. 3. Department of Public Health Sciences, University of Connecticut School of Medicine, Farmington, CT, USA. 4. Cancer Epidemiology and Health Outcomes, Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA. 5. Department of Medicine, Division of Epidemiology, Vanderbilt University Medical Center, Nashville, TN, USA. 6. Department of Public Health Sciences, University of Virginia, Charlottesville, VA, USA. 7. Office of Minority Health and Health Disparities Research, Georgetown Lombardi Comprehensive Cancer Center, Georgetown University Medical Campus, Washington DC, USA. 8. Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago School of Medicine and Division of Epidemiology and Biostatistics, School of Public Health, Chicago, IL, USA. 9. Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC, USA. 10. Department of Family Medicine and Community Health, Duke University Medical Center, Durham, NC, USA. 11. Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. 12. Department of Cancer Epidemiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA. 13. University of Southern California Norris Comprehensive Cancer Center, and Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California Norris Comprehensive Cancer Center, Los Angeles, CA, USA. 14. Slone Epidemiology Center at Boston University, Boston, MA, USA.
Abstract
BACKGROUND: Obesity disproportionately affects African American (AA) women and has been shown to increase ovarian cancer risk, with some suggestions that the association may differ by race. METHODS: We evaluated body mass index (BMI) and invasive epithelial ovarian cancer (EOC) risk in a pooled study of case-control and nested case-control studies including AA and White women. We evaluated both young adult and recent BMI (within the last 5 years). Associations were estimated using multi-level and multinomial logistic regression models. RESULTS: The sample included 1078 AA cases, 2582 AA controls, 3240 White cases and 9851 White controls. We observed a higher risk for the non-high-grade serous (NHGS) histotypes for AA women with obesity (ORBMI 30+= 1.62, 95% CI: 1.16, 2.26) and White women with obesity (ORBMI 30+= 1.20, 95% CI: 1.02, 2.42) compared to non-obese. Obesity was associated with higher NHGS risk in White women who never used HT (ORBMI 30+= 1.40, 95% CI: 1.08, 1.82). Higher NHGS ovarian cancer risk was observed for AA women who ever used HT (ORBMI 30+= 2.66, 95% CI: 1.15, 6.13), while in White women, there was an inverse association between recent BMI and risk of EOC and HGS in ever-HT users (EOC ORBMI 30+= 0.81, 95% CI: 0.69, 0.95, HGS ORBMI 30+= 0.73, 95% CI: 0.61, 0.88). CONCLUSION: Obesity contributes to NHGS EOC risk in AA and White women, but risk across racial groups studied differs by HT use and histotype.
BACKGROUND: Obesity disproportionately affects African American (AA) women and has been shown to increase ovarian cancer risk, with some suggestions that the association may differ by race. METHODS: We evaluated body mass index (BMI) and invasive epithelial ovarian cancer (EOC) risk in a pooled study of case-control and nested case-control studies including AA and White women. We evaluated both young adult and recent BMI (within the last 5 years). Associations were estimated using multi-level and multinomial logistic regression models. RESULTS: The sample included 1078 AA cases, 2582 AA controls, 3240 White cases and 9851 White controls. We observed a higher risk for the non-high-grade serous (NHGS) histotypes for AA women with obesity (ORBMI 30+= 1.62, 95% CI: 1.16, 2.26) and White women with obesity (ORBMI 30+= 1.20, 95% CI: 1.02, 2.42) compared to non-obese. Obesity was associated with higher NHGS risk in White women who never used HT (ORBMI 30+= 1.40, 95% CI: 1.08, 1.82). Higher NHGS ovarian cancer risk was observed for AA women who ever used HT (ORBMI 30+= 2.66, 95% CI: 1.15, 6.13), while in White women, there was an inverse association between recent BMI and risk of EOC and HGS in ever-HT users (EOC ORBMI 30+= 0.81, 95% CI: 0.69, 0.95, HGS ORBMI 30+= 0.73, 95% CI: 0.61, 0.88). CONCLUSION: Obesity contributes to NHGS EOC risk in AA and White women, but risk across racial groups studied differs by HT use and histotype.
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