PO.PS01.12 · 人群科学

Inflammation-related exposures and histotype- specific ovarian cancer risk in the Ovarian Cancer Association Consortium (OCAC)

编号 6261 展板 23 时间 4/21 02:00–05:00 区域 Section 33 主讲 Maxwell Akonde, BS

分会场 Environmental and Occupational Risk Factors, Infection, and Aging

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作者与单位

Maxwell Akonde¹, Britton Trabert², SHELLEY TWOROGER³, Allan Jensen⁴, Kathryn L. Terry⁵, Joshua Sampson⁶, Hoda Anton-Culver⁷, David Bowtell⁸, Elisa V. Bandera⁹, Angela Brooks-Wilson¹⁰, Andrew Berchuck¹¹, Daniel William Cramer¹², Linda S. Cook¹³, Julie M. Cunningham¹⁴, Jennifer A. Doherty¹⁵, Ellen L. Goode¹⁶, Marc T. Goodman¹⁷, Holly Ruth Harris¹⁸, Susanne K. Kjaer¹⁹, Nhu Le²⁰, Alice Wen-Ron Lee²¹, Francesmary Modugno²², Kirsten B. Moysich²³, Celeste Pearce²⁴, Malcolm C. Pike²⁵, Harvey A. Risch²⁶, Mary A. Rossing²⁷, Joellen M. Schildkrau²⁸, Daniel O. Stram²⁹, Rebecca Sutphen³⁰, David Van Den Berg³¹, Penelope M. Webb³², Anna Wu³³, Argyrios Ziogas³⁴, Nicolas A. Wentzensen³⁵

¹Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD,²University of Utah Huntsman Cancer Institute, Salt Lake City, UT,³Oregon Health and Science University, Knight Cancer Institute, Portland, OR,⁴Department of Lifestyle, Reproduction and Cancer, Danish Cancer Society Research Center, Copenhagen, Denmark,⁵Asst. Professor, Dept. of OB/GYN, Brigham and Women's Hospital, Boston, MA,⁶Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rocville, MD,⁷Chair & Professor, Dept. of Epidemiology, Department of Medicine, Genetic Epidemiology Research Institute, University of California, Irvine, Irvine, CA,⁸Cancer Genetics Laboratory, Research Division, Peter MacCallum Cancer Center, Melbourne, Australia,⁹Rutgers Cancer Institute of New Jersey, New Brunswick, NJ,¹⁰Head, Cancer Genetics, BC Cancer Research Centre, Vancouver, BC, Canada,¹¹Duke University Medical Center, Durham, NC,¹²Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA,¹³Epidemiology, School of Public Health, University of Colorado, Aurora, CO,¹⁴Mayo Clinic College of Medicine and Science, Rochester, MN,¹⁵Huntsman Cancer Institute, Department of Population Health Sciences, University of Utah, Salt Lake City, UT,¹⁶Mayo Clinic, Rochester, MN,¹⁷Cedars-Sinai Medical Center, Los Angeles, CA,¹⁸Fred Hutchinson Cancer Center, Seattle, WA,¹⁹Department of Virus, Lifestyle and Genes, Danish Cancer Institute, Copenhagen, Denmark,²⁰Cancer Control Research, BC Cancer Agency, 675 West 10th Avenue, Vancouver, BC, Canada,²¹California State University, Fullerton, Fullerton, CA,²²Womens Cancer Research Center, Magee-Womens Research Institute and Hillman Cancer Center, Pittsburgh, PA,²³Professor, Dept. of Epidemiology, Roswell Park Cancer Institute, Buffalo, NY,²⁴Univ. of Michigan School of Public Health, Ann Arbor, MI,²⁵Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY,²⁶Professor, Dept. of Epidemiology & Public Health, Yale Univ. School of Medicine, New Haven, CT,²⁷Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, WA,²⁸Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA,²⁹Department of Preventive Medicine, University of Southern California, Los Angeles, CA,³⁰Epidemiology Center, College of Medicine, University of South Florida, Tampa, FL,³¹Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA,³²Queensland Institute of Medical Research, Herston, Australia,³³Department of Population and Public Health Sciences, University of Southern California, Los Angeles, CA,³⁴Department of Medicine, Genetic Epidemiology Research Institute, University of California, Irvine, Irvine, CA,³⁵NCI Div. of Cancer Epidemiology & Genetics, Bethesda, MD

摘要 Abstract

Background: Chronic inflammation is implicated in ovarian carcinogenesis, but how different inflammation-related exposures individually or jointly affect histotype-specific associations remains unclear. Materials and Methods: We pooled data from 16 case-control studies in the Ovarian Cancer Association Consortium to evaluate associations of eight inflammation-related factors (anti-inflammatory: aspirin use, tubal ligation (TL); pro-inflammatory: endometriosis, obesity, lifetime ovulatory cycles (LOC), smoking, pelvic inflammatory disease (PID), polycystic ovary syndrome (PCOS)) with epithelial ovarian cancer (OvC) by histologic subtype. We examined individual associations and clustering of risk factors across histotypes and computed population attributable risk (PAR) for each factor. We assessed additive and multiplicative interactions for exposure combinations. Results: Associations with OvC risk differed by histotype (e.g., high-grade serous: aspirin: OR=0.90; 95%CI 0.82, 0.99; TL: OR=0.80; 95%CI 0.73, 0.88; overall serous: endometriosis: OR=1.17; 95%CI 1.03, 1.31; high LOC: OR=1.42; 95%CI 1.28, 1.58; obesity (low-grade serous): OR=1.50; 95%CI 1.14, 1.98). Clustering analyses showed highly correlated risk profiles in endometrioid and clear cell (r=0.91). High-grade serous and mucinous profiles were moderately correlated with endometrioid and clear cell (r=0.60) tumors. The profile for low-grade serous (r=0.36) tumors was distinct from other histotypes. PAR estimates suggested modifying aspirin use, TL, and LOCs could substantially reduce burdens of endometrioid, clear cell and mucinous tumors. Out of 28 exposure combinations tested in overall OvC and 189 by histotype, we observed 12 interactions. Not using aspirin regularly showed positive additive interactions with obesity and high LOCs, particularly in endometrioid tumors (obesity relative excess risk due to interaction (RERI)=0.74, 95%CI 0.31, 1.18; P int =0.001 for; LOCs RERI=0.80, 95%CI 0.03, 1.56; P int =0.04). Not using aspirin regularly also showed a positive additive interaction with endometriosis in clear cell tumors (RERI=1.77, 95%CI 0.03, 3.52; P int =0.05). Lack of TL showed positive interactions with obesity in endometrioid (RERI=0.86, 95%CI 0.17, 1.53; P int =0.01) and mucinous (RERI=1.10, 95%CI 0.23, 1.97; P int =0.01) tumors, while negative additive interactions were observed for smoking and endometriosis in endometrioid tumors (RERI=-1.12, 95%CI -2.19, -0.05; P int =0.04). A multiplicative interaction was observed between obesity and endometriosis in mucinous tumors (P int =0.01). Conclusion: The findings suggest ovarian tumorigenesis is strongly shaped by pro- and anti-inflammatory pathways that act largely independently. Further examining these pathways may clarify the origins of histotype heterogeneity and guide prevention strategies.

利益披露 Disclosure

M. Akonde, None.. S. Tworoger, None.. A. Jensen, None.. J. Sampson, None.. H. Anton-Culver, None.. D. Bowtell, None.. D. W. Cramer, None.. L. S. Cook, None.. J. A. Doherty, None.. S. K. Kjaer, None.. N. Le, None.. F. Modugno, None.. M. A. Rossing, None.. J. M. Schildkrau, None.. R. Sutphen, None.. D. Van Den Berg, None.. A. Wu, None.. A. Ziogas, None.

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