• Britton Trabert, Roberta B Ness, Wei-Hsuan Lo-Ciganic, Megan A Murphy, Ellen L Goode, Elizabeth M Poole, Louise A Brinton, Penelope M Webb, Christina M Nagle, Susan J Jordan, Australian Ovarian Cancer Study Group, Australian Cancer Study (Ovarian Cancer), Harvey A Risch, Mary Anne Rossing, Jennifer A Doherty, Marc T Goodman, Galina Lurie, Susanne K Kjær, Estrid Hogdall, Allan Jensen, Daniel W Cramer, Kathryn L Terry, Allison Vitonis, Elisa V Bandera, Sara Olson, Melony G King, Urmila Chandran, Hoda Anton-Culver, Argyrios Ziogas, Usha Menon, Simon A Gayther, Susan J Ramus, Aleksandra Gentry-Maharaj, Anna H Wu, Celeste Leigh Pearce, Malcolm C Pike, Andrew Berchuck, Joellen M Schildkraut, Nicolas Wentzensen, and Ovarian Cancer Association Consortium.
• Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD (BT, LAB, NW); University of Texas School of Public Health, Houston, TX (RBN); Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA (WL); Channing Division of Network Medicine (MAM, EMP) and Obstetrics and Gynecology Epidemiology Center (DWC, KLT), Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Epidemiology, Harvard School of Public Health, Boston, MA (MAM, EMP, DWC, KLT); Department of Health Sciences Research, Division of Epidemiology, Mayo Clinic, Rochester, MN (ELG); Queensland Institute of Medical Research, Brisbane, Australia (PMW, CMN, SJJ, Australian Ovarian Cancer Study Group, the Australian Cancer Study (Ovarian Cancer); Peter MacCallum Cancer Centre, East Melbourne, Australia (Australian Ovarian Cancer Study Group); Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT (HAR); Program in Epidemiology, Fred Hutchinson Cancer Research Center, Seattle, WA (MAR, JAD); Department of Community and Family Medicine, Section of Biostatistics & Epidemiology, Dartmouth Medical School, Lebanon, NH (JAD); Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA (MTG); Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI (GL); Virus, Lifestyle and Genes, Danish Cancer Society Research Center, Copenhagen, Denmark (SKK, EH, AJ); Gynaecologic Clinic, Copenhagen University Hospital, Copenhagen, Denmark (SKK); The Cancer Institute of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ (EVB, MGK, UC); Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY (SO); Department of Epidemiology, School of Medicine, University of California Irvine, Irvine, CA (HA, AZ); Department of Women's Cancer, University College London, EGA Institute for Wo
• J. Natl. Cancer Inst. 2014 Feb 1; 106 (2): djt431.

BackgroundRegular aspirin use is associated with reduced risk of several malignancies. Epidemiologic studies analyzing aspirin, nonaspirin nonsteroidal anti-inflammatory drug (NSAID), and acetaminophen use and ovarian cancer risk have been inconclusive.MethodsWe analyzed pooled data from 12 population-based case-control studies of ovarian cancer, including 7776 case patients and 11843 control subjects accrued between 1992 and 2007. Odds ratios (ORs) for associations of medication use with invasive epithelial ovarian cancer were estimated in individual studies using logistic regression and combined using random effects meta-analysis. Associations between frequency, dose, and duration of analgesic use and risk of ovarian cancer were also assessed. All statistical tests were two-sided.ResultsAspirin use was associated with a reduced risk of ovarian cancer (OR = 0.91; 95% confidence interval [CI] = 0.84 to 0.99). Results were similar but not statistically significant for nonaspirin NSAIDs, and there was no association with acetaminophen. In seven studies with frequency data, the reduced risk was strongest among daily aspirin users (OR = 0.80; 95% CI = 0.67 to 0.96). In three studies with dose information, the reduced risk was strongest among users of low dose (<100 mg) aspirin (OR = 0.66; 95% CI = 0.53 to 0.83), whereas for nonaspirin NSAIDs, the reduced risk was strongest for high dose (≥500 mg) usage (OR = 0.76; 95% CI = 0.64 to 0.91).ConclusionsAspirin use was associated with a reduced risk of ovarian cancer, especially among daily users of low-dose aspirin. These findings suggest that the same aspirin regimen proven to protect against cardiovascular events and several cancers could reduce the risk of ovarian cancer 20% to 34% depending on frequency and dose of use.

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