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American Journal of Epidemiology Vol. 136, No. 10: 1212-1220
Copyright © 1992 by The Johns Hopkins University School of Hygiene and Public Health
research-article |
Characteristics Relating to ovarian Cancer Risk: Collaborative Analysis of 12 US case-Control Studies
IV. The Pathogenesis of Epithlial Ovarian Cancer
1Division of Epidemiology, Department of a Health Research and Policy, Stanford University School of Medicine Stanford, CA
2Members of the Collaborative Ovarian Cancer Group: Dr. John T. Casagrande, Department of Preventive Medicine, University of Southern California, Los Angeles, CA; Dr. Daniel Cramer, Department of Obstetrics and Gynecotogy, Brigham and Women's Hospital, Boston, MA; Dr. Patricia Hartge, Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD; Dr. Jennifer L Keteey, Division of Epidemiology, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA; Dr. Marion Lee, Department of Epidemiology, University of California, San Francisco, San Francisco, CA; Dr. Nancy C. Lee, Women's Health and FertiHty Branch, Division of Reproductive Health, Centers for Disease Control, Atlanta, GA; Dr. Joseph L. Lyon, Department of Family and Community Medicine, The University of Utah Medical Center, Salt Lake City, UT; Dr. James R. Marshal, Department of Social and Preventive Medicine, State University of New York at Buffalo School of Medicine, Buffalo, NY; Dr. Larry McGowan, Division of Gynecologic Oncology, Department of Obstetrics and Gynecotogy, George Washington University Medical Center, Washington, DC; Dr. Phflip C. Nasca, New York State Department of Health, Bureau of Cancer Epidemiology, School of Public Health, Department of Epidemiology, Albany, NY; Dr. Ralph S. Paffenbarger, Jr., Division of Epidemiology, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA; Dr. Lynn Rosenberg, Slone Epidemiology Unit School of Public Health, Boston University School of Medicine, Brookline, MA; and Dr. Noel S. Weiss, Department of Epidemiology,
Reprint requests to Dr. Alice S. Whittemore, Stanford University School of Medicine, Department of Health Research and Policy, HRP Modular no. 2, Stanford CA 94305-5092
Two hypotheses have been proposed to explain the reduced risk of epithelial ovarian cancer associated with pregnancy and oral contraceptive use. The first states that some sequelae of ovulation increase the likelihood of malignancy and that pregnancies and oral contraceptives protect by suppressing ovulation. The second hypothesis states that circulating levels of pituitary gonadotropins increase the risk of malignancy and that pregnancies and oral contraceptives protect by suppressing secretion of these hormones. The authors evaluate the two hypotheses in light of combined data from 12 United States case-oxitrol studies of epithelial ovarian cancer in white women conducted from 1956 to 1986. While a number of observations support both hypotheses, there are exceptions. Differential risk reduction associated with pregnancy and oral contraceptive use (pregnancy being the more effective in young women and the less effective in older women) conflicts with the first "ovulation" hypothesis, while reduced risk associated with breast feeding and absence of altered risk associated with estrogen replacement therapy conflicts with the second "gonadotropin" hypothesis. Several findings would not have been predicted by either hypothesis, e.g., only weak trends relate cancer risk to age at menarche, and, among older women, no clear trends relate risk to age at menopause. Odds ratio attenuation due to errors in reporting personal characteristics may be responsible for some of these inconsistencies. Multidisciplinary research is needed to clarify the etkrfogic roles of ovulation and gonadotropin stimulation, both of which may enhance carcinogenesis in the ovarian epithelium. Am J Epidemiol 1992: 136: 1212–20
gonadotropins; ovarian neoplasms; ovulation; reproductions
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