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JNCI Journal of the National Cancer Institute 1999 91(17):1459-1467; doi:10.1093/jnci/91.17.1459
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 17, 1459-1467, September 1, 1999
© 1999 Oxford University Press


REVIEW

Possible Role of Ovarian Epithelial Inflammation in Ovarian Cancer

Roberta B. Ness, Carrie Cottreau

Affiliations of authors: R. B. Ness, Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, University of Pittsburgh Cancer Institute, and Magee-Womens Research Institute, Pittsburgh, PA; C. Cottreau, Department of Epidemiology, University of Pittsburgh Graduate School of Public Health.

Correspondence to: Roberta B. Ness, M.D., M.P.H., University of Pittsburgh Graduate School of Public Health, 130 DeSoto St., Rm. 513, Parran Hall, Pittsburgh, PA 15261 (e-mail: repro{at}vms.cis.pitt.edu).

Ovarian cancer is a commonly fatal disease for which prevention strategies have been limited, in part because of a lack of understanding of the underlying biology. This paper reviews the epidemiologic literature in the English language on risk factors and protective factors for ovarian cancer and proposes a novel hypothesis that a common mechanism underlying this disease is inflammation. Previous hypotheses about the causes of ovarian cancer have attributed risk to an excess number of lifetime ovulations or to elevations in steroid hormones. Inflammation may underlie ovulatory events because an inflammatory reaction is induced during the process of ovulation. Additional risk factors for ovarian cancer, including asbestos and talc exposure, endometriosis (i.e., ectopic implantation of uterine lining tissue), and pelvic inflammatory disease, cannot be directly linked to ovulation or to hormones but do cause local pelvic inflammation. On the other hand, tubal ligation and hysterectomy act as protective factors, perhaps by diminishing the likelihood that the ovarian epithelium will be exposed to environmental initiators of inflammation. Inflammation entails cell damage, oxidative stress, and elevations of cytokines and prostaglandins, all of which may be mutagenic. The possibility that inflammation is a pathophysiologic contributor to the development of ovarian cancer suggests a directed approach to future research



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