Abstract

This chapter describes the molecular mechanisms of disease progression of epithelial ovarian cancer. Ovarian cancer is neither a common nor a rare disease. Approximately 85% of ovarian cancers exhibit epithelial histology. Of the epithelial ovarian cancers, 90% are sporadic and occur in the absence of a strong family history. Some 10% of cases are hereditary, with ovarian or breast cancers in multiple generations of each kindred. Most hereditary cancers result from mutations of BRCA1 or BRCA2. Epidemiologic studies have generally failed to demonstrate chemical carcinogens that contribute to the development of sporadic ovarian cancer. One possible exception to this generalization is an association of ovarian cancer with the use of talc products, although the literature contains conflicting reports. Cigarette smoking has been associated with increased risk for a minority of ovarian cancers with mucinous histology. Several observations point to the importance of ovulation as a co-factor in the development of ovarian cancer. Factors that increase the number of ovulatory cycles also increase the risk of ovarian cancer, including early menarche, late menopause, and nulliparity. Conversely, factors that suppress ovulation—including multiple pregnancies and prolonged breastfeeding—decrease the risk of ovarian cancer.

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