Ovarian cancer is believed to result from "incessant ovulation." Release of an oocyte results in damage to ovarian epithelium. Aberrant repair of this damaged epithelium may result in cell changes ultimately leading to ovarian cancer. Conditions that decrease exposure to ovulation such as parity and breastfeeding are associated with
Table 4-1. Ovarian Cancer Risk
Population Ovarian Cancer Risk
General population 1.4% (1 in 70)
One first-degree relative with ovarian 4-5%
Two first-degree relatives with ovarian 7%
Deleterious BRCA1 mutation 30-40%
Deleterious BRCA2 mutation 15-25%
Hereditary nonpolyposis colorectal cancer 5-10%
a decreased risk of ovarian cancer. In contrast, nulliparity, early menarche, and late menopause all result in an increased number of ovulatory cycles and are linked to an increased risk of ovarian malignancy. Alternatively, exposure to progestins may lead to apoptosis in aberrant epithelial cells. Rodriguez and colleagues4 exposed macaques to combination oral contraceptive pills, to the estrogen component of oral contraceptive pills only, to the progestin component of oral contraceptive pills, or to no hormones. The ovarian epithelium of macaques exposed to the oral contraceptive pill or to the progestin component demonstrated only a statistically significant increase in the proportion of apoptotic cells. This apoptotic pathway can lead to ovarian cancer prevention. Therefore, based on their ability to suppress ovulation and their progestin-dominant formulation, oral contraceptive pills offer an attractive candidate for chemoprevention.
Prophylactic surgery for ovarian cancer involves removal of the adnexa bilaterally. Although this theoretically eliminates the risk of serous carcinomas of the ovary and fallopian tube, there remains a risk of primary peritoneal serous carcinoma. In addition, if the uterus remains in situ, the intramural portion of fallopian tube is at risk for the development of serous carcinoma.
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