New insights regarding pharmacologic approaches for ovarian cancer prevention

The pathogenesis of epithelial ovarian cancer is not completely understood, but it commonly is believed that the process of recurrent ovulation (incessant ovulation) causes genetic damage in ovarian epithelial cells and that sufficient genetic damage can lead to ovarian cancer in susceptible individuals. Under this model, it has been suggested that reproductive and hormonal factors, such as pregnancy and oral contraceptive use, decrease ovarian cancer risk mainly via their inhibitory effects on ovulation. There is mounting evidence that the ovarian epithelium is a hormonally responsive target organ whose biology can be impacted strongly by the local hormonal environment. Progestin-mediated apoptotic effects may be a major mechanism underlying the ovarian cancer protective effects of pregnancy (a high progestin state) and oral contraceptive pill use. Similarly, retinoids, vitamin D, and non-steroidal anti-inflammatory drugs may have biologic effects on the ovarian epithelium that are cancer preventive, whereas androgens may have stimulatory effects on the ovarian epithelium, leading to an increased ovarian cancer risk.