Last update:
06-Feb-2008

The incidence of ovarian cancer varies worldwide. There is a strong positive association of older age and family history with the risk of ovarian cancer, and a negative association of oral contraceptive use, increased parity and tubal ligation. There is evidence for more than one pathogenetic mechanism, and the various hypotheses proposed for include ovarian cancer pathogenesis, such as the "incessant ovulation" hypothesis, the "gonadotropin" hypothesis, the "pregnancy clearance" hypothesis, the "exogenous carcinogens" hypothesis, the "ovarian epithelial inflammation" hypothesis, and the "androgen and progesterone" hypothesis. Relevant studies focusing on oral contraceptive use and parity provide evidence supporting the incessant ovulation and the gonadotropin hypotheses, since both factors induce anovulation and are associated with decrease in gonadotropin levels. Conversely, the inverse association of breast-feeding and the positive association of a history of postmenopausal hormone use contradict the gonadotropin hypothesis. Studies that show a reduced risk with increasing parity support the pregnancy clearance hypothesis. Although the biological mechanism of the effects of tubal ligation remains unclear, the associated reduction in ovarian cancer risk is consistent with the theory of exogenous carcinogens. Other studies have provided evidence that ovarian epithelial inflammation (oxidative stress, cytokines, prostaglandins), and imbalance of androgens and progesterone may be involved in the pathogenesis of ovarian cancer. Multi-center stratified epidemiological studies including patients in different stages of the disease and with different histological types of ovarian cancer are needed to clarify the role of potential risk factors in ovarian cancer pathogenesis, in order to improve the prevention and the treatment of the disease.

Key words: Εpidemiology, Ovarian cancer, Pathogenesis.