Growth regulation of ovarian cancer.

The disease referred to as ovarian cancer is composed of those tumors derived from the ovarian surface epithelium. Ovarian cancer incidence peaks in postmenopausal women, when the hormonal milieu is in a state of flux. The ovarian carcinomas have histologic characteristics of classical endocrine responsive tissues. For example, the serous tumors are similar in appearance to the epithelium of the fallopian tube, the mucinous tumors to that of the endocervix, and the endometrioid tumors to that of the endometrium. These observations alone suggest a role for hormones in disease etiology and progression. In addition, much experimental evidence has accumulated that shows direct hormonal and growth factor effects on the normal and neoplastic ovarian surface epithelium and the potential for responsiveness based on the presence of specific receptors. The concept that growth stimulatory substances, by their impact on mitosis and cell number, may influence the rate of mutations that could confer malignant transformation serves as an additional mechanism by which growth stimulatory substances can influence ovarian cancer initiation. With the emergence of new molecular biology techniques, future studies should unravel the mechanisms by which steroid hormones, peptide hormones, and peptide growth factors influence the development of ovarian cancer.