Abstract
Epithelial ovarian cancer remains the most lethal of all the gynecologic malignancies, and is characterized by significant clinical heterogeneity. Variables include the number and site of metastases, surgical cytoreducibility of advanced stage disease, and differing responses to chemotherapy. While the majority of women with ovarian cancer enter remission following initial surgical cytoreduction and platinum-taxane chemotherapy, most will recur and ultimately succumb to progressive disease refractory to cytotoxic regimens. Epithelial ovarian cancers arise from the ovarian surface epithelium (OSE), which is an extension of the peritoneal mesothelium and contains a single layer of flat to cuboidal epithelial cells responsive to sex steroid hormones. While the complex interactions between the endocrine and cellular growth pathways are yet to be established, significant evidence suggests androgen signaling, through its specific receptor, plays an important role in modulating both risk of epithelial ovarian cancer as well as its tumor biology and behavior. This review examines the epidemiologic and molecular data supporting a role for androgens in ovarian carcinogensis and pathobiology.