The origin of epithelial ovarian cancer remains unknown. It is believed to develop from ovarian surface epithelium, post-ovulatory inclusion cysts, endometriosis and more recently the fimbrial end of the fallopian tube. Molecular evidence suggests that ovarian cancer may progress both through a step-wise mutation process (low-grade pathway, type I), and a separate pathway with high genetic instability leading to rapid metastasis without an identifiable precursor lesion (high-grade pathway, type II). This sub-classification explains the clinical and biological heterogeneity of ovarian cancer and highlights the importance for developing novel diagnostics and therapeutics targeting two unique diseases-type I and type II ovarian carcinomas. This article summarises current knowledge of the aetiology and molecular basis of ovarian cancer and discusses recent clinical strategies for type I and type II disease.