[Paradigm Shift in Ovarian Tumor Pathology from the View of Genomic Abnormalities].

A decade of accumulated evidence has led to significant progress and a paradigm shift in ovarian tumor pathology. Now, ovarian carcinoma is widely recognized as a heterogeneous group of neoplasms with regard to histogenesis and underlying molecular mechanisms. Ovarian carcinoma is, therefore, divided into 2 clinicopathologic groups: type 1 and type 2 tumors. Type 1 tumors arise in association with benign neoplastic conditions (adenoma-carcinoma sequence). They include endometriosis-related ovarian neoplasias, such as clear cell carcinoma and low-grade endometrioid carcinoma, which are derived from atypical endometriosis or adenofibroma, as well as mucinous carcinoma and low-grade serous carcinoma, which are commonly associated with mucinous and serous borderline tumors, respectively. In contrast, type 2 tumors, which arise de novo directly from the normal epithelium, include high-grade serous and endometrioid carcinoma, carcinosarcoma, and undifferentiated carcinoma. Notably, the hypothesis that most high-grade serous ovarian carcinoma is not of ovarian origin and, rather, is associated with serous tubal intraepithelial carcinoma (STIC), which is mostly found on the fimbrial end of the fallopian tube in up to 70% of cases of high-grade serous carcinoma, is universally accepted. Understanding ovarian carcinoma molecular pathogenesis should aid in developing effective therapeutic strategies for these particular tumors.