The Dualistic Model of Ovarian Carcinogenesis - Revisited, Revised, and Expanded Ovarian Cancer and Us OVARIAN CANCER and US Ovarian Cancer and Us

Blog Archives: Nov 2004 - present


Special items: Ovarian Cancer and Us blog best viewed in Firefox

Search This Blog

Saturday, August 27, 2016

The Dualistic Model of Ovarian Carcinogenesis - Revisited, Revised, and Expanded

full text (pdf)

Departments of Pathology, Gynecology and Obstetrics and Oncology, Johns Hopkins Medical Institutions, Baltimore, Maryland

Since our proposal of a dualistic model of epithelial ovarian carcinogenesis more than a decade ago, a large number of molecular and histopathologic studies were published that have provided important insights into the origin and molecular pathogenesis of this disease. This has required that the original model be revised and expanded to incorporate these findings. The new model divides type I tumors into three groups: i) endometriosis-related tumors that include endometrioid, clear cell, and seromucinous carcinomas; ii) low-grade serous carcinomas; and iii) mucinous carcinomas and malignant Brenner tumors. As in the previous model, type II tumors are composed, for the most part, of high-grade serous carcinomas that can be further subdivided into morphologic and molecular subtypes. Type I tumors develop from benign extraovarian lesions that implant on the ovary and which can subsequently undergo malignant transformation, whereas many type II carcinomas develop from intraepithelial carcinomas in the fallopian tube and, as a result, disseminate as carcinomas that involve the ovary and extraovarian sites, which probably accounts for their clinically aggressive behavior. The new molecular genetic data, especially those derived from next-generation sequencing, further underline the heterogeneity of ovarian cancer and identify actionable mutations. The dualistic model highlights these differences between type I and type II tumors which, it can be argued, describe entirely different groups of diseases.
Supported by the US Department of Defense grant OCRP-OC-100517, the Richard W. TeLinde Research Program, Johns Hopkins University, and the Roseman Ovarian Cancer Foundation (R.J.K. and I.M.S.); and NIH grant CA165807 (I.M.S.).


Post a Comment

Your comments?