Abstract
Ovarian cancer is associated with a high morbidity and mortality, and is the leading cause of gynecologic cancer-related death in the US. In recent years, the molecular pathophysiology of ovarian tumors has been better elucidated, allowing for the distinction of two tumor types: the more indolent type I tumors (encompassing endometrioid, clear cell, low-grade serous, and mucinous carcinomas) and the highly aggressive type II tumors (encompassing high-grade serous carcinomas and malignant mixed müllerian tumors). Type I tumors are related to abnormalities in the MAPK signaling pathway (KRAS and BRAF mutations), the PI3K/Akt2/PTEN pathway, and the Wnt/beta-catenin pathway, as well as mutations in other genes such as ARID1a, PPP2R1A, and HNF1-beta. Type II tumors, in contrast, are characterized by mutations in p53, as well as inactivation of BRCA1/2 and mutations in genes such as Notch3, Rsf-1, and NAC1. In this chapter, we discuss the characteristics and frequency of these molecular abnormalities, with an emphasis on their implications for diagnosis and treatment.
Original language | English (US) |
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Title of host publication | Molecular Surgical Pathology |
Publisher | Springer New York |
Pages | 129-149 |
Number of pages | 21 |
Volume | 9781461449003 |
ISBN (Electronic) | 9781461449003 |
ISBN (Print) | 1461448999, 9781461448990 |
DOIs | |
State | Published - May 1 2013 |
ASJC Scopus subject areas
- General Medicine