Molecular pathology of ovarian cancer

Kruti P. Maniar, Ie Ming Shih, Robert J. Kurman

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

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 languageEnglish (US)
Title of host publicationMolecular Surgical Pathology
PublisherSpringer New York
Pages129-149
Number of pages21
Volume9781461449003
ISBN (Electronic)9781461449003
ISBN (Print)1461448999, 9781461448990
DOIs
StatePublished - May 1 2013

ASJC Scopus subject areas

  • General Medicine

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