Abstract
Ovarian cancer is associated with 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 carcinosarcomas). 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 TP53, 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 |
|---|---|
| Title of host publication | Molecular Surgical Pathology |
| Subtitle of host publication | Second Edition |
| Publisher | Springer International Publishing |
| Pages | 271-296 |
| Number of pages | 26 |
| ISBN (Electronic) | 9783031351181 |
| ISBN (Print) | 9783031351174 |
| DOIs | |
| State | Published - 01 01 2023 |
| Externally published | Yes |
Bibliographical note
Publisher Copyright:© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2013, 2023.
Keywords
- BRAF mutation
- KRAS mutation
- Lynch syndrome
- Microsatellite instability
- Ovarian cancer
