A multistep model for ovarian tumorigenesis: the value of mutation analysis in the KRAS and BRAF genes

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Abstract
Epithelial ovarian tumours represent a complex group of histological subtypes and there has long been controversy over the question of a precursor lesion for these neoplasms. The application of mutation analysis of the KRAS and BRAF genes (members of the RAS‐RAF‐MEK‐ERK‐MAP kinase pathway) is consistent with the model for progression of mucinous carcinomas and a subset of serous carcinomas (the so‐called low‐grade serous carcinomas) through benign and borderline lesions. The relatively high incidence of BRAF and KRAS mutations in serous borderline tumours and low‐grade serous carcinomas, and their extremely low incidence/absence in high‐grade serous carcinomas, provide strong evidence that high‐grade carcinomas do not arise through this intermediate step. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.