A multistep model for ovarian tumorigenesis: the value of mutation analysis in the KRAS and BRAF genes.
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.
Russell
S E Hilary
SE
Department of Oncology, Queen's University Belfast, Belfast City Hospital, Belfast, UK. seh.russell@qub.ac.uk
McCluggage
W Glenn
WG
D018293:Cystadenoma, Serous / Q000235:genetics* / Q000473:pathology; D004848:Epithelium / Q000473:pathology; D005260:Female; D011905:Genes, ras / Q000235:genetics*; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D010051:Ovarian Neoplasms / Q000235:genetics* / Q000473:pathology; D048493:Proto-Oncogene Proteins B-raf; D019908:Proto-Oncogene Proteins c-raf / Q000235:genetics*
C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D019908:Proto-Oncogene Proteins c-raf