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

J Pathol. 2004 Jun;203(2):617-9. doi: 10.1002/path.1563.

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.

Publication types

  • Comment

MeSH terms

  • Cystadenoma, Serous / genetics*
  • Cystadenoma, Serous / pathology
  • Epithelium / pathology
  • Female
  • Genes, ras / genetics*
  • Humans
  • Models, Biological
  • Mutation
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / pathology
  • Proto-Oncogene Proteins B-raf
  • Proto-Oncogene Proteins c-raf / genetics*

Substances

  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • Proto-Oncogene Proteins c-raf