A multistep model for ovarian tumorigenesis: the value of mutation analysis in the KRAS and BRAF genes
Article first published online: 7 MAY 2004
Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 203, Issue 2, pages 617–619, June 2004
How to Cite
Russell, S. E. H. and McCluggage, W. G. (2004), A multistep model for ovarian tumorigenesis: the value of mutation analysis in the KRAS and BRAF genes. J. Pathol., 203: 617–619. doi: 10.1002/path.1563
- Issue published online: 7 MAY 2004
- Article first published online: 7 MAY 2004
- Manuscript Revised: 17 FEB 2004
- Manuscript Accepted: 16 FEB 2004
- Manuscript Received: 10 DEC 2003
- ovarian tumorigenesis;
- KRAS and BRAF mutation
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.