Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Molecular pathology of ovarian carcinomas

  • 70 Accesses

  • 38 Citations

Abstract

 There is evidence that ovarian cancer may be derived from the progressive transformation of benign and/or borderline tumours. Mutations involving different oncogenes and tumour suppressor genes accumulate during the process of malignant transformation, and the alterations of genes involved in the pathogenesis of familial ovarian cancer are probably early events in ovarian tumorigenesis. BRCA-1 and BRCA-2 act as classical tumour suppressor genes in hereditary tumours, but their role in sporadic tumours remains controversial; however, a high frequency of allele losses in BRCA-1 (17q) and BRCA-2 (13q) loci has been observed in both familial and sporadic tumours. The possible role of mismatch repair genes and microsatellite instability is also controversial, but a role for them has been proposed in borderline tumours. Mutations in K-ras are specific for mucinous tumours and may be related to mucinous differentiation. Finally, a role in tumour progression has been proposed for both c-erb B-2 and p53, but their practical value in prognosis remains questionable.

This is a preview of subscription content, log in to check access.

Author information

Additional information

Received: 29 May 1997 / Accepted: 2 April 1998

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Matias-Guiu, X., Prat, J. Molecular pathology of ovarian carcinomas. Virchows Archiv 433, 103–111 (1998). https://doi.org/10.1007/s004280050224

Download citation

  • Key words Ovary
  • Oncogenes
  • Tumour suppressor genes
  • Pathogenesis
  • Tumours