HISTOLOGY AND HISTOPATHOLOGY

Cellular and Molecular Biology



Review

Molecular genetics of ovarian carcinomas

J. Diebold

Pathological Institute, Ludwig-Maximilians-University of Munich, Germany

Offprint requests to: Priv.-Doz. Dr. med. J. Diebold, Pathologisches Institut der Universität, Thalkirchner Str. 36, D-80337 Munchen, Germany. Fax: +49-89-5160-4079. e-mail: Joachim.Diebold@lrz-muenchen.de

 

Summary. The phenotypic variability of epithelial ovarian neoplasms correlates with a diversity of changes at the molecular level. Invasive serous and un-differentiated ovarian carcinomas are characterized by p53 mutations with p53 protein accumulation, extensive loss of genetic material of chromosome 17 and complex changes on many other chromosomes, e.g. amplification of oncogenes. These alterations are seen only in a minority of mucinous and endometrioid carcinomas, mainly in advanced stages. Overexpression of bcl-2 is seen most frequently in endometrioid carcinomas (ca. 90% of cases), which in addition show microsatellite instability in around a third of the cases, as has been described in endometrioid endometrial carcinomas. KRAS mutations are characteristic for mucinous LMP tumors and mucinous carcinomas (40-50% of cases) and are also found in a third of serous LMP tumors. In addition, serous LMP tumors show mild microsatellite instability in 30%. However, complex chromosomal aberrations are never seen in these neoplasms. Histol. Histopathol. 14, 269-277 (1999)

 

Key words: Ovarian carcinoma, Molecular genetics, Molecular pathology

DOI: 10.14670/HH-14.269