[Molecular genetics of epithelial ovarian neoplasms: correlations with phenotype and biological behavior]

The phenotypic variability of epithelial ovarian neoplasms correlates with a diversity of changes on the molecular level. Invasive serous and undifferentiated ovarian carcinomas are characterized by p53 mutations, extensive loss of genetic material of chromosome 17 and complex changes on many other chromosomes. 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 cases, as has been described in endometrioid endometrial carcinomas. KRAS mutations are characteristic for mucinous LMP tumors (borderline tumors) and mucinous carcinomas (40-50% of cases). Furthermore, KRAS mutations have been described in around a third of serous LMP tumors, which in addition show microsatellite instability in up to 40% of cases. Serous LMP tumors never harbour complex chromosomal aberrations.