Benign, borderline, and malignant ovarian epithelial neoplasms will be examined by molecular and interphase cytogenetic techniques to determine whether ovarian carcinoma develops from progressive cancerization of benign tumors or arises de novo. Alterations in chromosome number, loss of heterozygosity, oncogene amplification and mutation, deletion of tumor suppressor genes, and microsatellite instability will be assessed. These will also be examined in benign-appearing, borderline, and malignant elements within heterogeneous carcinomas, and used to compare pure versus heterogeneous, and serous versus mucinous, tumors. The presence and pattern of nonrandom aberrations should provide insight into the process of tumorigenesis. Cumulative genetic changes would suggest a multistep progression from benign to malignant, while the presence of very different genetic abnormalities would suggest independent origins.
| Wolf, Nancy G; Farver, Carol; Abdul-Karim, Fadi W et al. (2003) Analysis of microsatellite instability and X-inactivation in ovarian borderline tumors lacking numerical abnormalities by comparative genomic hybridization. Cancer Genet Cytogenet 145:133-8 |
| Wolf, N G; Abdul-Karim, F W; Farver, C et al. (1999) Analysis of ovarian borderline tumors using comparative genomic hybridization and fluorescence in situ hybridization. Genes Chromosomes Cancer 25:307-15 |
| Wolf, N G; Abdul-Karim, F W; Schork, N J et al. (1996) Origins of heterogeneous ovarian carcinomas. A molecular cytogenetic analysis of histologically benign, low malignant potential, and fully malignant components. Am J Pathol 149:511-20 |
