Comparative genomic hybridization in inherited and sporadic ovarian tumorsin Israel

To gain an understanding of the molecular mechanisms of or arian cancer, we analyzed 16 ovarian tumors from Jewish Israeli patients by comparative gen omic hybridization: 12 invasive epithelial tumors (including three BRCA1 an d one BRCA2 mutation carriers), 2 primary peritoneal carcinomatosis, I pseu domyxoma peritoneii tumor, and 1 sertoli cell tumor. We similarly analyzed 1 normal ovary from a BRCA1 mutation carrier, and 3 metastases. The most co mmon abnormalities in epithelial tumors rr-ere amplification of 8q22.1-ter (8/12, 66.6%), 1q22-32.1 (5/22, 41.6%), 3q, 10p (4/12, 33.3% for each), and deletions of 9q (5/22, 41.6%) and 16q21-24 (4/12, 33.3%). All 3 BRCA1 muta tion carriers and 2 of 8 sporadic cases displayed 9q deletion, and 2 of 3 B RCA1 mutation carriers, but none of the sporadic cases, had deletion of chr omosome 19. The range of genetic changes in primary peritoneal tumors and e pithelial of ovarian cancers nas similar, though the mean number of alterat ions in the former rr as less (3.5/tumor versus 8/tumor). Our preliminary r esults may indicate that inherited predisposition to ovarian cancer possibl y entails preferential somatic deletions of chromosomes 9 and 19. (C) 2000 Elsevier Science Inc. All rights reserved.