To gain an understanding of the molecular mechanisms of ovarian cancer, we analyzed 16 ovarian tumors from Jewish Israeli patients by comparative genomic hybridization: 12 invasive epithelial tumors (including three BRCA1 and one BRCA2 mutation carriers), 2 primary peritoneal carcinomatosis, 1 pseudomyxoma peritoneii tumor, and 1 sertoli cell tumor. We similarly analyzed 1 normal ovary from a BRCA1 mutation carrier, and 3 metastases. The most common abnormalities in epithelial tumors were amplification of 8q22.1-ter (8/12, 66.6%), 1q22-32.1 (5/12, 41.6%), 3q, 10p (4/12, 33.3% for each), and deletions of 9q (5/12, 41.6%) and 16q21-24 (4/12, 33.3%). All 3 BRCA1 mutation carriers and 2 of 8 sporadic cases displayed 9q deletion, and 2 of 3 BRCA1 mutation carriers, but none of the sporadic cases, had deletion of chromosome 19. The range of genetic changes in primary peritoneal tumors and epithelial ovarian cancers was similar, though the mean number of alterations in the former was less (3.5/tumor versus 8/tumor). Our preliminary results may indicate that inherited predisposition to ovarian cancer possibly entails preferential somatic deletions of chromosomes 9 and 19.