Detection of numerical chromosome anomalies in interphase cells of ovarian carcinomas using fluorescence in situ hybridization
Brock, J.A.; Liu, W.H.; Smith, S.T.; Young, S.R.
Genes Chromosomes and Cancer 16(2): 120-129
1996
ISSN/ISBN: 1045-2257 PMID: 8818659 DOI: 10.1002/(sici)1098-2264(199606)16:2<120::aid-gcc6>3.0.co;2-1
Accession: 008441093
Fluorescence in situ hybridization was used in interphase cells of 30 ovarian carcinomas to detect numerical changes in copy number of 13 different centromeres (1, 2, 3, 4, 6, 7, 8, 10, 11, 12, 17, 18, and X). Thirty-seven percent of samples (11/30) were near diploid and demonstrated only minor changes in centromere copy number, involving gain and/or loss of one or a few centromeres. The most common changes included loss of centromeres 4,6, 17, and 18 and gain of centromere 1. The remaining 63% of samples were hyperdiploid and demonstrated a general increase in copy number of most or all centromeres examined. Among these samples, the centromere of chromosome I was most often found to be at higher copy number. Centromeres that were less often at increased copy or deleted within the hyperdiploid samples include centromeres 4, 17, 18, and X. These results suggest that tumor-suppressor genes that are located on chromosomes 4, 6, 17, and 18 may be involved in the development and progression of ovarian cancer.