Multiple polysomies in breast carcinomas: Preferential gain of chromosomes1, 5, 6, 7, 12, 16, 17, 18, and 19

Citation
A. Adeyinka et al., Multiple polysomies in breast carcinomas: Preferential gain of chromosomes1, 5, 6, 7, 12, 16, 17, 18, and 19, CANC GENET, 111(2), 1999, pp. 144-148
Citations number
27
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
CANCER GENETICS AND CYTOGENETICS
ISSN journal
01654608 → ACNP
Volume
111
Issue
2
Year of publication
1999
Pages
144 - 148
Database
ISI
SICI code
0165-4608(199906)111:2<144:MPIBCP>2.0.ZU;2-H
Abstract
Chromosome G-banding analysis of metaphase cells from 16 primary breast car cinomas revealed the presence of multiple polysomies in near-diploid as wel l as in polyploid cells. Chromosome 17 was preferentially gained in 7 tumor s, followed in frequency by chromosomes 1, 12, and 19 (5 tumors each), and chromosomes 5, 6, 7, 16, and 18 (4 tumors each). Eleven of the 16 carcinoma s had, apart from the clones exhibiting the numerical gains, other unrelate d clones. Nine of these 11 cases had clones with structural chromosome aber rations, 5 of which had structural aberrations involving the short arm of c hromosome 3. The biologic significance, if any: of this seemingly nonrandom coexistence of multiple polysomies with structural aberrations of 3p is at present not known. The pattern of numerical chromosome aberrations observe d in the present study is comparable to previous results from fluorescence in situ hybridization (FISH) studies, with the use of centromeric probes on interphase cells. However, unlike FISH studies, which have been focused on chromosomes 1, 3, 7, 8, 11, 16, and 17, the cytogenetic results reveal tha t other chromosomes also may be nonrandomly gained as part of multiple poly somies in breast carcinomas. In addition, the tumors with multiple polysomi es were generally of high histologic grade and with metastasis to axillary lymph nodes, suggesting that multiple whole-chromosome gains may be a pathw ay of genetic evolution or progression or both in some breast carcinomas. ( C) Elsevier Science Inc., 1999. All rights reserved.