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
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.