Schlegel J, Scherthan H, Arens N, Stumm G, Kiessling M
Abt. Neuropathologie, Universität Marburg, Germany.
J Neuropathol Exp Neurol. 1996 Jan;55(1):81-7. doi: 10.1097/00005072-199601000-00008.
The aim of the present study was to detect complex genetic alterations in human glioblastoma multiforme (GBM) by comparative genomic in situ hybridization (CGH). Of the 24 GBM that were examined, increased fluorescence intensities indicating chromosomal polysomy of chromosome 7 and gene amplification at chromosome 7p were found in 42% of the tumors. In addition, signal enhancement of chromosome 19 was present in 29% and at 12q13-15 in 21% of the tumors. We also detected reduction of fluorescence intensities indicating gross deletions on chromosomes 10 (58%), 9p (46%), and 13 (29%). There was a close correlation of CGH results when compared with Southern analysis of the EGFR gene localized on chromosome 7 and loss of heterozygosity detection of chromosome 9 and 10 by microsatellite PCR. A close correlation was also observed between copy number changes of chromosome 7 and deletions of chromosome 10. Amplification of chromosome 12q and deletions of chromosomes 9p and 13 seemed to be complementary in the tumors investigated in the present study.
本研究的目的是通过比较基因组原位杂交（CGH）检测多形性胶质母细胞瘤（GBM）中的复杂基因改变。在所检测的24例GBM中，42%的肿瘤出现荧光强度增加，提示7号染色体多体性及7p染色体基因扩增。此外，29%的肿瘤出现19号染色体信号增强，21%的肿瘤出现12q13 - 15信号增强。我们还检测到荧光强度降低，提示10号染色体（58%）、9p染色体（46%）和13号染色体（29%）存在大片段缺失。与位于7号染色体上的表皮生长因子受体（EGFR）基因的Southern分析以及通过微卫星PCR检测9号和10号染色体杂合性缺失相比，CGH结果具有密切相关性。7号染色体拷贝数变化与10号染色体缺失之间也观察到密切相关性。在本研究中所调查的肿瘤中，12q染色体扩增以及9p和13号染色体缺失似乎具有互补性。
