Chromosome 7 rearrangements in glioblastomas; loci adjacent to EGFR are independently amplified
Chromosome 7 rearrangements in glioblastomas; loci adjacent to EGFR are independently amplified
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DOI：
10.1097/00005072-199812000-00005
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发表时间：
1998-12-01
影响因子：
3.2
通讯作者：
Collins, VP
中科院分区：
文献类型：
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作者：
Liu, L;Ichimura, K;Collins, VP
在人类胶质母细胞瘤中发现的第一个被扩增的基因是位于7p12的EGFR。最近，7q31的MET基因也被报道扩增。我们对47例胶质母细胞瘤的7号染色体进行了FISH、RFLP和微卫星分析。4%（2/47）有1个着丝粒，26%（12/47）有2个，32%（15/47）有3个，4%（2/47）有4个，34%（16/47）有7号染色体着丝粒数目可变的亚群。在47例肿瘤中，有25例（53%）在每个信息位点观察到的等位基因失衡模式相似，与FISH数据一致，表明完整染色体拷贝的丢失或获得。在32%的肿瘤（15/47）中，在染色体的不同位点上观察到不同的等位基因失衡，这表明在二体、三体、四体或多体的背景下，7号染色体的部分缺失或增加。在121个胶质母细胞瘤的扩展系列中研究了扩增，在47个肿瘤（39%）的7p12区域发现了扩增。42个肿瘤显示EGFR扩增，其中12个具有广泛的扩增，包括许多邻近的位点，总是只涉及1个等位基因。5个肿瘤（11%）的扩增子不包括EGFR，这表明该区域的其他未知基因是扩增的目标。未发现MET扩增。研究结果表明，7号染色体的拷贝数变化是常见的，并且在胶质母细胞瘤中，许多基因可能在7p12处扩增。
The first gene found to be amplified in human glioblastomas was EGFR at 7p12. More recently the MET gene at 7q31 was also reported amplified. We have studied chromosome 7 in a series of 47 glioblastomas by FISH, RFLP and microsatellite analysis. Four per cent (2/47) had 1 centromere, 26% (12/47) 2, 32% (15/47) 3, 4% (2/47) 4, and 34% (16/47) had subpopulations with variable numbers of chromosome 7 centromeres. In 25 of the 47 tumors (53%) the pattern of allelic imbalance observed at each informative locus was similar and in accord with the FISH data, indicating loss or gain of complete chromosome copies. In 32% of tumors (15/47) varying allelic imbalance was seen at different loci along the chromosome indicative of loss or gain of parts of chromosome 7 on a background of disomy, trisomy, tetrasomy, or polysomy. Amplification was studied in an extended series of 121 glioblastomas, and was seen at the 7p12 region in 47 tumors (39%). Forty-two tumors showed amplification of EGFR and 12 of these had extensive amplicons including a number of adjacent loci, always involving only 1 allele. The amplicons of 5 tumors (11%) did not include EGFR, indicating that other unidentified genes in the region are targeted for amplification. Amplification of MET was not found. The findings show that copy number changes of chromosome 7 are common and that a number of genes may be targeted for amplification at 7p12 in glioblastomas.