微卫星
杂合子丢失
放大器
生物
比较基因组杂交
遗传学
南方斑点
分子生物学
遗传标记
基因复制
等位基因
细胞遗传学
癌变
拷贝数变化
肉瘤
基因
拷贝数分析
聚合酶链反应
基因组DNA
基因定位
常染色体
等色体
作者
M. J. Wolf,M. Tarkkanen,T. J. Hulsebos,M. L. Larramendy,A. Forus,O. Myklebost,L. A. Aaltonen,I. Elomaa,S. Knuutila
标识
DOI:10.1002/(sici)1097-0215(19990730)82:3
摘要
The structure of the 17p amplicon from 9 human sarcoma specimens evaluated by comparative genomic hybridization (CGH) has been studied by analyzing 28 microsatellite markers by PCR. Eleven sarcoma specimens showing no DNA copy number increases at 17p by CGH were analyzed as control samples. Five specimens were analyzed by Southern blotting using probes that have previously shown amplification at the 17p12 region in astrocytoma and high-grade osteosarcoma samples. Microsatellite marker analyses revealed that all samples but 1 showing copy number increases at 17p by CGH displayed allelic imbalance that confirmed the CGH findings. Seven of these 9 cases displayed gain in copy number by microsatellite marker analysis. Four cases displaying gain in copy number were associated with loss of heterozygosity at other loci. Southern blot analysis showed amplification in 3 cases, all of them had shown copy number increases by CGH and microsatellite marker analysis, except one case, which was not included in the microsatellite marker analysis. Our results reveal the complexity of the 17p amplicon in sarcomas, suggesting that multiple target genes are involved in tumorigenesis
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