LOSS OF HETEROZYGOSITY ON CHROMOSOMES-3, CHROMOSOME-13, AND CHROMOSOME-17 IN SMALL-CELL CARCINOMA AND ON CHROMOSOME-3 IN ADENOCARCINOMA OF THE LUNG

LOSS OF HETEROZYGOSITY ON CHROMOSOMES-3, CHROMOSOME-13, AND CHROMOSOME-17 IN SMALL-CELL CARCINOMA AND ON CHROMOSOME-3 IN ADENOCARCINOMA OF THE LUNG
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DOI:
10.1073/pnas.84.24.9252
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发表时间:
1987-12-01
影响因子:
11.1
通讯作者:
SUGIMURA, T
SUGIMURA, T
中科院分区:
综合性期刊1区
文献类型:
--
作者:
YOKOTA, J;WADA, M;SUGIMURA, T

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通过分子遗传学方法,使用多态性DNA标记,检测等位基因缺失的特定染色体区域,我们分析了可能的损失的染色体杂合性在5个不同的组织学类型的肺癌从47例患者。在小细胞癌中,三个不同染色体位点的等位基因缺失发生率极高:7例患者中7例(100%)在染色体3 p上检测到杂合性缺失,11例患者中10例(91%)在13 q上检测到杂合性缺失,5例患者中5例(100%)在17 p上检测到杂合性缺失。小细胞癌中这些位点的缺失甚至在没有任何转移临床证据的肿瘤中也观察到。此外,染色体3 p和13 q上的杂合性丢失发生在NMYC扩增和染色体11 p缺失之前。腺癌中染色体3 p的杂合性丢失率也很高[5/6例(83%)]。31例非小细胞肺癌患者中10例(32%)和12例患者中3例(25%)染色体13 q和17 p杂合性丢失。这些结果表明,涉及染色体3 p,13 q和17 p序列的隐性遗传变化可能在小细胞癌的发生中起重要作用,染色体3 p上的那些可能在腺癌的发生中起重要作用。
By a molecular genetic approach using polymorphic DNA markers that detect allelic deletion of specific chromosomal regions, we analyzed for possible loss of chromosomal heterozygosity in five different histological types of lung cancers obtained from 47 patients. In small-cell carcinomas, the incidence of allelic deletions at three different chromosomal loci was extremely high: loss of heterozygosity was detected on chromosomes 3p in 7 of 7 patients (100%), 13q in 10 of 11 patients (91%), and 17p in 5 of 5 patients (100%). The deletions at these loci in small-cell carcinomas were observed even in the tumors without any clinical evidence of metastasis. Furthermore, loss of heterozygosity on chromosomes 3p and 13q occurred prior to NMYC amplification and chromosome 11p deletion. Loss of heterozygosity on chromosome 3p was also detected with high frquency in adenocarcinomas [5 of 6 patients (83%)]. Heterozygosity of chromosomes 13q and 17p was lost in 10 of 31 patients (32%) and in 3 of 12 patients (25%), respectively, of lung cancers other than small-cell carcinomas. These results indicate that recessive genetic changes involving sequences on chromosomes 3p, 13q, and 17p may play important roles in the genesis of small-cell carcinoma, and those on chromosome 3p may play an important role in the genesis of adenocarcinoma.