DELETIONS IN HUMAN-CHROMOSOME ARM-11P AND ARM-13Q IN PRIMARY HEPATOCELLULAR CARCINOMAS
DELETIONS IN HUMAN-CHROMOSOME ARM-11P AND ARM-13Q IN PRIMARY HEPATOCELLULAR CARCINOMAS
复制标题
DOI：
10.1159/000132593
复制
发表时间：
1988-01-01
期刊：
影响因子：
--
通讯作者：
ROGLER, CE
中科院分区：
文献类型：
--
作者：
WANG, HP;ROGLER, CE
使用检测限制性片段长度多态性的探针对大多数人类染色体上的基因座上的正常肝脏和肝细胞癌（HCC）基因型进行比较。 14 个肿瘤中有 6 个表现出 11p 上一种或多种标记物杂合性的丧失。 10 名患者提供了 13q 基因座的信息，这 10 名患者中的 5 名表现出一种或多种 13q 标记的杂合性丢失。总共，14 名患者中有 9 名显示 11p 或 13q 上一个或多个位点的多态性等位基因丢失。对另外 16 条染色体上的基因座的调查表明，这些缺失并不是由于 HCC 杂合性普遍丧失所致。定量密度测定显示，10 个缺失中的每一个都导致肿瘤组织中剩余等位基因的半合性（无重复）。与遗传性胚胎肿瘤（其中剩余染色体重复是规则）相反，简单缺失似乎是这些成人非遗传性 HCC 杂合性丧失的主要机制。这些数据表明，乙型肝炎病毒携带者中出现的肝癌是一组遗传异质性肿瘤，其中一些可能是通过 13q 改变产生的，一些是通过 11p 改变产生的，一些是两条染色体都改变了，还有一些是两条染色体都完好。
Normal liver and hepatocellular carcinoma (HCC) genotypes were compared at loci on most of the human chromosomes with probes that detect restriction fragment length polymorphisms. Six of fourteen tumors exhibited loss of heterozygosity of one or more markers on 11p. Ten patients were informative for loci on 13q, and 5 of these 10 exhibited loss of heterozygosity for one or more of the 13q markers. Altogether, 9 of the 14 patients showed loss of a polymorphic allele for one or more loci on either 11p or 13q. A survey of loci on 16 additional chromosomes indicated that the deletions were not due to a general loss of heterozygosity in HCCs. Quantitative densitometry showed that each of the 10 deletions resulted in hemizygosity (no reduplication) of the remaining allele in tumor tissue. In contrast to hereditary embryonal tumors, in which reduplication of the remaining chromosome is the rule, simple deletion appears to be the primary mechanism responsible for the loss of heterozygosity in these adult, nonhereditary HCCs. These data show that HCCs arising in hepatitis B virus carriers are a genetically heterogeneous group of tumors, some of which may arise through 13q alterations, some through 11p alterations, some with both chromosomes altered, and some with both intact.