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肝细胞癌中的杂合性缺失

[Loss of heterozygosity in hepatocellular carcinoma].

作者信息

Takahashi K, Kudo J, Ishibashi H, Niho Y

机构信息

First Department of Internal Medicine, Faculty of Medicine, Kyushu University.

出版信息

Nihon Rinsho. 1993 Feb;51(2):370-4.

PMID:8096550
Abstract

Several genetic events are necessary for a cell to become malignant. Some of these events are activations of protooncogenes and loss of normal functions of tumor suppressor genes. Recently loss of heterozygosity at specific loci on some chromosomes have been observed in several tumors. Loss of heterozygosity in the tumor suggests that a certain tumor suppressor gene may reside near the locus of the probe by which the loss of heterozygosity was demonstrated. In hepatocellular carcinoma, loss of heterozygosity on chromosome 1p, 4q, 5q, 10q, 11p, 13q, 16q, 17p and 22q are observed. Inactivation of tumor suppressor genes on these chromosomes may play important roles in tumorigenesis or progression of hepatocellular carcinoma.

摘要

细胞发生恶性转化需要多个遗传事件。其中一些事件是原癌基因的激活以及肿瘤抑制基因正常功能的丧失。最近,在几种肿瘤中观察到某些染色体上特定位点的杂合性缺失。肿瘤中的杂合性缺失表明某个肿瘤抑制基因可能位于用于证明杂合性缺失的探针位点附近。在肝细胞癌中,观察到1p、4q、5q、10q、11p、13q、16q、17p和22q染色体上的杂合性缺失。这些染色体上肿瘤抑制基因的失活可能在肝细胞癌的发生或进展中起重要作用。

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