摘要
肿瘤的发生和演化是一个多步骤的过程,肝癌也不例外。分子生物学及流行病学的研究结果表明,在人原发性肝癌(PHC)发生、演化过程中,一些癌基因或相关基因的结构或表达发生了改变;一些抗癌基因受到抑制或发生丢失;嗜肝病毒对肝细胞的恶性转化起了促进作用。这些基因和病毒在PHC的发生、发展过程中的作用是分阶段、协同和累积的。以下,结合我们实验室近几年的工作对癌基因及其相关基因。
Tumorigenesis is a complex, multistep process. In human primary hepatic cancer(PHC), epidemiological and molecular biological studies have shown that many molecu-lar events involved in the initiation and development of this cancer. In this review, aneffort has been made to summarize previous results from our lab as well as other's andto present a simple model for the genetic basis of PHC which includes following threeevents: 1. Over-expression of some oncogenes and related genes, such as N-ras, c-myc,p53, c-ets-2,IGF-Ⅱ,IGF-Ⅱ R and c-fms. 2. Allelic losses of putative antioncogenes. 3.Hepadnavirus infection. It is hoped that this may lead to some clues to the eluoidation ofmolecular mechanisms of human liver carcinogenesis.
出处
《肿瘤》
CAS
CSCD
北大核心
1991年第3期123-125,共3页
Tumor
