乙型肝炎病毒与肝细胞癌的最新进展。

IF 3.5 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1990-11-01
C E Rogler
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引用次数: 0

摘要

本次会议回顾的数据强化了HBV可能通过多种机制促进肝癌发展的观点,包括通过插入诱变激活癌基因(c-myc和N-myc),表达作为反式激活因子和可能的癌蛋白的病毒蛋白(X和pre-S2/S),以及通过酶介导的整合进入宿主基因组引入染色体缺陷。然而,并非所有这些机制在每种肿瘤中都起作用。因此,未来的工作将旨在更详细地描述每种机制并确定其在致癌过程中的相对重要性。
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Recent advances in hepatitis B viruses and hepatocellular carcinoma.

The data reviewed at this meeting reinforce the notion that HBV may contribute to the development of liver cancer through a variety of mechanisms, including activation of oncogenes (c-myc and N-myc) by insertional mutagenesis, expression of viral proteins (X and pre-S2/S) that function as trans-activators and possibly oncoproteins, and introduction of chromosomal defects through enzymatically mediated integration into the host genome. Not all of these mechanisms appear to be active in every tumor, however. Thus, future work will be aimed at characterizing each mechanism in more detail and determining its relative importance in the carcinogenic process.

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