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从肝脏的组织再生理解肝细胞癌的产生
引用本文:姜润德,李春海. 从肝脏的组织再生理解肝细胞癌的产生[J]. 中华肝胆外科杂志, 2002, 8(6): 323-328
作者姓名:姜润德  李春海
作者单位:100850,北京市,军事医学科学院附属医院肿瘤分子生物学研究室
摘    要:肝细胞性肝癌以其高发病率和高恶性行为而著称,占我国癌症死亡的第二位。尽管流行病学资料已强烈提示乙肝病毒的感染及其它致癌因子的作用与肝细胞癌的发生具有相关性,但这种相关关系是如何建立起来的,近几十年来分子生物学的研究至今没有提出令人信服的解释,但却使我们对肝细胞癌发生机制的认识过于复杂化了。本文从肝的组织发生和组织再生入手,结合乙肝病毒感染后肝组织的病理发展过程及当今干细胞研究的最新结论,从发育生物学观点探讨了肝细胞癌发生的机制。这一模式使得肝细胞癌若干令人费解的生物学现象,譬如低分化状态、AFP的表达、端粒酶激活、病毒的低复制或不复制及病毒蛋白的低表达或不表达状态、染色体结构的紊乱及(或)突变、肝癌的多中心性起源等,变得易于理解。尤其重要的是,这一模式使得我们有理由研究如何通过改变肝癌组织的微环境来诱导癌细胞向正常细胞分化,而达到治愈肝细胞癌的目的。

关 键 词:肝脏 组织再生 肝细胞癌 乙型肝炎病毒 干细胞
修稿时间:2001-09-04

Understanding hepatocarcinogenesis from liver regeneration
JIANG Runde,LI Chunhai. Understanding hepatocarcinogenesis from liver regeneration[J]. Chinese Journal of Hepatobiliary Surgery, 2002, 8(6): 323-328
Authors:JIANG Runde  LI Chunhai
Affiliation:JIANG Runde,LI Chunhai. Department of Molecular Tumor Biology,Chinese Academy of Military Medical Sciences,Beijing 100850,P. R. China
Abstract:Notorious for its high incidence and high degree of malignancy, hepatocellular carcinoma (HCC) has already been regarded as the second most common cause of cancer death in China. Although epidemic data strongly suggest that hepatitis B virus infection as well as some other factors may be closely related to hepatocarcinogenesis, we still have not found how the relationship was established. Even modern molecular biological researches have not ye provided us with a convincing interpretation but just more bewildering data that make us much harder to achieve a satisfactory comprehension. In this study, the authors logically investigated the mechansism of hepatocellular carcinogenesis from the point of developmental biology, which was accomplished in combination with liver development, liver regeneration, pathological development of liver tissue after hepatitis B virus infection and recent achievement in stem cell researches. This model also enable us to easily understand some biological characteristics of hepatocellular carcinoma cells, most of which had been evasive to our understanding for so long a time. They include low differentiation state, AFP expression, activation of telomerase, low or no copy of replication of HBV DNA, low or no expression of virus proteins, structural disorder of chromosome and/or aneuploid state and/or gene mutations and, multicenter origin. Most importantly, from understanding of this model, we shall stand on a reasonable ground to search effective methods, perhaps by ways of altering microenvironment of cancer tissue, to induce malignant cells to differentiae into normal mature cells so as to completely put cancers under control.
Keywords:Carcinoma  hepatocellular  Liver regeneration  Hepatitis B virus  Carcinogenesis  Stem cell
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