概念模型对乙肝病毒相关肝细胞癌萌生

StephenW

Conceptual models for the initiation of hepatitis B virus-associated hepatocellular carcinoma

    Thomas Tu1,2,3, Magdalena A. Budzinska2,3, Nicholas A. Shackel2,3,4 andAllison R. Jilbert1,*

Article first published online: 9 FEB 2015

DOI: 10.1111/liv.12773

© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Issue

Liver International

Volume 35, Issue 7, pages 1786–1800, July 2015
Article has an altmetric score of 1


    1    Department of Molecular and Cellular Biology, School of Biological Sciences, University of Adelaide, Adelaide, SA, Australia
    2    Liver Cell Biology, Centenary Institute, Sydney, NSW, Australia
    3    Sydney Medical School, University of Sydney, Sydney, NSW, Australia
    4    A.W. Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital, Sydney, NSW, Australia

* Correspondence
A/Prof Allison R. Jilbert,
Department of Molecular and Cellular Biology, School of Biological Sciences, University of Adelaide, SA 5005, Australia
Tel: +61 8 8313 3263
Fax: +61 8 8313 5338
e-mail: [email protected]


Abstract

Although chronic hepatitis B virus (HBV) infection is a known risk factor for the development of hepatocellular carcinoma (HCC), the steps involved in the progression from normal liver to HCC are poorly understood. In this review, we apply five conceptual models, previously proposed by Vineis et al. to explain carcinogenesis in general, to explore the possible steps involved in the initiation and evolution of HBV-associated HCC. Available data suggest that the most suitable and inclusive model is based on evolution of hepatocyte subpopulations. In this evolutionary model, HCC-associated changes are driven by selection and subsequent clonal expansion of phenotypically altered hepatocyte subpopulations in the microenvironment of the HBV-infected liver. This model can incorporate the wide range of mechanisms proposed to play a role in the initiation of HCC including oncogenic HBV proteins, integration of HBV DNA and chronic inflammation of the liver. The model may assist in the early prevention, detection and treatment of HCC and may guide future studies of the initiation of HBV-associated HCC.

StephenW

概念模型对乙肝病毒相关肝细胞癌萌生

    托马斯Tu1,2,3，马格达莱纳A. Budzinska2,3，尼古拉斯·Shackel2,3,4 andAllison R. Jilbert1，*

文章首次在线发表：2015年2月9日

DOI：10.1111 / liv.12773

2014年©约翰·威利父子A / S。由John Wiley＆Sons出版有限公司

问题

肝国际

第35卷，第7期，页1786至1800年，2015年7月
文章有altmetric比分1


    分子和细胞生物学，生物科学学院，阿德莱德大学，阿德莱德，SA，澳大利亚1系
    2肝细胞生物学研究所百年，悉尼，新南威尔士，澳大利亚
    3悉尼医学院，悉尼，悉尼，澳大利亚新南威尔士州大学
    4 A.W.莫罗胃肠病学和肝脏中心，皇家阿尔弗雷德王子医院，悉尼，新南威尔士，澳大利亚

*通讯
A /艾利森教授R. Jilbert，
分子和细胞生物学，生物科学学院，阿德莱德大学，SA 5005，澳大利亚部
联系电话：+61 8313 8 3263
传真：+61 8313 8 5338
电子邮件：[email protected]


抽象

虽然慢性乙型肝炎病毒（HBV）感染是肝细胞癌的发展（HCC）的一个已知危险因子，参与的进程从正常肝与肝癌中的步骤是知之甚少。在这次审查中，我们应用5概念模型，先前提出的Vineis等。解释癌变在一般情况下，探索涉及HBV相关HCC的起始和发展的可能步骤。现有数据表明，最适合和包容性的模型是基于肝细胞亚群的进化。在这个进化模型，HCC-相关的变化是通过选择和表型改变肝细胞亚群在HBV感染肝脏微环境的后续克隆性扩张的推动下。该模型可以将广泛的机制提出要发挥在肝癌的启动，包括致癌HBV蛋白，整合的HBV DNA和肝脏的慢性炎症的作用。该模型可帮助肝癌的早期预防，发现和治疗，并可以引导乙肝相关肝癌的起始未来的研究。

StephenW

全文:
http://onlinelibrary.wiley.com/doi/10.1111/liv.12773/pdf