Volume 35, Issue 7, pages 1786–1800, July 2015
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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.
作者: StephenW 时间: 2015-6-13 15:45
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，*