Virus associated malignancies: the role of viral hepatitis in hepatocellular carcinoma.
Virus associated malignancies: the role of viral hepatitis in hepatocellular carcinoma.
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DOI：
10.1016/j.semcancer.2014.01.004
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发表时间：
2014-06
影响因子：
14.5
通讯作者：
Rice CM
中科院分区：
文献类型：
--
作者：
Shlomai A;de Jong YP;Rice CM
肝细胞癌（HCC）是世界范围内第三大致死性癌症，其发病率持续增加。涉及B型肝炎病毒（HBV）或丙型肝炎病毒（HCV）感染的慢性病毒性肝炎是HCC的主要病因，使得HCC预防成为抗病毒治疗的主要目标。虽然最近的临床观察和转化研究增强了我们对HCC发生和发展的分子机制的理解，但仍有许多未知因素。目前的数据表明，HCC肿瘤是高度复杂和异质性的多个分子通路的异常功能的结果。这种复杂的生物学至少在一定程度上是这种致命癌症缺乏高效靶向治疗的原因。此外，HBV和HCV感染对HCC发展的直接或间接影响仍然是一个有争议的问题。因此，病毒性肝炎相关的HCC是否源于病毒特异性因素和/或涉及炎症和组织再生的一般机制仍然是一个问题。在这篇综述中，我们总结了肝癌的一般机制，强调了今天可用的新技术产生的数据。我们还强调了HBV和HCV可能参与HCC发病机制的特定途径。然而，需要改进目前两种病毒的体外和体内系统，以严格定义时间序列和特定途径失调，从而推动慢性肝炎病毒感染和HCC之间的密切临床联系。
Hepatocellular carcinoma (HCC) is the third leading fatal cancer worldwide and its incidence continues to increase. Chronic viral hepatitis involving either hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is the leading etiology for HCC, making HCC prevention a major goal of antiviral therapy. While recent clinical observations and translational research have enhanced our understanding of the molecular mechanisms driving the initiation and progression of HCC, much remains unknown. Current data indicates that HCC tumors are highly complex and heterogeneous resulting from the aberrant function of multiple molecular pathways. This complex biology is responsible, at least in part, for the absence of highly efficient target-directed therapies for this deadly cancer. Additionally, the direct or indirect effect of HBV and HCV infection on the development of HCC is still a contentious issue. Thus, the question remains whether viral hepatitis-associated HCC stems from virus-specific factors, and/or from a general mechanism involving inflammation and tissue regeneration. In this review we summarize general mechanisms implicated in HCC, emphasizing data generated by new technologies available today. We also highlight specific pathways by which HBV and HCV could be involved in HCC pathogenesis. However, improvements to current in vitro and in vivo systems for both viruses will be needed to rigorously define the temporal sequence and specific pathway dysregulations that drive the strong clinical link between chronic hepatitis virus infection and HCC.
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