肝细胞癌与非酒精性脂肪性肝炎：现状
Hepatocellular carcinoma and non-alcoholic steatohepatitis: The state of play.
作者信息
Charrez Bérénice, Qiao Liang, Hebbard Lionel
机构信息
Bérénice Charrez, Lionel Hebbard, Department of Molecular and Cell Biology, James Cook University, Townsville, QLD 4811, Australia.
出版信息
World J Gastroenterol. 2016 Feb 28;22(8):2494-502. doi: 10.3748/wjg.v22.i8.2494.
Abstract
Hepatocellular carcinoma (HCC) is now the fifth cancer of greatest frequency and the second leading cause of cancer related deaths worldwide. Chief amongst the risks of HCC are hepatitis B and C infection, aflatoxin B1 ingestion, alcoholism and obesity. The latter can promote non-alcoholic fatty liver disease (NAFLD), that can lead to the inflammatory form non-alcoholic steatohepatitis (NASH), and can in turn promote HCC. The mechanisms by which NASH promotes HCC are only beginning to be characterized. Here in this review, we give a summary of the recent findings that describe and associate NAFLD and NASH with the subsequent HCC progression. We will focus our discussion on clinical and genomic associations that describe new risks for NAFLD and NASH promoted HCC. In addition, we will consider novel murine models that clarify some of the mechanisms that drive NASH HCC formation.
摘要
肝细胞癌（HCC）目前是全球发病率第五高的癌症，也是癌症相关死亡的第二大主要原因。HCC的主要风险包括乙型和丙型肝炎感染、黄曲霉毒素B1摄入、酗酒和肥胖。后者可导致非酒精性脂肪性肝病（NAFLD），进而发展为炎症性非酒精性脂肪性肝炎（NASH），继而引发HCC。NASH促进HCC发生的机制才刚刚开始被阐明。在这篇综述中，我们总结了近期的研究发现，这些发现描述了NAFLD和NASH与随后的HCC进展之间的关系。我们将重点讨论临床和基因组关联，这些关联揭示了NAFLD和NASH引发HCC的新风险。此外，我们还将探讨一些新型小鼠模型，这些模型有助于阐明驱动NASH-HCC形成的部分机制。
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