Oe Natsumi, Takeda Haruhiko, Eso Yuji, Takai Atsushi, Marusawa Hiroyuki
Department of Gastroenterology, Red Cross Osaka Hospital, Osaka 5438555, Japan.
Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto 6068501, Japan.
Pathogens. 2022 Apr 1;11(4):430. doi: 10.3390/pathogens11040430.
Hepatocellular carcinoma (HCC) arises in the background of chronic liver diseases, including hepatitis and liver cirrhosis caused by hepatitis C virus (HCV) infection. It is well known that HCV eradication using antiviral drugs can efficiently inhibit hepatocarcinogenesis. Recent advances in and development of direct-acting antiviral (DAA) drugs has revolutionized the treatment of HCV infection, and the vast majority of HCV patients can achieve HCV eradication using DAAs. However, mounting evidence clearly indicates that HCC inevitably occurs in a subset of patients after successful viral eradication using DAA therapy. Cancer is a genetic disease, and the accumulation of genetic and epigenetic aberrations may cause hepatocarcinogenesis in chronically damaged liver, even after virus elimination. In this review, we highlight HCC development after HCV eradication and discuss the current understanding of the molecular mechanisms of tumorigenesis after virus elimination, focusing on the genetic and epigenetic background of chronically damaged liver tissues.
肝细胞癌(HCC)发生于慢性肝病背景下,包括丙型肝炎病毒(HCV)感染所致的肝炎和肝硬化。众所周知,使用抗病毒药物根除HCV可有效抑制肝癌发生。直接抗病毒(DAA)药物的最新进展和研发彻底改变了HCV感染的治疗方式,绝大多数HCV患者使用DAA药物可实现HCV根除。然而,越来越多的证据清楚表明,在使用DAA疗法成功根除病毒后,一部分患者不可避免地会发生HCC。癌症是一种遗传性疾病,即使在病毒清除后,遗传和表观遗传异常的积累也可能在长期受损的肝脏中导致肝癌发生。在本综述中,我们重点介绍HCV根除后的HCC发展,并讨论目前对病毒清除后肿瘤发生分子机制的理解,重点关注长期受损肝组织的遗传和表观遗传背景。