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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
Published on: September 12, 2019
Viral hepatocarcinogenesis: from infection to cancer
Alexander Tan1, Shiou-Hwie Yeh, Chun-Jen Liu
1Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan.
Abstract:
Hepatocellular carcinoma (HCC) is a worldwide health issue that has started receiving attention but is still poorly understood. However, the hepatitis B virus (HBV) and the hepatitis C virus (HCV) are known to be two major causative agents of HCC. They differ in their modes of infection, their treatment options, their genomes and their carcinogenic abilities. However, both share a link with HCC through alterations of the host genome. In order to continue in our search for the mechanisms behind viral hepatocarcinogenesis, the individual entities (HBV, HCV, HCC and host), their natural history, treatment options and genomic properties must be further understood. Additionally, an understanding of the genomics, the link between the entities, is crucial for the success of the ongoing search for therapeutic options for HCC. Similar to most types of cancer, hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocyte. As technology advances and research continues, the genetic changes and influences among these entities will prove essential to improved diagnostic and therapeutic options. It remains a challenge to provide a clear picture of the connection between virus and cancer. We review (i) the epidemiological link between HBV/HCV infection to HCC; (ii) prevention and control of chronic hepatitis B or C in reducing HCC risk; and (iii) genetic characters of viruses and hosts and the mechanisms associated with HCC susceptibilities, with the intention of providing a direction for future research and treatment.
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