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Molecular Carcinogenesis of HBV-Related HCC

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Hepatitis B Virus and Liver Disease

Abstract

Primary liver cancer is the second most common cause of death due to cancer worldwide, and a vast majority of primary liver cancer is the hepatocellular carcinoma (HCC) subtype. Although a number of etiologies are recognized to cause HCC, HBV infection accounts for over 50% of diagnosed HCC cases. HBV infection leads to the development of HCC through a variety of mechanisms. Indirectly, viral infection leads to repetitive liver injury through oxidative stress, the immune response, and telomere shortening, eventually causing cellular transformation. Integration of viral DNA into the host genome can indirectly lead to carcinogenesis by inducing genomic instability, as well as directly causing oncogenesis by preferentially integrating into genomic loci of known oncogenes. The activity of the HBV X protein (HBx) has been demonstrated to directly promote transformation and hepatocarcinogenesis in a number of ways, including activating cancer-related pathways and altering cellular epigenetic and noncoding RNA expression. In this chapter, we will summarize the current scientific knowledge of the ways in which HBV infection can lead to HCC.

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Correspondence to Xin W. Wang .

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© 2018 Springer Nature Singapore Pte Ltd.

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Fako, V., Wang, X.W. (2018). Molecular Carcinogenesis of HBV-Related HCC. In: Kao, JH., Chen, DS. (eds) Hepatitis B Virus and Liver Disease. Springer, Singapore. https://doi.org/10.1007/978-981-10-4843-2_8

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  • DOI: https://doi.org/10.1007/978-981-10-4843-2_8

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  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-10-4842-5

  • Online ISBN: 978-981-10-4843-2

  • eBook Packages: MedicineMedicine (R0)

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