Abstract
Chronic infection with hepatitis viruses represents the major causative factor for end-stage liver diseases, including liver cirrhosis and primary liver cancer (hepatocellular carcinoma, HCC). In this review, we highlight the current understanding of the molecular mechanisms that drive the hepatocarcinogenesis associated with chronic hepatitis virus infections. While chronic inflammation (associated with a persistent, but impaired anti-viral immune response) plays a major role in HCC initiation and progression, hepatitis viruses can also directly drive liver cancer. The mechanisms by which hepatitis viruses induce HCC include: hepatitis B virus DNA integration into the host cell genome; metabolic reprogramming by virus infection; induction of the cellular stress response pathway by viral gene products; and interference with tumour suppressors. Finally, we summarise the limitations of hepatitis virus-associated HCC model systems and the development of new techniques to circumvent these shortcomings.
Acknowledgements
Work in the authors’ laboratory was supported by the Deutsche Forschungsgemeinschaft (TRR179, TP9 to R.B.).
References
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©2017 Walter de Gruyter GmbH, Berlin/Boston
Articles in the same Issue
- Frontmatter
- Guest Editorial
- Viruses and cancer: molecular relations and perspectives
- HIGHLIGHT: VIRUSES AND CANCER
- Chronic viral hepatitis and its association with liver cancer
- The biology of JC polyomavirus
- Rhadinoviral interferon regulatory factor homologues
- Human papillomavirus first and second generation vaccines–current status and future directions
- Employing RNA viruses to fight cancer: novel insights into oncolytic virotherapy
- Modulation of oncogenic signaling networks by Kaposi’s sarcoma-associated herpesvirus
- Mechanisms and strategies of papillomavirus replication
- Review
- MicroRNAs are important regulators of drug resistance in colorectal cancer
- Research Articles/Short Communications
- Molecular Medicine
- In vitro modelling of familial amyloidotic polyneuropathy allows quantitative detection of transthyretin amyloid fibril-like structures in hepatic derivatives of patient-specific induced pluripotent stem cells
Articles in the same Issue
- Frontmatter
- Guest Editorial
- Viruses and cancer: molecular relations and perspectives
- HIGHLIGHT: VIRUSES AND CANCER
- Chronic viral hepatitis and its association with liver cancer
- The biology of JC polyomavirus
- Rhadinoviral interferon regulatory factor homologues
- Human papillomavirus first and second generation vaccines–current status and future directions
- Employing RNA viruses to fight cancer: novel insights into oncolytic virotherapy
- Modulation of oncogenic signaling networks by Kaposi’s sarcoma-associated herpesvirus
- Mechanisms and strategies of papillomavirus replication
- Review
- MicroRNAs are important regulators of drug resistance in colorectal cancer
- Research Articles/Short Communications
- Molecular Medicine
- In vitro modelling of familial amyloidotic polyneuropathy allows quantitative detection of transthyretin amyloid fibril-like structures in hepatic derivatives of patient-specific induced pluripotent stem cells