Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma

Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid...

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Veröffentlicht in:World journal of gastroenterology : WJG Jg. 26; H. 38; S. 5759
Hauptverfasser: D'souza, Simmone, Lau, Keith Ck, Coffin, Carla S, Patel, Trushar R
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 14.10.2020
Schlagworte:
Carcinoma, Hepatocellular
Hepatitis B - complications
Hepatitis B virus - genetics
Hepatitis, Viral, Human
Humans
Liver Neoplasms
Hallmarks of cancer
Viral hepatitis
Hepatitis delta virus co-infection
Molecular mechanisms
Hepatocellular carcinoma
Hepatitis B virus
Hepatitis C virus
Chronic viral infection
ISSN:2219-2840, 2219-2840
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Zusammenfassung:Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid tumors like HCC are complex and have heterogeneous tumor genomic profiles contributing to complexity in diagnosis and management. Chronic infection with hepatitis B virus (HBV), hepatitis delta virus (HDV), and hepatitis C virus (HCV) are the greatest etiological risk factors for HCC. Due to the significant role of chronic viral infection in HCC development, it is important to investigate direct (viral associated) and indirect (immune-associated) mechanisms involved in the pathogenesis of HCC. Common mechanisms used by HBV, HCV, and HDV that drive hepatocarcinogenesis include persistent liver inflammation with an impaired antiviral immune response, immune and viral protein-mediated oxidative stress, and deregulation of cellular signaling pathways by viral proteins. DNA integration to promote genome instability is a feature of HBV infection, and metabolic reprogramming leading to steatosis is driven by HCV infection. The current review aims to provide a brief overview of HBV, HCV and HDV molecular biology, and highlight specific viral-associated oncogenic mechanisms and common molecular pathways deregulated in HCC, and current as well as emerging treatments for HCC.
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ObjectType-Feature-2
ObjectType-Review-3
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ISSN:2219-2840
2219-2840
DOI:10.3748/wjg.v26.i38.5759