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Hepatitis C virus-induced hepatocellular carcinoma.

Goossens N, Hoshida Y - Clin Mol Hepatol (2015)

Bottom Line: Host factors also play a major role in HCV-induced HCC as evidenced by genomic studies identifying polymorphisms in immune, metabolic, and growth signaling systems associated with increased risk of HCC.Despite highly effective direct-acting antiviral agents, the morbidity and incidence of liver-related complications of HCV, including HCC, is likely to persist in the near future.Clinical markers to selectively identify HCV subjects at higher risk of developing HCC have been reported however they require further validation, especially in subjects who have experienced sustained virological response.

View Article: PubMed Central - PubMed

Affiliation: Division of Liver Diseases, Department of Medicine, Liver Cancer Program, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, USA. ; Division of Gastroenterology and Hepatology, Geneva University Hospital, Geneva, Switzerland.

ABSTRACT
Hepatitis C virus (HCV) is a leading etiology of hepatocellular carcinoma (HCC). The interaction of HCV with its human host is complex and multilayered; stemming in part from the fact that HCV is a RNA virus with no ability to integrate in the host's genome. Direct and indirect mechanisms of HCV-induced HCC include activation of multiple host pathways such as liver fibrogenic pathways, cellular and survival pathways, interaction with the immune and metabolic systems. Host factors also play a major role in HCV-induced HCC as evidenced by genomic studies identifying polymorphisms in immune, metabolic, and growth signaling systems associated with increased risk of HCC. Despite highly effective direct-acting antiviral agents, the morbidity and incidence of liver-related complications of HCV, including HCC, is likely to persist in the near future. Clinical markers to selectively identify HCV subjects at higher risk of developing HCC have been reported however they require further validation, especially in subjects who have experienced sustained virological response. Molecular biomarkers allowing further refinement of HCC risk are starting to be implemented in clinical platforms, allowing objective stratification of risk and leading to individualized therapy and surveillance for HCV individuals. Another role for molecular biomarker-based stratification could be enrichment of HCC chemoprevention clinical trials leading to smaller sample size, shorter trial duration, and reduced costs.

No MeSH data available.


Related in: MedlinePlus

Natural history and biological drivers of HCV-induced HCC development. Some figures sourced from www.servier.com under a Creative Commons Attribution 3.0 Unported License. HCV, hepatitis C virus; HCC, hepatocellular carcinoma; LPS, lipopolysaccharide; SNP, single nucleotide polymorphism.
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Related In: Results  -  Collection

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Figure 1: Natural history and biological drivers of HCV-induced HCC development. Some figures sourced from www.servier.com under a Creative Commons Attribution 3.0 Unported License. HCV, hepatitis C virus; HCC, hepatocellular carcinoma; LPS, lipopolysaccharide; SNP, single nucleotide polymorphism.

Mentions: HCV-induced HCC development is a multi-step process that may progress over 20-40 years and involves a number of steps: establishment of chronic HCV infection, chronic hepatic inflammation, progressive liver fibrosis, initiation of neoplastic clones accompanied by irreversible somatic genetic/epigenetic alterations, and progression of the malignant clones in a carcinogenic tissue microenvironment (Fig. 1). Each step of HCV-induced hepatocarcinogenesis is a potential target for therapeutic intervention or chemoprevention.12 Unlike HBV which can integrate into the host genome leading to potential direct carcinogenic activity, HCV is a RNA virus with limited integration of its genetic material into the host's genome. Therefore, the carcinogenic potential of HCV is generally assumed to be linked to indirect mechanisms, although the lack of a convenient in vitro model system to study biology is a major obstacle for the understanding of the mechanisms linking HCV infection, inflammation and carcinogenesis.1314


Hepatitis C virus-induced hepatocellular carcinoma.

Goossens N, Hoshida Y - Clin Mol Hepatol (2015)

Natural history and biological drivers of HCV-induced HCC development. Some figures sourced from www.servier.com under a Creative Commons Attribution 3.0 Unported License. HCV, hepatitis C virus; HCC, hepatocellular carcinoma; LPS, lipopolysaccharide; SNP, single nucleotide polymorphism.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493352&req=5

Figure 1: Natural history and biological drivers of HCV-induced HCC development. Some figures sourced from www.servier.com under a Creative Commons Attribution 3.0 Unported License. HCV, hepatitis C virus; HCC, hepatocellular carcinoma; LPS, lipopolysaccharide; SNP, single nucleotide polymorphism.
Mentions: HCV-induced HCC development is a multi-step process that may progress over 20-40 years and involves a number of steps: establishment of chronic HCV infection, chronic hepatic inflammation, progressive liver fibrosis, initiation of neoplastic clones accompanied by irreversible somatic genetic/epigenetic alterations, and progression of the malignant clones in a carcinogenic tissue microenvironment (Fig. 1). Each step of HCV-induced hepatocarcinogenesis is a potential target for therapeutic intervention or chemoprevention.12 Unlike HBV which can integrate into the host genome leading to potential direct carcinogenic activity, HCV is a RNA virus with limited integration of its genetic material into the host's genome. Therefore, the carcinogenic potential of HCV is generally assumed to be linked to indirect mechanisms, although the lack of a convenient in vitro model system to study biology is a major obstacle for the understanding of the mechanisms linking HCV infection, inflammation and carcinogenesis.1314

Bottom Line: Host factors also play a major role in HCV-induced HCC as evidenced by genomic studies identifying polymorphisms in immune, metabolic, and growth signaling systems associated with increased risk of HCC.Despite highly effective direct-acting antiviral agents, the morbidity and incidence of liver-related complications of HCV, including HCC, is likely to persist in the near future.Clinical markers to selectively identify HCV subjects at higher risk of developing HCC have been reported however they require further validation, especially in subjects who have experienced sustained virological response.

View Article: PubMed Central - PubMed

Affiliation: Division of Liver Diseases, Department of Medicine, Liver Cancer Program, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, USA. ; Division of Gastroenterology and Hepatology, Geneva University Hospital, Geneva, Switzerland.

ABSTRACT
Hepatitis C virus (HCV) is a leading etiology of hepatocellular carcinoma (HCC). The interaction of HCV with its human host is complex and multilayered; stemming in part from the fact that HCV is a RNA virus with no ability to integrate in the host's genome. Direct and indirect mechanisms of HCV-induced HCC include activation of multiple host pathways such as liver fibrogenic pathways, cellular and survival pathways, interaction with the immune and metabolic systems. Host factors also play a major role in HCV-induced HCC as evidenced by genomic studies identifying polymorphisms in immune, metabolic, and growth signaling systems associated with increased risk of HCC. Despite highly effective direct-acting antiviral agents, the morbidity and incidence of liver-related complications of HCV, including HCC, is likely to persist in the near future. Clinical markers to selectively identify HCV subjects at higher risk of developing HCC have been reported however they require further validation, especially in subjects who have experienced sustained virological response. Molecular biomarkers allowing further refinement of HCC risk are starting to be implemented in clinical platforms, allowing objective stratification of risk and leading to individualized therapy and surveillance for HCV individuals. Another role for molecular biomarker-based stratification could be enrichment of HCC chemoprevention clinical trials leading to smaller sample size, shorter trial duration, and reduced costs.

No MeSH data available.


Related in: MedlinePlus