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Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...

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Related Experiment Video

Updated: May 15, 2026

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
06:38

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

Hepatitis C virus and hepatocarcinogenesis.

Soung Won Jeong1, Jae Young Jang, Raymond T Chung

  • 1Institute for Digestive Research, Digestive Disease Center, Department of Internal Medicine, Soonchunhyang University College of Medicine, Seoul, Korea.

Clinical and Molecular Hepatology
|January 17, 2013
PubMed
Summary

Hepatitis C virus (HCV) infection contributes to liver cancer (hepatocellular carcinoma) through complex genetic and epigenetic changes. Understanding these mechanisms is key for developing targeted therapies for HCV-related HCC.

Keywords:
Hepatitis C virusHepatocellular carcinomaMolecular

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A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma

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Related Experiment Videos

Last Updated: May 15, 2026

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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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

A Protocol for Analyzing Hepatitis C Virus Replication
13:04

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma
12:24

A Three-Dimensional Spheroid Model to Investigate the Tumor-Stromal Interaction in Hepatocellular Carcinoma

Published on: September 30, 2021

Area of Science:

  • Hepatology
  • Virology
  • Oncology

Background:

  • Hepatitis C virus (HCV) is an RNA virus implicated in liver disease.
  • HCV infection contributes to hepatocellular carcinoma (HCC) through complex molecular mechanisms.
  • HCV proteins interact with host cells, influencing pathways related to cell survival and proliferation.

Purpose of the Study:

  • To review the current understanding of hepatocarcinogenesis induced by HCV infection.
  • To explore the genetic and epigenetic alterations involved in HCV-related HCC.
  • To highlight the need for molecular classification for personalized therapy.

Main Methods:

  • Review of current literature on HCV pathogenesis and HCC.
  • Analysis of gene expression profiles and messenger RNA.
  • Examination of cellular signal transduction pathways affected by viral proteins.

Main Results:

  • HCV infection involves slow, multi-step oncogenic processes including genetic/epigenetic alterations.
  • Stellate cell transdifferentiation may link to HCC development.
  • Viral proteins impact cell survival, proliferation, migration, and transformation.

Conclusions:

  • HCV-induced hepatocarcinogenesis is complex and heterogeneous.
  • Further molecular classification of HCC is necessary.
  • Understanding molecular complexities may lead to effective chemoprevention and personalized therapies for HCV-related HCC.