Chronic inflammation, immune escape, and oncogenesis in the liver: a unique neighborhood for novel intersections

JK Stauffer, AJ Scarzello, Q Jiang, RH Wiltrout - Hepatology, 2012 - Wiley Online Library
JK Stauffer, AJ Scarzello, Q Jiang, RH Wiltrout
Hepatology, 2012Wiley Online Library
Sustained hepatic inflammation, driven by alcohol consumption, nonalcoholic fatty liver
disease, and/or chronic viral hepatitis (hepatitis B and C), results in damage to parenchyma,
oxidative stress, and compensatory regeneration/proliferation. There is substantial evidence
linking these inflammation‐associated events with the increased incidence of hepatocellular
carcinogenesis. Although acute liver inflammation can play a vital and beneficial role in
response to liver damage or acute infection, the effects of chronic liver inflammation …
Abstract
Sustained hepatic inflammation, driven by alcohol consumption, nonalcoholic fatty liver disease, and/or chronic viral hepatitis (hepatitis B and C), results in damage to parenchyma, oxidative stress, and compensatory regeneration/proliferation. There is substantial evidence linking these inflammation‐associated events with the increased incidence of hepatocellular carcinogenesis. Although acute liver inflammation can play a vital and beneficial role in response to liver damage or acute infection, the effects of chronic liver inflammation, including liver fibrosis and cirrhosis, are sufficient in a fraction of individuals to initiate the process of transformation and the development of hepatocellular carcinoma. This review highlights immune‐dependent mechanisms that may be associated with hepatocellular oncogenesis, including critical transformative events/pathways in the context of chronic inflammation and subverted tolerogenesis. (HEPATOLOGY 2012)
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