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Gastroenterology Research and Practice
Volume 2010 (2010), Article ID 518674, 8 pages
Review Article

TLRs, Alcohol, HCV, and Tumorigenesis

Department of Molecular Microbiology and Immunology, 503B-HMR, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA

Received 16 April 2010; Accepted 19 December 2010

Academic Editor: Timothy R. Billiar

Copyright © 2010 Keigo Machida. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic liver damage caused by viral infection, alcohol, or obesity can result in increased risk for hepatocellular carcinoma (HCC). Ample epidemiological evidence suggests that there is a strong synergism between hepatitis C virus (HCV) and alcoholic liver diseases (ALD). The Toll-like receptor (TLR) signaling pathway is upregulated in chronic liver diseases. Alcoholism is associated with endotoxemia that stimulates expression of proinflammatory cytokine expression and inflammation in the liver and fat tissues. Recent studies of HCC have centered on cancer-initiating stem cell (CSC), including detection of CSC in cancer, identification of CSC markers, and isolation of CSC from human HCC cell lines. Synergism between alcohol and HCV may lead to liver tumorigenesis through TLR signaling.