Abstract

HCC is a rapidly increasing cancer worldwide. Most HCC rises in the setting of chronic and advanced liver disease caused by viral hepatitis, alcohol use, non-alcoholic liver disease or their combination. We found that in the mouse model, alcohol alone does not induce HCC, however, it can promote HCC development after a carcinogen exposure. Multiple mechanisms are involved in carcinogenesis and alcohol affects many of those including epithelial-mesenchymal transition, cancer stem marker expression and inflammation as evidenced in our HCC model.

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