New Molecular Insights into Hepatitis and Hepatic Cancer

Dear Colleagues,

Hepatocellular carcinoma (HCC) is among the top ten most frequent tumor types worldwide. Major etiologies include hepatitis B, hepatitis C, chronic alcoholism, and nonalcoholic steatohepatitis. Mortality is high by the time of diagnosis because the tumor is already in advanced stages, and treatment options are limited. Various imaging techniques have successfully identified early tumors when cures could be accomplished by surgical resection, but these approaches are not commonly employed because early tumors are often asymptomatic. Like most solid tumors, HCC is multi-step and often multi-focal by the time it is detected. The result is that different nodules may be both phenotypically and genotypically heterogeneous, making treatment and cure quite challenging. Part of the problem here is the lack of reproducible serum biomarkers to help identify patients with early tumors. Clearly, multiple therapeutic approaches will be needed to successfully treat HCC, and these are under development, but since HCC is a chronic disease, even multiple therapies run the risk of selecting for therapeutic-induced resistance. In hepatitis virus-associated cancers, the emphasis has been to target virus gene expression and replication by various means, and while this has helped to ameliorate chronic liver disease (CLD) prior to the appearance of cancer, there is still a long way to go before host molecules and pathways that contribute to the hallmarks of cancer are adequately targeted to result in a cure. Given that the pathogenesis of HCC is immune-mediated independent of etiology, additional approaches being explored include therapeutic vaccination and immunotherapy, although success here has been limited. Immunomodulation of CLD is also being developed to change the course of the disease so that the risk of progression to HCC is reduced. Since the progression of CLD is a major risk factor for progression to end-stage liver disease (cirrhosis) and HCC, early intervention years prior to the development of cancer may be a viable approach not only to target hepatitis but also to prevent or slow down the appearance of fibrosis and cirrhosis, thereby re-establishing liver homeostasis.

Chapter 1: Epidemiology of HCC due to HBV, HCV, alcoholism, and nonalcoholic steatohepatitis.
Chapter 2: Stages of chronic liver disease leading to fibrosis, cirrhosis, and HCC; pathologic changes in liver morphology and function as disease progresses.
Chapter 3: Imaging techniques used to detect early HCC; success rates.
Chapter 4: Current treatments for HCC and limitations. Antiviral therapies in disease pathogenesis.
Chapter 5: The cellular and molecular basis for phenotypic and genotypic heterogeneity in CLD and HCC. Molecular pathways common to CLD independent of etiology.
Chapter 6: The limitations in establishing reliable serum and/or tissue biomarkers for CLD and HCC. 
Chapter 7: Current immunological approaches to HCC treatment (immunotherapy and therapeutic vaccination, etc.).
Chapter 8: Immunomodulation of CLD to reduce the risk of progression to HCC.

Prof. Dr. Mark A. Feitelson
Guest Editor

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• hepatitis
• alcoholic and non-alcoholic steatohepatitis
• HBV and HCV
• hepatic Cancer
• hepatocellular carcinoma
• chronic liver disease
• cellular and molecular basis
• signaling pathways
• antiviral therapies
• immunotherapy
• therapeutic advances