Speaker: Prof. Matthias Heikenwälder (DKFZ)
Organizer: Westdeutsches Tumorzentrum
Registration necessary: no
Chronic hepatitis is the main driver of liver cancer, the second most common cause for cancer related death in humans. Several different etiologies have been shown to cause chronic liver disease with prominent inflammation including chronic viral infections with Hepatitis B or C (HBV, HCV) but also chronic alcohol consumption or chronic high caloric diet in combination with a sedentary life style. Due to the consumption of high caloric food combined with increased sedentary lifestyle, overweight and obesity incidence has grown rapidly in Western countries (e.g. USA, Europe) but notably also in developing countries (e.g. India, China), affecting both adults and children. Although chronic viral infections are still the leading cause for hepatocellular carcinoma (HCC), alcoholic steatohepatitis (ASH), non-alcoholic fatty liver (NAFL) and subsequent non-alcoholic steatohepatitis (NASH) have become important etiologies for HCC. We and others have generated and characterized several pre-clinical mouse models that enable studying the mechanisms of inflammation induced liver cancer (e.g. NASH development and NASH to HCC transition in the context of a metabolic syndrome). Remarkably, these models recapitulate several human pathophysiological hallmarks of inflammation induced HCC. It has become apparent that adaptive immune cells but also innate immune cells play an important role in driving NAH and subsequent HCC - and at the same time actively participate in tumor surveillance. Here, I will report on the different kinds of innate and adaptive immune cells that can drive NASH and primary liver cancer like HCC or cholangiocarcinoma (iCC). I will discuss the characterization and identification of novel targets to treat inflammation induced liver cancer (e.g. in the context of NASH).
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Picture: © Universitätsklinikum Essen