Inflammation induced tissue damage and carcinogenesis

The causal relationship between chronic inflammation, tissue damage, fibrosis and carcinogenesis is well established by epidemiological studies. Various etiologies, including chronic alcohol consumption, chronic drug abuse, autoimmune disorders, toxins (e.g. aflatoxin B) or infections with viruses (e.g. Hepatitis B and Hepatitis C virus) or bacteria (e.g. Helicobacter pylori) can lead to chronic inflammation, tissue damage and carcinogenesis. Aberrant expression of cytotoxic cytokines by immune but also non-immune cells is thought to be critically involved in the initial induction of inflammation and its progression towards a chronic state.
 
Our laboratory focuses on understanding the inflammatory signaling pathways (e.g. cytokines and chemokines) and cellular mechanisms responsible for the induction and maintenance of chronic inflammation, finally leading to tissue destruction and cancer. One focus of this laboratory is to elucidate the pathomechanisms of Hepatitis B (HBV) and Hepatitis C (HCV) viruses, by far the most common cause of chronic hepatitis in humans. HBV and HCV infections are frequently associated with hepatocellular carcinoma, the most prevalent primary human liver cancer. However, the cellular and molecular mechanisms driving hepatitis-induced liver cancer remain elusive.
 
Moreover, our work involves the generation of mouse models for chronic inflammatory disorders in different organs (e.g. pancreas, muscle, CNS) as well as work with human tissue and body fluids. Besides we aim at translating our research into a clinical setting and therefore are currently initiating a first clinical trial.

Funding

Work in our laboratory is currently funded by the following foundations: