AG Michalski
Christoph Michalski
Bo Kong
Simon Rieder
Ivane Abiatari
Natalya Valkovska
Manja Thorwith
Charlotte Bruse
Sina Fritzsche
Georg Leinenkugel
Wilhelm Schönherr
Patrick Winterhalter
Susanne Raulefs
Ivonne Regel
Philipp Bruns
Chiara Tosolini
Bakyt Sabyrbekov
Benedikt Schmid
Weiwei Wu
Chronic inflammation, pancreatic
and liver carcinogenesis
Most, if not all tumors are accompanied by inflammation and infiltration of immune cells. More recent epidemiological data also shows that chronic inflammation and the development of cancer are associated, but cancer-associated inflammation is a double-edged sword: On the one hand, it can be a sign of a reaction of the host’s immune system against cancer but, on the other hand, inflammation may promote malignant transformation; additionally, inflammation also increases the (local) environmental pressure which again might induce an “evolutionary” selection of more aggressive cancer cell clones. Interestingly, several recent reports have demonstrated that oncogenic transformation – induced by the activation of oncogenic mutations – itself is accompanied by a so-called intrinsic (i.e. epithelial-intrinsic) inflammation. The initial reaction to such transformations of epithelial cells is potentially sensed by receptors of the innate immune system (i.e. Toll-like receptors; probably both on immune cells and epithelia) as a “first line of defense”. Our research group thus focuses on elucidating the molecular mechanisms underlying oncogenic mutation-driven intrinsic inflammation and the innate immune reaction towards such changes in the epithelial cell compartment. To this end, we employ primary epithelial and immune cell cultures, genetically-engineered mouse models of pancreatic and hepatocellular cancer and mouse models of acute and chronic pancreatic and liver inflammation.