Research Group for Molecular Gastroenterology & Tumor Biology

A major cause of carcinogenesis is the cellular adaptation to persistent stress due to chronic inflammatory processes - e.g. of epithelial cells of the intestine or pancreas during ulcerative colitis or chronic pancreatitis. Under the influence of immune cells (e.g. macrophages, granulocytes) and their effectors (ROS/RNS, IL1β, IL6, TNFα, TGFβ1) and the resulting oxidative and inflammatory stress, epithelial protective mechanisms are consolidated under the control of transcription factors such as nuclear factor-κB (NF-κB) or nuclear factor-E2 related factor-2 (Nrf2). This can also result in a malignant phenotype, e.g. in connection with increased apoptosis protection, increased proliferation or migration behaviour, changes in metabolism and the development of resistance to therapy. Thus, NF-κB and Nrf2 undoubtedly play an important role in the development of tumors, e.g. colorectal carcinoma or ductal pancreatic carcinoma. Accordingly, NF-κB and Nrf2 are of great interest as target structures for more efficient diagnostic/therapeutic measures. A prerequisite for this is an exact understanding of the modalities of how NF-κB and Nrf2 unfold their tumour-promoting properties or how these can be specifically influenced.

Using different examination models and with special consideration of the tumour-stroma interaction, our research group has been working on this topic for many years. The spectrum of investigations ranges from cell culture experiments to animal experiments and patient-based analyses. This ensures that the findings, which are initially based on basic research, can also be reproduced in a clinical context.