Working group Heßmann

Research focus

Genetic alterations in the pancreatic acinar cell, including mutation, deletion or amplification of major oncogenes and tumorsuppressors play a pivotal role in pancreatic cancer development and progression. In addition to genetic events, pancreatic cancer is characterized by a plethora of epigenetic alterations that influence gene expression without changes in the DNA itself. Epigenetic mechanisms control gene expression at all levels of protein synthesis, e.g. via DNA methylation, chromatin alterations or expression of non-coding RNAs. In contrast to genetic alterations, epigenetic changes are reversible. Therefore, the regulators accountable for epigenetic dysregulation represent promising therapeutic targets in cancer therapy.

Our group focuses on the impact of chromatin dysregulation in the development and progression of pancreatic cancer. We utilize a plethora of functional, biochemical and molecular methods in human and murine tumor cells to dissect the influence of selected chromatin regulators in pancreatic carcinogenesis and progression. Within and without the conext of the KFO 5002 and with the help of transgenic mice and “Patient-derived-Xenograft” models of pancreatic cancer we further investigate the therapeutic potential of targeting chromatin dysregulation in this dreadful malignant disease. Together, we aim to govern mechanistic insights into chromatin-associated alterations in pancreatic cancer and evaluate therapeutic strategies to tackle epigenetic dysregulation in this disease.