Summary

Pancreatic cancer is considered as an almost incurable disease due to late diagnosis, rapid spread and negligible response to treatment. Therefore, our aim is to develop concepts to prevent pancreatic cancer development analogous to statins, which prevent coronary heart disease. Acinar-to-ductal metaplasia is the earliest step in pancreatic carcinogenesis, which we are characterizing in a panel of murine in vivo and murine/human in vitro systems. Metabolic requirements and common signaling events as potential vulnerabilities are analyzed using high throughput approaches. In addition, sc-RNA-sequencing is performed to generate a comprehensive atlas of cell populations in early neoplastic lesions to define dynamic cellular, signaling and metabolic changes at a single cell level. Understanding the role of ROS and its interconnection with metabolic rewiring is another aim of the lab. The overall goal is the development of strategies to prevent pancreatic cancer.