The Kimmelman lab is focused on the study of pancreatic cancer metabolism. Together this work has defined the altered metabolism of pancreatic cancer and has elucidated novel therapeutic approaches. A major focus of the lab is a form of metabolic scavenging known as autophagy. The Kimmelman lab was the first to identify that pancreatic cancers have elevated basal autophagy which is required for continued proliferation through its importance in their metabolism. This work has provided fundamental insights into the importance of autophagy in Ras-driven cancers and multiple clinical trials have now opened to test this therapeutic approach. The lab continues to explore the role autophagy in pancreatic cancer metabolism and recently identified a novel autophagy receptor for ferritin that is critical for iron metabolism. Additionally, studies from the lab have demonstrated how central carbon metabolism is altered in pancreatic cancer and that oncogenic Kras regulates many of these alterations. Using a novel pancreatic cancer mouse model, they discovered that oncogenic Kras maintains pancreatic tumor growth in part through the rewiring of anabolic glucose metabolism. Additionally, they have identified a novel metabolic pathway in pancreatic tumors that is essential for their growth by maintaining redox balance. Importantly, normal cells do not require this pathway and therefore this may be an attractive therapeutic target in pancreatic cancer patients. Work in the lab continues to define the precise role of various carbon sources in the metabolism of these tumors.