Department of Radiation Oncology
University of California, Los Angeles (UCLA)
Los Angeles, CA
Potentiating radiation therapy in pancreatic cancer
Aim: Basic Science / Cancer Biology
Pancreatic ductal adenocarcinomas (PDAC), commonly referred to as pancreatic cancer, are lethal, in part, due to a remarkable resistance to current therapies, including radiation therapy. For reasons that remain obscure, radiation fails to improve outcomes for pancreatic cancer patients even in the non-metastatic setting. In this proposal we hypothesize that the master regulator of cellular oxidative balance, NRF2, promotes tumor survival to oxidative stress during radiation by regulating the transcription of a metabolic genes that feed into antioxidant pathways. Our preliminary data suggest that inhibiting the NRF2 pathway can sensitize pancreatic cancer cells to radiation, strongly supporting our hypothesis and our long-term goal of developing novel ways to improve radiation therapy outcomes for pancreatic cancer patients.