October 23, 2017
Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer death in the US and despite some advances in treatment approaches, the long-term survival of patients remains extremely poor. Mutations in KRAS are a hallmark of this cancer type, occurring in >90% of cases, making this gene an attractive therapeutic target. New research from the laboratory of Tyler Jacks, a David H. Koch Professor of Biology and director of the Koch Institute, investigated whether PDAC cells are dependent on KRAS for their growth. Using CRISPR/ Cas9 to completely delete KRAS, the researchers determined that a subset of PDAC cells are still able to survive. However, the cells that do survive are sensitive to inhibitors of the PI3K pathway, suggesting that the simultaneous inhibition of KRAS and PI3K would be a viable combinatorial therapeutic strategy.