Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive form of cancer, carrying a dismal five-year survival rate of only ~4%. We hypothesize that the combination of oncogenic mutations and changes in the stiffness of the microenvironment is required to drive a cancer-like phenotype of increased growth, changes in morphology, and increased ERK activity. The dynamic and modular nature of this system allows us to test the effect of further perturbations on ERK signaling and growth with the goal of understanding how these factors contribute to PanIN to PDAC progression and identify targets for interception.
