Abstract PL03-03: K-RAS dependency in pancreatic cancer

Abstract

Abstract 2015 AACR-NCI-EORTC K-RAS dependency in Pancreatic Cancer David Tuveson, M.D., Ph.D., Cold Spring Harbor Laboratory Efforts to inhibit the KRAS oncogene in pancreatic cancer have focused on classical downstream pathways and empirically identified dependencies. We have developed organoid models of mouse and human pancreatic cancer to expedite such translational approaches for this disease. We find that organoid models of PDA demonstrate ERBB pathway activation in response to dual MEK/AKT inhibition, and that this feature is absent in non-neoplastic organoids. Furthermore, organoid models predict the limited activity of EGFR specific inhibitors in PDA patients that are also receiving MEK or AKT inhibitors. These models have also been an invaluable resource for probing new dependencies in PDA, and will be discussed. Citation Format: David A. Tuveson. K-RAS dependency in pancreatic cancer. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr PL03-03.