Pancreatic ductal adenocarcinoma (PDAC) is dependent on mutant KRAS and elevated autophagy for growth. Previously, we and others demonstrated that pharmacological inhibition of the KRAS ERK-MAPK pathway caused increased autophagic flux. Targeting this increased autophagic flux with inhibitors that block autophagic pr...
Seamus E. Degan, Mallory K. Roach, Jonathan M. DeLiberty et al.· Cancer Research· 0 citations
Mutational activation of the KRAS oncogene occurs in over 90% of pancreatic ductal adenocarcinoma (PDAC) patients, and plays a crucial role in tumor initiation, progression, and tumor maintenance. Historically considered undruggable, there has recently been a surge in efforts to develop and improve drugs that target...
Sarah E. Ackermann, Seamus E. Degan, Wen-Hsuan Chang et al.· Cancer Research· 0 citations
Combined treatment with the AXL inhibitor bemcentinib together with the RAS(ON) multi-selective tri-complex inhibitor RMC-7977 (RASi) or the ERK-selective inhibitor SCH772984 (ERKi) significantly enhanced growth suppression in human KRAS-mutant pancreatic and lung cancer models.
Yan-Pang Ching, Shruthi Narayanan, Jeffrey A. Klomp et al.· bioRxiv· 0 citations
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