AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
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Together, these studies comprehensively define the KRASi-induced proteome and identify ALPP/ALPPL2 as a promising cell surface target for combination with KRASi to enhance response and forestall KRASi resistance.
Direct inhibition of oncogenic RAS has emerged as a clinically active therapeutic strategy for RAS-addicted cancers, including pancreatic ductal adenocarcinoma (PDAC). However, resistance is likely to limit the durability of therapeutic response, motivating combination strategies that target adaptive survival mechani...
The adaptive response to KRASG12C inhibitors (KRASi) in KRASG12C-mutant lung adenocarcinoma models is profile using an integrated genetic, transcriptomic, and mass-spectrometry-based quantitative temporal proteomic platform.
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...
These studies establish a comprehensive proteomic resource for the PDAC/KRASi research community and identify ALPP/ALPPL2 as a promising cell surface target for combination with KRASi to drive deeper, sustained responses and prevent or forestall KRASi resistance.
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.
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