Channing J. Der

This study shows that combining AXL inhibition with RAS or ERK inhibitors enhances efficacy in KRAS-mutant cancers by overcoming resistance mechanisms.

This study identifies KEAP1 loss as a resistance mechanism to KRAS inhibitors in pancreatic and lung cancer and shows that combining glutamine inhibition with KRAS inhibitors can overcome this resistance.

This study shows that p53 and YAP/TAZ-TEAD activities regulate metaplastic heterogeneity in pancreatic cancer by influencing differentiation states and molecular subtypes.

This study shows that ONC201 inhibits KRAS-mutant pancreatic cancer growth and overcomes resistance to RAS inhibitors by activating ClpP and altering metabolic pathways.

The paper shows that p53 activity regulates YAP/TAZ-TEAD complexes to shape transcriptional landscapes during tumorigenesis by altering TEAD binding and gene regulatory networks.

This study identifies TRIP13 as a key factor protecting KRAS-mutant pancreatic cancer cells from DNA replication stress and therapy-induced damage.

This study evaluates the therapeutic potential of RMC-7977, a broad-spectrum RAS inhibitor, in pancreatic ductal adenocarcinoma models, showing strong anti-tumor effects with minimal impact on normal tissues.

The paper engineers threshold-based selection systems in C. elegans to identify novel downstream effectors by disrupting embryonic morphogenesis with conditional CED-10/Rac activation.