Rory L. Smoot

The paper identifies LCK-driven EGFR activation as a therapeutic target in cholangiocarcinoma, showing EGFR activity predicts response to EGFR inhibition.

This study identifies AKT as a regulator of YAP stability and shows that AKT inhibition triggers ESCRT-dependent YAP degradation, enhancing the efficacy of RAS inhibition in pancreatobiliary cancers.

This study identifies therapy-induced senescent-like cancer cells as drivers of immunosuppression in cholangiocarcinoma by promoting macrophage-mediated suppression of CD8+ T cells.

This study identifies biomarkers and resistance mechanisms to SFK-YAP inhibition in cholangiocarcinoma using multiomic profiling and shows synergy with chemotherapy.

The paper identifies frequent EPHA2 mutations in cholangiocarcinoma and shows they disrupt forward signaling, suggesting EPHA2 acts as a tumor suppressor.