Yang Zheng

This study identifies a stress-lipid kinase axis in NEPC driven by PIKfyve, revealing a synthetic vulnerability between PIKfyve and FASN that can be exploited for therapeutic targeting.

This study shows that degrading p300/CBP in prostate cancer suppresses tumor growth more effectively than inhibiting their activity, highlighting their role in maintaining the active AR enhanceosome.

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.

This study identifies a therapeutic vulnerability in POU2F-POU2AF-driven cancers by showing that targeting the mSWI/SNF complex with a PROTAC degrader reduces tumor growth in preclinical models.

This study shows that PIKfyve inhibition enhances dendritic cell function and improves immunotherapy efficacy in tumor models.

This paper develops an orally bioavailable PROTAC degrader of mSWI/SNF ATPases for prostate cancer and identifies resistance mechanisms through long-term treatment.