Caleb Cheng

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 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 shows CDK12 loss drives prostate cancer development and identifies CDK13 as a therapeutic target through paralog-based synthetic lethality in CDK12-mutant tumors.

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