Yuanyuan Qiao

This paper identifies a druggable chromatin vulnerability in suppressive neutrophils that can restore antitumor immunity through mSWI/SNF antagonists.

A bifunctional AR–p300/CBP molecule, DALTAC-1, forces a non-native contact between AR and p300 domains, silences AR enhancers and regresses AR-driven prostate tumors in mice while sparing AR-negative lines.

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 NSD2 as a critical component of the AR neo-enhanceosome in prostate cancer, showing its role in AR enhancer circuitry and tumor progression.

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.