Stephanie J. Miner

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

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