Lanbo Xiao

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

This study shows that HSF1 forms stress-induced condensates with divergent transcriptional outcomes, impacting transcriptional responses during different stress conditions.

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

The paper tracks RNA localization to processing bodies using single-molecule microscopy and shows that RNA functionality influences their dynamic recruitment to PBs.