Somnath Mahapatra

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 maps the mouse prostate's cellular organization and identifies key determinants of castration resistance using single-cell and spatial transcriptomics.

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 humanized mouse models of metastatic prostate cancer to evaluate therapies, showing improved immune interactions and response to hormonal and immunotherapies.

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