Abhijit Parolia

This study shows lactate epigenetically regulates cell states in H3K27M diffuse midline gliomas by modifying histones, and targeting CBP/p300 reduces tumor heterogeneity and improves preclinical outcomes.

This study modifies a molecule to create two variants with different target selectivity, showing how small structural changes can control degradation activity.

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 genomic drivers of progression and therapeutic outcomes in mCRPC and develops a multi-omic classifier to predict patient survival across multiple therapies.

The paper identifies fedratinib as a drug that increases endoplasmic reticulum-mitochondria contact sites by inhibiting BRD4, revealing a novel epigenetic pathway linking ERMCS to cellular metabolism.

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 lineage-specific transcription factor profiles in prostate cancer progression, revealing dynamic shifts during NE transdifferentiation and proposing a three-phase model.

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 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.