A. Parolia

NSD2 is a requisite subunit of the AR/FOXA1 neo-enhanceosome in promoting prostate tumorigenesis

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.

p300/CBP degradation is required to disable the active AR enhanceosome in prostate cancer

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.

CDK12 Loss Promotes Prostate Cancer Development While Exposing Vulnerabilities to Paralog-Based Synthetic Lethality

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.

Development of an orally bioavailable mSWI/SNF ATPase degrader and acquired mechanisms of resistance in prostate cancer

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

PIKfyve controls dendritic cell function and tumor immunity

This study shows that PIKfyve inhibition enhances dendritic cell function and improves immunotherapy efficacy in tumor models.

BRD4-mediated epigenetic regulation of endoplasmic reticulum-mitochondria contact sites is governed by the mitochondrial complex III

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.

Targeting the mSWI/SNF Complex in POU2F-POU2AF Transcription Factor-Driven Malignancies

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.

Distinct mutational processes shape selection of MHC class I and class II mutations across primary and metastatic tumors

The paper identifies distinct mutational processes in MHC class I and II genes across primary and metastatic tumors, showing positive selection for mutations disrupting immune interfaces and linking them to immune checkpoint inhibitor response.

Multivalent proteins rapidly and reversibly phase-separate upon osmotic cell volume change

The paper shows multivalent proteins rapidly phase-separate during hyperosmotic stress and reversibly dissolve upon osmotic rescue, impacting transcription termination.