Chromatin Remodeling and Cancer

High resolution interaction surface mapping by PRISMA reveals novel ARID1A interactions

This study uses PRISMA to identify and map novel ARID1A interactions at high sequence resolution, revealing new interactors and a regulatory mechanism involving CDK2 phosphorylation.

Systematic drug profiling across BAF complex perturbations reveals distinct dependencies

This study systematically profiles drug responses in BAF complex perturbations, revealing subtype-specific vulnerabilities and resistance patterns to genotoxic and cytotoxic compounds.

CHD1 is a synthetic lethal vulnerability in MYC-driven breast cancer

The paper identifies CHD1 as a synthetic lethal target in MYC-driven breast cancer, showing that its loss suppresses tumor growth and induces cell death in MYC-overexpressing models.

Diverse Mechanisms of SMARCB1 Inactivation and Genome Maintenance Defects in Ultra-Rare Malignant Rhabdoid Tumors

This study identifies diverse mechanisms of SMARCB1 inactivation and genome maintenance defects in malignant rhabdoid tumors through multi-omics profiling of patient-derived models.

mSWI/SNF complex inhibition sensitizes KRAS-mutant lung cancers to targeted therapies via epithelial-mesenchymal subversion

This study shows that inhibiting mSWI/SNF complexes enhances the effectiveness of KRAS inhibitors in lung cancers by reversing epithelial-mesenchymal transition resistance.

Chromatin compaction upon CDK12 inhibition drives long gene silencing and a combinatorial lethal dependency on PAF1

This study shows CDK12 inhibition causes chromatin compaction and long gene silencing, revealing a lethal dependency on PAF1 for cell survival in prostate cancer.

Structural basis for BCL7B-mediated ncBAF-nucleosome engagement

This study resolves the structural mechanism of ncBAF-nucleosome interaction, showing BCL7B's role in chromatin remodeling and its connection to nuclear actin networks.

Tumour suppressors LKB1 and SMARCA4 functionally interact to regulate gene expression of diverse biological processes in lung cancer

This study investigates how LKB1 and SMARCA4 interact to regulate gene expression in lung cancer, showing they function together in a linear pathway and are similarly affected in mutant cells and human tumors.

BAF complex-independent gene activation by SS18::SSX

This study shows that SS18::SSX can drive transcription independently of BAF complex interaction and relies on EP300 for gene activation, suggesting new therapeutic targets for synovial sarcoma.

SS18-SSX co-opts P300 to sustain oncogenic transcription independent of SWI/SNF activity

This study shows SS18-SSX sustains oncogenic transcription without needing SWI/SNF activity, identifies P300 as a critical co-factor, and demonstrates targeting P300 or SWI/SNF as therapeutic strategies.

CRISPR-enabled genetic screens identify synthetic lethal targets across frequently altered cancer drivers

This study identifies synthetic lethal interactions between cancer drivers and tractable targets using CRISPR screens and cancer dependency data, offering new drug targets for therapy.

Chromatin remodeling with combined FACT and BET inhibition disrupts oncogenic transcription in Diffuse Midline Glioma

This study shows that combining FACT and BET inhibition disrupts oncogenic transcription and extends survival in Diffuse Midline Glioma models.

The PBAF chromatin remodeling complex contributes to metal homeostasis through Mtf1 regulation

The paper shows that the PBAF chromatin remodeling complex regulates metal homeostasis in myoblasts via Mtf1, with metal supplementation compensating for some complex deficiencies.

A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform

The paper identifies SWIFT, a SWI/SNF subunit domain that mediates transcription factor interactions, showing its role in chromatin targeting and cancer cell proliferation.

Identification of SMARCA1 as a key regulator for Colorectal Cancer

The paper identifies SMARCA1 as a key regulator in colorectal cancer metastasis through analysis of histone modification recognition proteins in cancer cell lines.

Generation and characterization of a mouse model of conditional Chd4 knockout in the endometrial epithelium.

This study generates a mouse model with conditional Chd4 knockout in the endometrial epithelium and finds no significant structural or functional changes or tumorigenesis.

Spatial dissection of ADC/RPT targets defines therapeutic opportunities inrhabdoid tumors

The paper identifies surface protein targets for ADC and RPT in rhabdoid tumors through transcriptomic and spatial analysis, revealing subgroup-specific expression patterns.

Redundancy masks functional specificity of SMARCD paralogs in neurodevelopment

The paper shows that SMARCD paralogs exhibit functional redundancy but also specialized roles in neurodevelopment, with SMARCD3 uniquely regulating oxidative phosphorylation.

Cell State Chaos Underpins the Evolution of SMARCA4-Deficient Dedifferentiated Endometrial Cancer

This study shows that SMARCA4 loss in endometrial cancer leads to cell state chaos, not stemness, causing dedifferentiation through epigenomic dysregulation.

Menin-MLL1 complex cooperates with NF-Y to promote HCC survival

This study identifies the menin-MLL1 complex as essential for HCC survival and shows it cooperates with NF-Y to regulate oncogenic gene transcription.

SMARCA2 is an essential and potent cofactor for a specific subset of the glucocorticoid response in A549 cells

The paper identifies SMARCA2 as a critical cofactor for a subset of glucocorticoid response genes in A549 cells through a CRISPR screen and functional analysis.

Targeting of SUMOylation leads to cBAF complex stabilization and disruption of the SS18::SSX transcriptome in Synovial Sarcoma

This study shows that inhibiting SUMOylation with TAK-981 stabilizes cBAF complexes and disrupts the SS18::SSX-driven transcriptome in synovial sarcoma, leading to tumor inhibition.

Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in dedifferentiated endometrial carcinomas

This study identifies shifted mSWI/SNF subcomplex stoichiometry in DDEC/UEC cancers and shows that SMARCA4/2 inhibitors reduce tumor growth and synergize with chemotherapy.

Spatially-resolved Photoproximity Profiling of MYC Identifies a MYC-BAF Liability in Cancer Cells

This paper introduces siPROX, a spatially resolved photoproximity method to map MYC interactomes, revealing BAF complex interactions as a therapeutic target in MYC-driven cancers.

ARID1A regulates histone octamer transfer activity of human canonical BAF complex

This study identifies ARID1A's role in histone octamer transfer by BAF complexes, showing it is required for this activity but not for nucleosome binding or sliding.

ARID1A and ARID1B safeguard B cell identity, prevent myeloid transformation and expose therapeutic vulnerabilities in lymphoma

This study investigates the roles of ARID1A and ARID1B in B cell development and lymphoma, showing their importance in preventing myeloid transformation and revealing therapeutic targets.

SUMO2 Inhibition Reverses Aberrant Epigenetic Rewiring Driven by Synovial Sarcoma Fusion Oncoproteins and Impairs Sarcomagenesis

This study identifies SUMO2 as a selective vulnerability in synovial sarcoma, showing that SUMO2 inhibition reverses SS18-SSX-driven gene expression and impairs tumor growth.

Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas

The paper identifies ATR as a target for combination EZH2 epigenetic therapy in SMARCB1-deficient sarcomas, showing that EZH2 inhibition promotes DNA damage via PGBD5, and that ATR inhibition enhances therapeutic responses.

Structural and functional basis of PU.1-BAF interaction enables targeting of lineage-specific transcription

This paper identifies the structural basis of PU.1-BAF interaction and shows small molecules can disrupt it, offering a new therapeutic strategy for cancer.

Expression of LTR and LINE1 transposable elements defines atypical teratoid/rhabdoid tumor subtypes

This study identifies distinct TE transcription profiles in ATRT subtypes, revealing unique patterns in ATRT-MYC that may inform new therapeutic strategies.