Chromatin Remodeling and Cancer

SOX2 is a dispensable modulator of NUT carcinoma oncogenesis in mouse

This study shows SOX2 is not required for NUT carcinoma initiation or maintenance in mice, challenging its assumed oncogenic role and suggesting limited utility for SOX2-targeted therapies.

Tissue-Specific Co-Expression Patterns of BAF Complexes Provide Regulatory Insights Across Human Tissues with Implications for Endocrine and Non-Endocrine Functions

The paper analyzes BAF complex gene co-expression across human tissues to identify tissue-specific regulatory patterns and their functional implications.

MORC2 phosphorylation fine tunes its DNA compaction activity

This study characterizes MORC2 phosphorylation's role in DNA compaction and chromatin remodelling, showing it regulates ATP hydrolysis and DNA binding.

How cBAF and PBAF regulate the nucleosomal and subnucleosomal landscape of promoters, enhancers and REST repressor binding sites

The paper investigates how cBAF and PBAF chromatin remodeling complexes regulate nucleosomal and subnucleosomal structures at promoters, enhancers, and REST sites, revealing distinct functional roles for their subunits.

Synaptic Activity Causes Minute-scale Changes in BAF Complex Composition and Function

The paper investigates how synaptic activity rapidly alters BAF complex composition and function in neurons, revealing phosphorylation and chromatin remodeling effects within minutes.

CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly

The paper identifies Mlf2 and Rbm15 as regulators of SWI/SNF complex activity through CRISPR screening in mouse embryonic stem cells, revealing their roles in chromatin remodeling and m6A RNA methylation.

Clonal lineage tracing and parallel multiomics profiling reveal transcriptional diversification induced by ARID1A deficiency

This study uses an integrated platform to show that ARID1A deficiency increases transcriptomic and epigenetic heterogeneity in cancer cells through stochastic and constrained chromatin changes.

SMARCA4 is essential for early-stage tumor development but its loss promotes late-stage cancer progression in small-cell lung cancer

This study shows SMARCA4 is important for early tumor development in SCLC but its loss promotes late-stage cancer progression through altered tumor-NK cell interactions.

First Generation Tools for the Modeling of Capicua (CIC) - Family Fusion Oncoprotein-Driven Cancers

The paper develops synthetic CIC-family fusion oncoproteins to study their distinct transcriptional effects in cancer.

The SWI/SNF PBAF complex facilitates REST occupancy at repressive chromatin

The paper shows that the PBAF complex in melanoma facilitates REST occupancy at repressive chromatin, leading to upregulation of synaptic transcripts when ARID2 is mutated.

Phenotypic and Functional Characterization of Oncohistone Mutations in Breast Cancers

This study identifies and characterizes 17 high frequency oncohistone mutations in breast cancer that promote cancer-related phenotypes and may act as potential cancer drivers.

H3F3A K27M Mutations Drives a Repressive Transcriptome by Modulating Chromatin Accessibility, Independent of H3K27me3 in Diffuse Midline Glioma

Challenges and opportunities for drug repurposing in cancers based on synthetic lethality induced by tumor suppressor gene mutations

This paper identifies potential drug repurposing opportunities through synthetic lethality by analyzing CRISPR screens and drug sensitivity data, but finds pharmacological inhibitors often fail to mimic genetic KO effects.

Recurrent breakpoints in the BRD4 locus reduce toxicity associated with gene amplification

This study shows that BRD4 gene deletions reduce toxicity from overexpression in ovarian and breast cancers, providing evidence for a novel mechanism in cancer progression.

SMARCA4 mutation induces tumor cell-intrinsic defects in enhancer landscape and resistance to immunotherapy

This study shows that SMARCA4 mutations in lung cancer disrupt enhancer landscapes and innate immune gene expression, leading to immunotherapy resistance.

ATRX safeguards cellular identity during C. elegans development

This study shows that XNP-1, the C. elegans homologue of ATRX, maintains cellular identity by preventing ectopic germline gene expression, and its loss leads to developmental defects.

Integrative analysis of patient-derived tumoroids and ex vivo organoid modeling of ARID1A loss in bladder cancer reveals therapeutic molecular targets

The paper identifies CHEK1 and BIRC5 as therapeutic targets in ARID1A-deficient bladder cancer using patient-derived tumoroids and public datasets.

Loss of ARID1A accelerates prostate tumourigenesis with a proliferative collagen-poor phenotype through co-operation with AP1 subunit cFos

This study identifies Arid1a loss as a driver of aggressive prostate cancer in mice, accelerating tumorigenesis and promoting a proliferative, collagen-poor phenotype through cooperation with cFos.

Loss of SMARCB1 evokes targetable epigenetic vulnerabilities in Epithelioid Sarcoma

This study investigates how SMARCB1 loss in Epithelioid Sarcoma rewires epigenetic regulation, revealing therapeutic vulnerabilities through functional multi-omics analysis.

Plant BCL-Domain Homologues play a conserved role in SWI/SNF complex stability

This study identifies BDH proteins as conserved subunits of plant SWI/SNF complexes, showing their role in complex stability and hypocotyl elongation through interactions with ARP4-ARP7.

Long non-coding RNAs direct the SWI/SNF complex to cell-specific enhancers

This study identifies long non-coding RNAs (lncRNAs) as guides for the SWI/SNF complex to cell-specific enhancers, revealing a mechanism for chromatin accessibility and gene expression control.

BAZ1A, an Imitation Switch (ISWI) protein, interacts and facilitates the recruitment of E2F1 to activate the E2F transcription program

This study identifies BAZ1A as a key component of an ISWI complex that recruits E2F1 to activate the E2F transcription program, promoting G1-S progression in glioma cells.

A STAG2-PAXIP1/PAGR1 axis suppresses lung tumorigenesis

This study identifies a STAG2-PAXIP1/PAGR1 tumor-suppressive axis in lung cancer by showing their combined role in suppressing oncogenic KRAS-driven tumorigenesis.

Activity-assembled nBAF complex mediates rapid immediate early gene transcription by regulating RNA Polymerase II productive elongation.

This study shows the nBAF complex facilitates activity-induced transcription of IEGs by regulating RNA Polymerase II elongation through its assembly and ATPase activity.

Differential Modulation of Polycomb-Associated Histone Marks by cBAF, pBAF, and gBAF Complexes

The paper shows that cBAF complexes, but not gBAF or pBAF, remove polycomb repressive histone marks from the Nkx2.9 locus in mESCs, leading to transcriptional activation.

Integrated multiomic profiling reveals SWI/SNF subunit-specific pathway alterations and targetable vulnerabilities

The paper identifies pathway alterations and targetable vulnerabilities in SWI/SNF-defective cancers through multiomic profiling and drug screening.

Synovial Sarcoma Chromatin Dynamics Reveal a Continuum in SS18:SSX Reprograming

This study examines the epigenomic states of synovial sarcoma using multi-omics analysis, revealing a continuum of epigenomic states and identifying H3K4me3 inhibition as a potential therapeutic strategy.

SS18::SSX redistributes BAF chromatin remodelers selectively to activate and repress transcription

This paper shows SS18::SSX fusion protein alters BAF chromatin remodeler distribution, leading to transcriptional activation and repression by changing histone modifications at regulatory regions.

Differential requirements for different subfamilies of the mammalian SWI/SNF chromatin remodeling enzymes in myoblast differentiation

The paper investigates the roles of three mSWI/SNF subfamilies in myoblast differentiation, finding distinct requirements for BAF and ncBAF complexes, while PBAF is dispensable.

Cell state-dependent chromatin targeting in NUT carcinoma

The paper shows that BRD4-NUT fusion protein creates chromatin megadomains whose locations depend on the initial cell state, not genetic variation.