Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Epigenome Programming by H3.3K27M Mutation Creates a Dependence of Pediatric Glioma on SMARCA4

28 Oct 2022

Abstract excerpt

Patients with diffuse midline gliomas that are H3K27 altered (DMG) display a dismal prognosis. However, the molecular mechanisms underlying DMG tumorigenesis remain poorly defined. Here we show that SMARCA4, the catalytic subunit of the mammalian SWI/SNF chromatin remodeling complex, is essential for the proliferation, migration, and invasion of DMG cells and tumor growth in patient-derived DMG xenograft models....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chromatin Remodeling and Cancer
Share to Genomics and Chromatin Dynamics
Share to Glioma Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36305747
DOI: 10.1158/2159-8290.cd-21-1492

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Epigenome Programming by H3.3K27M Mutation Creates a Dependence of Pediatric Glioma on SMARCA4PMID 36305747Read ↗

Targeting SWI/SNF ATPases in H3.3K27M diffuse intrinsic pontine gliomas.Semantic proximity Read ↗

H3F3A K27M mutations drive a repressive transcriptome by modulating chromatin accessibility independent of H3K27me3 in Diffuse Midline Glioma.Semantic proximity Read ↗

SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation.Semantic proximity Read ↗

H3F3A K27M Mutations Drives a Repressive Transcriptome by Modulating Chromatin Accessibility, Independent of H3K27me3 in Diffuse Midline GliomaSemantic proximity Read ↗

BMP2 and BMP7 cooperate with H3.3K27M to promote quiescence and invasiveness in pediatric diffuse midline gliomasSemantic proximity Read ↗

H3.3K27M Mutation Controls Cell Growth and Resistance to Therapies in Pediatric Glioma Cell LinesSemantic proximity Read ↗

Epigenetic activation of a RAS/MYC axis in H3.3K27M-driven cancerSemantic proximity Read ↗

Super elongation complex as a targetable dependency in diffuse midline gliomaSemantic proximity Read ↗

BMP2 and BMP7 cooperate with H3.3K27M to promote quiescence and invasiveness in pediatric diffuse midline gliomas.Semantic proximity Read ↗

SUV39H1 regulates progression of pediatric diffuse high-grade gliomas through modulation of β-catenin/TCF4 levelsSemantic proximity Read ↗

Dual Targeting of Histone Deacetylases and MYC as Potential Treatment Strategy for H3-K27M Pediatric GliomasSemantic proximity Read ↗

Common molecular features of H3K27M DMGs and PFA ependymomas map to hindbrain developmental pathways.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.