ATRX loss promotes tumor growth and impairs nonhomologous end joining DNA repair in glioma.

doi:10.1126/scitranslmed.aac8228

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

Community

Back to search

Article

ATRX loss promotes tumor growth and impairs nonhomologous end joining DNA repair in glioma.

Science translational medicine - 2 Mar 2016

Koschmann Carl, Calinescu Anda-Alexandra, Nunez Felipe J, Mackay Alan, Fazal-Salom Janet, Thomas Daniel, Mendez Flor, Kamran Neha, Dzaman Marta, Mulpuri Lakshman, Krasinkiewicz Johnathon, Doherty Robert, Lemons Rosemary, Brosnan-Cashman Jacqueline A, Li Youping, Roh Soyeon, Zhao Lili, Appelman Henry, Ferguson David, Gorbunova Vera, Meeker Alan, Jones Chris, Lowenstein Pedro R, Castro Maria G

Abstract excerpt

Recent work in human glioblastoma (GBM) has documented recurrent mutations in the histone chaperone protein ATRX. We developed an animal model of ATRX-deficient GBM and showed that loss of ATRX reduces median survival and increases genetic instability. Further, analysis of genome-wide data for human gliomas showed that ATRX mutation is associated with increased mutation rate at the single-nucleotide variant (SNV)...

Read the complete abstract on PubMed

Topics

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

Share to Chromosomes, Mammalian

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DNA End-Joining Repair

Share to DNA Helicases

Share to Glioma

Share to Microsatellite Instability

Share to Telomere Homeostasis

Share to Transposases

Share to X-linked Nuclear Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 26936505
DOI: 10.1126/scitranslmed.aac8228
PMCID: PMC5381643

Genes

ATRX

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ATRX loss promotes tumor growth and impairs nonhomologous end joining DNA repair in glioma.PMID 26936505Read ↗

Mutant ATRX: uncovering a new therapeutic target for glioma.Semantic proximity Read ↗

The Role of ATRX in Glioma BiologySemantic proximity Read ↗

Atrx inactivation drives disease-defining phenotypes in glioma cells of origin through global epigenomic remodeling.Semantic proximity Read ↗

G-quadruplex DNA drives genomic instability and represents a targetable molecular abnormality in ATRX-deficient malignant gliomaSemantic proximity Read ↗

Loss of ATRX confers DNA repair defects and PARP inhibitor sensitivitySemantic proximity Read ↗

Loss of ATRX, associated with DNA methylation pattern of chromosome end, impacted biological behaviors of astrocytic tumors.Semantic proximity Read ↗

DNA repair genes in astrocytoma tumorigenesis, progression and therapy resistanceSemantic proximity Read ↗

ATRX, a guardian of chromatinSemantic proximity Read ↗

ATRX loss induces multiple hallmarks of the alternative lengthening of telomeres (ALT) phenotype in human glioma cell lines in a cell line-specific mannerSemantic proximity Read ↗

Whole-exome sequencing identifies ATRX mutation as a key molecular determinant in lower-grade glioma.Semantic proximity Read ↗

<i>Atrx</i> deletion impairs cGAS-STING signaling and increases response to radiation and oncolytic herpesvirus in sarcomaSemantic proximity Read ↗

The Chromatin Remodeler ATRX: Role and Mechanism in Biology and CancerSemantic proximity Read ↗

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