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

doi:10.1038/s41467-018-03476-6

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Article

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

Nature communications - 13 Mar 2018

Danussi Carla, Bose Promita, Parthasarathy Prasanna T, Silberman Pedro C, Van Arnam John S, Vitucci Mark, Tang Oliver Y, Heguy Adriana, Wang Yuxiang, Chan Timothy A, Riggins Gregory J, Sulman Erik P, Lang Frederick F, Creighton Chad J, Deneen Benjamin, Miller C Ryan, Picketts David J, Kannan Kasthuri, Huse Jason T

Abstract excerpt

Mutational inactivation of the SWI/SNF chromatin regulator ATRX occurs frequently in gliomas, the most common primary brain tumors. Whether and how ATRX deficiency promotes oncogenesis by epigenomic dysregulation remains unclear, despite its recent implication in both genomic instability and telomere dysfunction. Here we report that Atrx loss recapitulates characteristic disease phenotypes and molecular features...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 29535300
DOI: 10.1038/s41467-018-03476-6
PMCID: PMC5849741

Genes

ATRX

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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.

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