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Article

RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.

Cell reports - 23 May 2017

Loke Justin, Assi Salam A, Imperato Maria Rosaria, Ptasinska Anetta, Cauchy Pierre, Grabovska Yura, Soria Natalia Martinez, Raghavan Manoj, Delwel H Ruud, Cockerill Peter N, Heidenreich Olaf, Bonifer Constanze

Abstract excerpt

Acute myeloid leukemia (AML) is a heterogeneous disease caused by mutations in transcriptional regulator genes, but how different mutant regulators shape the chromatin landscape is unclear. Here, we compared the transcriptional networks of two types of AML with chromosomal translocations of the RUNX1 locus that fuse the RUNX1 DNA-binding domain to different regulators, the t(8;21) expressing RUNX1-ETO and the...

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Share to CCAAT-Enhancer-Binding Protein-alpha
Share to Chromatin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromosomes, Human

Share to Core Binding Factor Alpha 2 Subunit

Share to GATA2 Transcription Factor

Share to Gene Knockdown Techniques

Share to Leukemia, Myeloid, Acute

Share to Translocation, Genetic

Source

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Identifiers

PMID: 28538183
DOI: 10.1016/j.celrep.2017.05.005
PMCID: PMC5457485

Genes

RUNX1
GATA2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

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RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.PMID 28538183Read ↗

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