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Article

Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature.

Cell reports - 4 Aug 2015

Cauchy Pierre, James Sally R, Zacarias-Cabeza Joaquin, Ptasinska Anetta, Imperato Maria Rosaria, Assi Salam A, Piper Jason, Canestraro Martina, Hoogenkamp Maarten, Raghavan Manoj, Loke Justin, Akiki Susanna, Clokie Samuel J, Richards Stephen J, Westhead David R, Griffiths Michael J, Ott Sascha, Bonifer Constanze, Cockerill Peter N

Abstract excerpt

Acute myeloid leukemia (AML) is characterized by recurrent mutations that affect the epigenetic regulatory machinery and signaling molecules, leading to a block in hematopoietic differentiation. Constitutive signaling from mutated growth factor receptors is a major driver of leukemic growth, but how aberrant signaling affects the epigenome in AML is less understood. Furthermore, AML cells undergo extensive clonal...

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Share to Core Binding Factor Alpha 2 Subunit
Share to fms-Like Tyrosine Kinase 3

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Leukemic

Share to Leukemia, Myeloid, Acute

Share to MAP Kinase Signaling System

Share to Mitogen-Activated Protein Kinase Kinases

Share to Protein Structure, Tertiary

Share to Transcription Factor AP-1

Source

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Identifiers

PMID: 26212328
DOI: 10.1016/j.celrep.2015.06.069
PMCID: PMC4726916

Genes

FLT3
RUNX1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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