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Article

An AML1-ETO/miR-29b-1 regulatory circuit modulates phenotypic properties of acute myeloid leukemia cells.

Oncotarget - 20 Jun 2017

Zaidi Sayyed K, Perez Andrew W, White Elizabeth S, Lian Jane B, Stein Janet L, Stein Gary S

Abstract excerpt

Acute myeloid leukemia (AML) is characterized by an aggressive clinical course and frequent cytogenetic abnormalities that include specific chromosomal translocations. The 8;21 chromosomal rearrangement disrupts the key hematopoietic RUNX1 transcription factor, and contributes to leukemia through recruitment of co-repressor complexes to RUNX1 target genes, altered subnuclear localization, and deregulation of the...

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Share to Chromosomes, Human, Pair 21
Share to Chromosomes, Human, Pair 8

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Co-Repressor Proteins

Share to Core Binding Factor Alpha 2 Subunit

Share to Gene Expression Regulation, Leukemic

Share to Leukemia, Myeloid

Share to Oncogene Proteins, Fusion

Share to RUNX1 Translocation Partner 1 Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 28611288
DOI: 10.18632/oncotarget.18127
PMCID: PMC5522207

Genes

RUNX1

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.

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