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Article

Integrative genetic analysis of mouse and human AML identifies cooperating disease alleles.

The Journal of experimental medicine - 11 Jan 2016

Hatlen Megan A, Arora Kanika, Vacic Vladimir, Grabowska Ewa A, Liao Willey, Riley-Gillis Bridget, Oschwald Dayna M, Wang Lan, Joergens Jacob E, Shih Alan H, Rapaport Franck, Gu Shengqing, Voza Francesca, Asai Takashi, Neel Benjamin G, Kharas Michael G, Gonen Mithat, Levine Ross L, Nimer Stephen D

Abstract excerpt

t(8;21) is one of the most frequent chromosomal abnormalities observed in acute myeloid leukemia (AML). However, expression of AML1-ETO is not sufficient to induce transformation in vivo. Consistent with this observation, patients with this translocation harbor additional genetic abnormalities, suggesting a requirement for cooperating mutations. To better define the genetic landscape in AML and distinguish driver...

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Topics

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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 Core Binding Factor Alpha 2 Subunit

Share to Gene Expression Regulation, Leukemic

Share to Gene Knockout Techniques

Share to Oncogene Proteins, Fusion

Share to Protein Tyrosine Phosphatase, Non-Receptor Type 11

Share to RUNX1 Translocation Partner 1 Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 26666262
DOI: 10.1084/jem.20150524
PMCID: PMC4710200

Genes

PTPN11
TET2

Variants

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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