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Article

Targeting CDK1 promotes FLT3-activated acute myeloid leukemia differentiation through C/EBPα.

The Journal of clinical investigation - 1 Aug 2012

Radomska Hanna S, Alberich-Jordà Meritxell, Will Britta, Gonzalez David, Delwel Ruud, Tenen Daniel G

Abstract excerpt

Mutations that activate the fms-like tyrosine kinase 3 (FLT3) receptor are among the most prevalent mutations in acute myeloid leukemias. The oncogenic role of FLT3 mutants has been attributed to the abnormal activation of several downstream signaling pathways, such as STAT3, STAT5, ERK1/2, and A...

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Share to CCAAT-Enhancer-Binding Protein-alpha
Share to CDC2 Protein Kinase
Share to fms-Like Tyrosine Kinase 3

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Leukemia, Myeloid, Acute

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Source

Open in PubMed Open full text

Identifiers

PMID: 22797303
DOI: 10.1172/JCI43354
PMCID: PMC3408728

Genes

CDK1
FLT3
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-22797303-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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Targeting CDK1 promotes FLT3-activated acute myeloid leukemia differentiation through C/EBPα.PMID 22797303Read ↗

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An essential pathway links FLT3-ITD, HCK and CDK6 in acute myeloid leukemia.Semantic proximity Read ↗

Palbociclib treatment of FLT3-ITD+ AML cells uncovers a kinase-dependent transcriptional regulation of FLT3 and PIM1 by CDK6.Semantic proximity Read ↗

CDK2 destabilizes tumor suppressor C/EBPα expression through ubiquitin-mediated proteasome degradation in acute myeloid leukemia.Semantic proximity Read ↗

Internal tandem duplication mutation of FLT3 blocks myeloid differentiation through suppression of C/EBPalpha expression.Semantic proximity Read ↗

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