ArticleBlood2012
Terminal myeloid differentiation in vivo is induced by FLT3 inhibition in FLT3/ITD AML.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
102 citing papers in PubMed, 170 citations in OpenAlex.
- FDA Approval Summary: Gilteritinib for Relapsed or Refractory Acute Myeloid Leukemia with aClinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- A phase 1/2 study of the oral FLT3 inhibitor pexidartinib in relapsed/refractory FLT3-ITD-mutant acute myeloid leukemia.Blood advances · 2020Trial
- Hematopoietic niche drives FLT3-ITD acute myeloid leukemia resistance to quizartinibHaematologica · 2019Trial
- Trial
- Differentiation Syndrome Associated With Enasidenib, a Selective Inhibitor of Mutant Isocitrate Dehydrogenase 2: Analysis of a Phase 1/2 Study.JAMA oncology · 2018Trial
- A next-generation sequencing-based assay for minimal residual disease assessment in AML patients withBlood advances · 2018Trial
- Selective inhibition of FLT3 by gilteritinib in relapsed or refractory acute myeloid leukaemia: a multicentre, first-in-human, open-label, phase 1-2 study.The Lancet. Oncology · 2017Trial
- Quizartinib elicits differential responses that correlate with karyotype and genotype of the leukemic clone.Leukemia · 2016Trial
- Trial
- Timing of response in patients with relapsed/refractoryBlood neoplasia · 2026Article
- Revisiting retinoic acid in AML therapy: mechanisms of action and rational combination strategies.British journal of cancer · 2026Review
- Targeting oncogenic FLT3 uncovers a ferroptosis vulnerability through selenocysteine recoding in acute myeloid leukaemia.Nature cell biology · 2026Article
- FLT3-ITD signals for CEBPA and p53 proteolysis by the ubiquitin-proteosome pathway.Research square · 2026Article
- FLT3-ITD signals for CEBPA and p53 proteolysis by the ubiquitin-proteosome pathway.bioRxiv : the preprint server for biology · 2026Article
- Identification and Management of Differentiation Syndrome in Emergency Settings: A Narrative Review.Cancers · 2026Review
- Targeting ZMIZ1 induces differentiation in acute myeloid leukemia via chromatin remodeling.Signal transduction and targeted therapy · 2026Article
- Targeting WNK1 Releases Differentiation Block in Acute Myeloid Leukemia.bioRxiv : the preprint server for biology · 2026Article
- Differentiation Syndrome in Acute Myeloid Leukemia: Molecular Mechanisms, Clinical Spectrum, and Emerging Therapeutic Paradigms.International journal of molecular sciences · 2026Review
- Targeting nucleotide metabolism and epigenetic regulation to overcome the differentiation blockade in AML.Leukemia research reports · 2026Review
- Post-HCT maintenance therapy for AML: who, when, why, how long?Hematology. American Society of Hematology. Education Program · 2025Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
A hallmark of cancer is the disruption of differentiation within tumor cells. Internal tandem duplication mutations of the FLT3 kinase (FLT3/ITD) occur commonly in acute myeloid leukemia (AML) and are associated with poor survival, leading to efforts to develop FLT3 kinase inhibitors. However, FLT3 inhibitors have thus far met with limited success, inducing only a clearance of peripheral blasts with minimal BM responses. Quizartinib is a novel potent and selective FLT3 inhibitor currently being studied in clinical trials. In 13 of 14 FLT3/ITD AML patients with normal karyotype treated with quizartinib, we observed terminal myeloid differentiation of BM blasts in association with a clinical differentiation syndrome. The single patient whose blasts failed to differentiate had a preexisting C/EBPα mutation and another developed a C/EBPα mutation at disease progression, suggesting a mechanism of resistance to FLT3 inhibition. In vitro, in primary blasts cocultured with human BM stroma, FLT3 inhibition with quizartinib induced cell-cycle arrest and differentiation rather than apoptosis. The present study is the first description of terminal differentiation of cancer cells in patients treated with a tyrosine kinase inhibitor. These data highlight the importance of the differentiation block in the patho-genesis of AML.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.