ArticleCell reports2013
FLT3-ITDs instruct a myeloid differentiation and transformation bias in lymphomyeloid multipotent progenitors.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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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
36 citing papers in PubMed, 42 citations in OpenAlex.
- Clinical Significance of FLT3-ITD Variation Allele Frequency in Acute Myeloid Leukemia: A Multicenter Study.Hematological oncology · 2026Article
- Recrudescence of a FLT3 wild-type CMML clone after allogeneic stem cell transplant for FLT3-ITD acute myeloid leukemia.The oncologist · 2026Article
- IGFBP7 regulates cell proliferation and migration through JAK/STAT pathway in gastric cancer and is regulated by DNA and RNA methylation.Journal of cellular and molecular medicine · 2024Article
- A Review of FLT3 Kinase Inhibitors in AML.Journal of clinical medicine · 2023Review
- An Update on FLT3 in Acute Myeloid Leukemia: Pathophysiology and Therapeutic Landscape.Current oncology reports · 2023Review
- Article
- Context is key for FLT3-ITD.Blood · 2023Article
- Article
- Exploration and identification of anoikis-related genes in polycythemia vera.Frontiers in genetics · 2023Article
- SETBP1 overexpression acts in the place of class-defining mutations to drive FLT3-ITD-mutant AML.Blood advances · 2021Article
- Mouse Models of Myeloid Malignancies.Cold Spring Harbor perspectives in medicine · 2021Review
- Inflammasome Activation in Myeloid Malignancies-Friend or Foe?Frontiers in cell and developmental biology · 2021Review
- Metabolic reprogramming of the myeloid lineage by Schistosoma mansoni infection persists independently of antigen exposure.PLoS pathogens · 2021Article
- Single-Cell Analysis of Neonatal HSC Ontogeny Reveals Gradual and Uncoordinated Transcriptional Reprogramming that Begins before Birth.Cell stem cell · 2020Article
- Direct role of FLT3 in regulation of early lymphoid progenitors.British journal of haematology · 2018Article
- The Myc/Max/Mxd Network Is a Target of Mutated Flt3 Signaling in Hematopoietic Stem Cells in Flt3-ITD-Induced Myeloproliferative Disease.Stem cells international · 2018Article
- Article
- PRKCH regulates hematopoietic stem cell function and predicts poor prognosis in acute myeloid leukemia.Experimental hematology · 2017Article
- Niche-mediated depletion of the normal hematopoietic stem cell reservoir by Flt3-ITD-induced myeloproliferation.The Journal of experimental medicine · 2017Article
- Runx1 Orchestrates Sphingolipid Metabolism and Glucocorticoid Resistance in Lymphomagenesis.Journal of cellular biochemistry · 2017Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
Whether signals mediated via growth factor receptors (GFRs) might influence lineage fate in multipotent progenitors (MPPs) is unclear. We explored this issue in a mouse knockin model of gain-of-function Flt3-ITD mutation because FLT3-ITDs are paradoxically restricted to acute myeloid leukemia even though Flt3 primarily promotes lymphoid development during normal hematopoiesis. When expressed in MPPs, Flt3-ITD collaborated with Runx1 mutation to induce high-penetrance aggressive leukemias that were exclusively of the myeloid phenotype. Flt3-ITDs preferentially expanded MPPs with reduced lymphoid and increased myeloid transcriptional priming while compromising early B and T lymphopoiesis. Flt3-ITD-induced myeloid lineage bias involved upregulation of the transcription factor Pu.1, which is a direct target gene of Stat3, an aberrantly activated target of Flt3-ITDs, further establishing how lineage bias can be inflicted on MPPs through aberrant GFR signaling. Collectively, these findings provide new insights into how oncogenic mutations might subvert the normal process of lineage commitment and dictate the phenotype of resulting malignancies.
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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.