ArticleOncotarget2012
FLT3 in lineage specification and plasticity.
Article in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- From monoclonals to bispecific T cell engagers: the evolving antibody-based therapy landscape in acute myeloid leukemia.Frontiers in immunology · 2026Review
- Flow Cytometric Identification of Hematopoietic and Leukemic Blast Cells for Tailored Clinical Follow-Up of Acute Myeloid Leukemia.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FLT3 is a receptor tyrosine kinase that is expressed in CD34+ hematopoietic stem/ progenitor cells (HSPCs) and is important for both normal myeloid and lymphoid differentiation. FLT3 expression in Pax5 negative lymphoid precursors coincides with a window of multilineage differentiation potential in mice and humans. Recent work has shown that FLT3 activating mutations can collaborate with a Nup98-HoxD13 mutation to induce an aggressive acute leukemia. The leukemic initiating population in this model displayed properties of both lymphoid and myeloid precursors, making it a useful tool to study the role of FLT3 in lineage plasticity. Through a variety of assays, the leukemic initiating population was shown to be restricted to myeloid differentiation, suggesting that the B-lineage properties in these cells are due to the priming of lymphoid transcription programs in multipotent progenitors rather than a true capacity for B-cell maturation. The development of an undifferentiated myeloid leukemia in this model, also has implications for the role of FLT3 in the inhibition of myeloid differentiation. Here we discuss the insights gained from this model.
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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.