ArticleBlood2012
Knock-in of a FLT3/ITD mutation cooperates with a NUP98-HOXD13 fusion to generate acute myeloid leukemia in a mouse model.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed, 64 citations in OpenAlex.
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- High-Throughput Identification, Modeling, and Analysis of Cancer Driver Genes In Vivo.Cold Spring Harbor perspectives in medicine · 2023Review
- Layered immunity and layered leukemogenicity: Developmentally restricted mechanisms of pediatric leukemia initiation.Immunological reviews · 2023Review
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- Context is key for FLT3-ITD.Blood · 2023Article
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- Cut-like homeobox 1 (CUX1) tumor suppressor gene haploinsufficiency induces apoptosis evasion to sustain myeloid leukemia.Nature communications · 2021Article
- Review
- Mouse Models of Myeloid Malignancies.Cold Spring Harbor perspectives in medicine · 2021Review
- Mechanistic insights and potential therapeutic approaches for NUP98-rearranged hematologic malignancies.Blood · 2020Review
- Novel Approaches to Target Mutant FLT3 Leukaemia.Cancers · 2020Review
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- Transforming activities of theHaematologica · 2020Article
- FLT3-ITD cooperates with Rac1 to modulate the sensitivity of leukemic cells to chemotherapeutic agents via regulation of DNA repair pathways.Haematologica · 2019Article
- Review
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- Nuclear factor of activated T-cells, NFATC1, governs FLT3Journal of hematology & oncology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Constitutive activation of FLT3 by internal tandem duplication (ITD) is one of the most common molecular alterations in acute myeloid leukemia (AML). FLT3/ITD mutations have also been observed in myelodysplastic syndrome patients both before and during progression to AML. Previous work has shown that insertion of an FLT3/ITD mutation into the murine Flt3 gene induces a myeloproliferative neoplasm, but not progression to acute leukemia, suggesting that additional cooperating events are required. We therefore combined the FLT3/ITD mutation with a model of myelodysplastic syndrome involving transgenic expression of the Nup98-HoxD13 (NHD13) fusion gene. Mice expressing both the FLT3/ITD and NHD13 transgene developed AML with 100% penetrance and short latency. These leukemias were driven by mutant FLT3 expression and were susceptible to treatment with FLT3 tyrosine kinase inhibitors. We also observed a spontaneous loss of the wild-type Flt3 allele in these AMLs, further modeling the loss of the heterozygosity phenomenon that is seen in human AML with FLT3-activating mutations. Because resistance to FLT3 inhibitors remains an important clinical issue, this model may help identify new molecular targets in collaborative signaling pathways.
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