ArticleThe Journal of clinical investigation2009
The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
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- Acute myeloid leukemia with rare recurring translocations-an overview of the entities included in the international consensus classification.Annals of hematology · 2024Review
- SPOC domain proteins in health and disease.Genes & development · 2023Review
- Advances in molecular characterization of pediatric acute megakaryoblastic leukemia not associated with Down syndrome; impact on therapy development.Frontiers in cell and developmental biology · 2023Review
- Revealing the intratumoral heterogeneity of non-DS acute megakaryoblastic leukemia in single-cell resolution.Frontiers in oncology · 2022Article
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- RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020Review
- Acute Megakaryocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
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- NFrontiers in oncology · 2019Review
- Pediatric Acute Myeloid Leukemia (AML): From Genes to Models Toward Targeted Therapeutic Intervention.Frontiers in pediatrics · 2019Review
Corrections and comments
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Authors and funding
19 authors at 9 institutions in 4 countries.
Funding
Abstract
Acute megakaryoblastic leukemia (AMKL) is a form of acute myeloid leukemia (AML) associated with a poor prognosis. The genetics and pathophysiology of AMKL are not well understood. We generated a knockin mouse model of the one twenty-two-megakaryocytic acute leukemia (OTT-MAL) fusion oncogene that results from the t(1;22)(p13;q13) translocation specifically associated with a subtype of pediatric AMKL. We report here that OTT-MAL expression deregulated transcriptional activity of the canonical Notch signaling pathway transcription factor recombination signal binding protein for immunoglobulin kappa J region (RBPJ) and caused abnormal fetal megakaryopoiesis. Furthermore, cooperation between OTT-MAL and an activating mutation of the thrombopoietin receptor myeloproliferative leukemia virus oncogene (MPL) efficiently induced a short-latency AMKL that recapitulated all the features of human AMKL, including megakaryoblast hyperproliferation and maturation block, thrombocytopenia, organomegaly, and extensive fibrosis. Our results establish that concomitant activation of RBPJ (Notch signaling) and MPL (cytokine signaling) transforms cells of the megakaryocytic lineage and suggest that specific targeting of these pathways could be of therapeutic value for human AMKL.
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Registered trials
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