ArticleLeukemia2017
AMKL chimeric transcription factors are potent inducers of leukemia.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 40 citations in OpenAlex.
- Condensates in fusion oncoprotein-driven leukemia: new biology and therapeutic opportunities.Trends in cancer · 2026Review
- Fully human anti-FOLR1 T-cell engager demonstrates potent activity in CBFA2T3::GLIS2 acute megakaryoblastic leukemia.Blood neoplasia · 2026Article
- A stem cell differentiation model reveals two alternative fates in CBFA2T3::GLIS2-driven acute megakaryoblastic leukemia initiation.Communications biology · 2025Article
- Overexpression of miR-99a promoted expansion and suppressed differentiation of hematopoietic stem/progenitor cells.Scientific reports · 2025Article
- Malignant Bone-Forming Neoplasm With NIPBL::BEND2 Fusion.Genes, chromosomes & cancer · 2024Article
- CBFA2T3-GLIS2 mediates transcriptional regulation of developmental pathways through a gene regulatory network.Nature communications · 2024Article
- 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
- CBFA2T3-GLIS2 model of pediatric acute megakaryoblastic leukemia identifies FOLR1 as a CAR T cell target.The Journal of clinical investigation · 2022Article
- c-Mpl-del, a c-Mpl alternative splicing isoform, promotes AMKL progression and chemoresistance.Cell death & disease · 2022Article
- [Blocking PAK1 kinase activity promotes the differentiation of acute megakaryocytic leukemia cells and induces their apoptosis].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022Article
- Case report: Novel NIPBL-BEND2 fusion gene identified in osteoblastoma-like phosphaturic mesenchymal tumor of the fibula.Frontiers in oncology · 2022Article
- Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022Review
- Intrinsically disordered Meningioma-1 stabilizes the BAF complex to cause AML.Molecular cell · 2021Article
- Article
- The Genome-Wide Impact ofInternational journal of molecular sciences · 2020Article
- Role of Meningioma 1 for maintaining the transformed state in MLL-rearranged acute myeloid leukemia: potential for therapeutic intervention?Haematologica · 2020Article
- High WBP5 expression correlates with elevation of HOX genes levels and is associated with inferior survival in patients with acute myeloid leukaemia.Scientific reports · 2020Article
- Emerging Roles of GLI-Similar Krüppel-like Zinc Finger Transcription Factors in Leukemia and Other Cancers.Trends in cancer · 2019Review
- Long-read sequencing unveils IGH-DUX4 translocation into the silenced IGH allele in B-cell acute lymphoblastic leukemia.Nature communications · 2019Article
- A high-throughput screen indicates gemcitabine and JAK inhibitors may be useful for treating pediatric AML.Nature communications · 2019Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Acute megakaryoblastic leukemia in patients without Down syndrome is a rare malignancy with a poor prognosis. RNA sequencing of fourteen pediatric cases previously identified novel fusion transcripts that are predicted to be pathological including CBFA2T3-GLIS2, GATA2-HOXA9, MN1-FLI and NIPBL-HOXB9. In contrast to CBFA2T3-GLIS2, which is insufficient to induce leukemia, we demonstrate that the introduction of GATA2-HOXA9, MN1-FLI1 or NIPBL-HOXB9 into murine bone marrow induces overt disease in syngeneic transplant models. With the exception of MN1, full penetrance was not achieved through the introduction of fusion partner genes alone, suggesting that the chimeric transcripts possess a unique gain-of-function phenotype. Leukemias were found to exhibit elements of the megakaryocyte erythroid progenitor gene expression program, as well as unique leukemia-specific signatures that contribute to transformation. Comprehensive genomic analyses of resultant murine tumors revealed few cooperating mutations confirming the strength of the fusion genes and their role as pathological drivers. These models are critical for both the understanding of the biology of disease as well as providing a tool for the identification of effective therapeutic agents in preclinical studies.
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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.