ArticlePloS one2014
Cell fate decisions in malignant hematopoiesis: leukemia phenotype is determined by distinct functional domains of the MN1 oncogene.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- The BAFfling story of MN1-induced leukemogenesis.Molecular cell · 2021Article
- Intrinsically disordered Meningioma-1 stabilizes the BAF complex to cause AML.Molecular cell · 2021Article
- MN1 gene loss-of-function mutation causes cleft palate in a pedigree.Brain : a journal of neurology · 2021Article
- Article
- Sustained fetal hematopoiesis causes juvenile death from leukemia: evidence from a dual-age-specific mouse model.Blood advances · 2020Article
- Role of Meningioma 1 for maintaining the transformed state in MLL-rearranged acute myeloid leukemia: potential for therapeutic intervention?Haematologica · 2020Article
- Gain-of-Function MN1 Truncation Variants Cause a Recognizable Syndrome with Craniofacial and Brain Abnormalities.American journal of human genetics · 2020Article
- MN1 C-terminal truncation syndrome is a novel neurodevelopmental and craniofacial disorder with partial rhombencephalosynapsis.Brain : a journal of neurology · 2020Article
- Acquisition of an oncogenic fusion protein is sufficient to globally alter the landscape of miRNA expression to inhibit myogenic differentiation.Oncotarget · 2017Article
- Article
- Meis2 as a critical player in MN1-induced leukemia.Blood cancer journal · 2017Article
- MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia.The Journal of clinical investigation · 2016Article
- Chromosome 22q12.1 microdeletions: confirmation of the MN1 gene as a candidate gene for cleft palate.European journal of human genetics : EJHG · 2016Article
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Authors and funding
19 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive molecular profiling of leukemias and preleukemic diseases has revealed that distinct clinical entities, like acute myeloid (AML) and T-lymphoblastic leukemia (T-ALL), share similar pathogenetic mutations. It is not well understood how the cell of origin, accompanying mutations, extracellular signals or structural differences in a mutated gene determine the phenotypic identity of leukemias. We dissected the functional aspects of different protein regions of the MN1 oncogene and their effect on the leukemic phenotype, building on the ability of MN1 to induce leukemia without accompanying mutations. We found that the most C-terminal region of MN1 was required to block myeloid differentiation at an early stage, and deletion of an extended C-terminal region resulted in loss of myeloid identity and cell differentiation along the T-cell lineage in vivo. Megakaryocytic/erythroid lineage differentiation was blocked by the N-terminal region. In addition, the N-terminus was required for proliferation and leukemogenesis in vitro and in vivo through upregulation of HoxA9, HoxA10 and Meis2. Our results provide evidence that a single oncogene can modulate cellular identity of leukemic cells based on its active gene regions. It is therefore likely that different mutations in the same oncogene may impact cell fate decisions and phenotypic appearance of malignant diseases.
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