ArticleThe Journal of clinical investigation2016
MLL1 and DOT1L cooperate with meningioma-1 to induce acute myeloid leukemia.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Menin Inhibition in Acute Myeloid Leukemia: Rewiring Leukemic Transcriptional Networks.International journal of molecular sciences · 2026Review
- [Clinical characteristics and prognostic analysis of adult KMT2A-associated acute myeloid leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Menin inhibitors for the treatment of acute myeloid leukemia: challenges and opportunities ahead.Journal of hematology & oncology · 2024Review
- Refinement of Risk-Stratification of Cytogenetically Normal Acute Myeloid Leukemia Adult Patients by MN1 Expression.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- The Diverse Roles of ETV6 Alterations in B-Lymphoblastic Leukemia and Other Hematopoietic Cancers.Advances in experimental medicine and biology · 2024Review
- Acute myeloid leukemia: from NGS, through scRNA-seq, to CAR-T. dissect cancer heterogeneity and tailor the treatment.Journal of experimental & clinical cancer research : CR · 2023Review
- A Novel Pathogenic Variant in theJournal of pediatric genetics · 2023Article
- The Role of Histone Modification in DNA Replication-Coupled Nucleosome Assembly and Cancer.International journal of molecular sciences · 2023Review
- BRD9-containing non-canonical BAF complex maintains somatic cell transcriptome and acts as a barrier to human reprogramming.Stem cell reports · 2022Article
- Intrinsically disordered Meningioma-1 stabilizes the BAF complex to cause AML.Molecular cell · 2021Article
- Article
- DOT1L inhibitors block abnormal self-renewal induced by cohesin loss.Scientific reports · 2021Article
- Restoring MLL reactivates latent tumor suppression-mediated vulnerability to proteasome inhibitors.Oncogene · 2020Article
- Specific patterns of H3K79 methylation influence genetic interaction of oncogenes in AML.Blood advances · 2020Article
- Article
- Role of Meningioma 1 for maintaining the transformed state in MLL-rearranged acute myeloid leukemia: potential for therapeutic intervention?Haematologica · 2020Article
- Meningioma 1 is indispensable for mixed lineage leukemia-rearranged acute myeloid leukemia.Haematologica · 2020Article
- Yeats4 drives ILC lineage commitment via activation ofThe Journal of experimental medicine · 2019Article
- Characterization and targeting of malignant stem cells in patients with advanced myelodysplastic syndromes.Nature communications · 2018Article
- Integrative analysis reveals functional and regulatory roles of H3K79me2 in mediating alternative splicing.Genome medicine · 2018Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Meningioma-1 (MN1) overexpression is frequently observed in patients with acute myeloid leukemia (AML) and is predictive of poor prognosis. In murine models, forced expression of MN1 in hematopoietic progenitors induces an aggressive myeloid leukemia that is strictly dependent on a defined gene expression program in the cell of origin, which includes the homeobox genes Hoxa9 and Meis1 as key components. Here, we have shown that this program is controlled by two histone methyltransferases, MLL1 and DOT1L, as deletion of either Mll1 or Dot1l in MN1-expressing cells abrogated the cell of origin-derived gene expression program, including the expression of Hoxa cluster genes. In murine models, genetic inactivation of either Mll1 or Dot1l impaired MN1-mediated leukemogenesis. We determined that HOXA9 and MEIS1 are coexpressed with MN1 in a subset of clinical MN1hi leukemia, and human MN1hi/HOXA9hi leukemias were sensitive to pharmacologic inhibition of DOT1L. Together, these data point to DOT1L as a potential therapeutic target in MN1hi AML. In addition, our findings suggest that epigenetic modulation of the interplay between an oncogenic lesion and its cooperating developmental program has therapeutic potential in AML.
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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.