ArticleLeukemia2015
Runx1 is required for hematopoietic defects and leukemogenesis in Cbfb-MYH11 knock-in mice.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- The Inv(16) Oncogene CBFB::MYH11 is Required for the Survival of Leukemia Cells in the Blood and Spleen, but not the Bone Marrow.Oncogene · 2026Article
- Multi omics and mechanistic investigation reveals CBFB as a prognostic biomarker in gastric cancer.Discover oncology · 2026Article
- Article
- CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice.The Journal of clinical investigation · 2025Article
- Leukemic Cells Infiltrate the Ovaries Without Damaging Ovarian Reserve in an Acute Myeloid Leukemia Mouse Model.Endocrinology · 2025Article
- Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein.The Journal of clinical investigation · 2023Article
- RUNX1-Survivin Axis Is a Novel Therapeutic Target for Malignant Rhabdoid Tumors.Molecules and cells · 2022Article
- Multi-omics reveals mitochondrial metabolism proteins susceptible for drug discovery in AML.Leukemia · 2022Article
- RUNX1 transactivates BCR-ABL1 expression in Philadelphia chromosome positive acute lymphoblastic leukemia.Cancer science · 2022Article
- RUNX1 Upregulates CENPE to Promote Leukemic Cell Proliferation.Frontiers in molecular biosciences · 2021Article
- Article
- CHD7 and Runx1 interaction provides a braking mechanism for hematopoietic differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- CROX (Cluster Regulation of RUNX) as a Potential Novel Therapeutic Approach.Molecules and cells · 2020Review
- RUNX1 Dosage in Development and Cancer.Molecules and cells · 2020Review
- Use of polymeric CXCR4 inhibitors as siRNA delivery vehicles for the treatment of acute myeloid leukemia.Cancer gene therapy · 2020Article
- Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription.Cancers · 2019Review
- HDAC1 Is a Required Cofactor of CBFβ-SMMHC and a Potential Therapeutic Target in Inversion 16 Acute Myeloid Leukemia.Molecular cancer research : MCR · 2019Article
- IL1RL1 is dynamically expressed on Cbfb-MYH11Scientific reports · 2019Article
- Genetic compensation of RUNX family transcription factors in leukemia.Cancer science · 2018Review
- Divergence in DNA Specificity among Paralogous Transcription Factors Contributes to Their Differential In Vivo Binding.Cell systems · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
CBFβ-SMMHC (core-binding factor β-smooth muscle myosin heavy chain), the fusion protein generated by the chromosome 16 inversion fusion gene, CBFB-MYH11, is known to initiate leukemogenesis. However, the mechanism through which CBFβ-SMMHC contributes to leukemia development is not well understood. Previously, it was proposed that CBFβ-SMMHC acts by dominantly repressing the transcription factor RUNX1 (Runt-related protein 1), but we recently showed that CBFβ-SMMHC has activities that are independent of RUNX1 repression. In addition, we showed that a modified CBFβ-SMMHC with decreased RUNX1-binding activity accelerates leukemogenesis. These results raise questions about the importance of RUNX1 in leukemogenesis by CBFβ-SMMHC. To test this, we generated mice expressing Cbfb-MYH11 in a Runx1-deficient background, resulting from either homozygous Runx1-null alleles (Runx1(-/-)) or a single dominant-negative Runx1 allele (Runx1(+/lz)). We found that loss of Runx1 activity rescued the differentiation defects induced by Cbfb-MYH11 during primitive hematopoiesis. During definitive hematopoiesis, RUNX1 loss also significantly reduced the proliferation and differentiation defects induced by Cbfb-MYH11. Importantly, Cbfb-MYH11-induced leukemia had much longer latency in Runx1(+/lz) mice than in Runx1-sufficient mice. These data indicate that Runx1 activity is critical for Cbfb-MYH11-induced hematopoietic defects and leukemogenesis.
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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.