ArticleProceedings of the National Academy of Sciences of the United States of America2004
Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 136 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
- CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice.The Journal of clinical investigation · 2025Article
- The co-receptor Neuropilin-1 enhances proliferation in inv(16) acute myeloid leukemia via VEGF signaling.Leukemia · 2025Article
- Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein.The Journal of clinical investigation · 2023Article
- PLAGL1 is associated with prognosis and cell proliferation in pancreatic adenocarcinoma.BMC gastroenterology · 2023Article
- Pathogenic Mechanisms in Acute Myeloid Leukemia.Current treatment options in oncology · 2022Review
- Gene Transcription as a Therapeutic Target in Leukemia.International journal of molecular sciences · 2021Review
- Genetic Variants ofFrontiers in oncology · 2021Article
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- Molecular characterization of a second myeloid neoplasm developing after treatment for acute myeloid leukemia.Leukemia · 2020Article
- Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription.Cancers · 2019Review
- Construction of miRNA-target networks using microRNA profiles of CVB3-infected HeLa cells.Scientific reports · 2019Article
- Increased miR-214 expression suppresses cell migration and proliferation in Hirschsprung disease by interacting with PLAGL2.Pediatric research · 2019Article
- Review
- Aberrant Clonal Hematopoiesis following Lentiviral Vector Transduction of HSPCs in a Rhesus Macaque.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- HDAC1 Is a Required Cofactor of CBFβ-SMMHC and a Potential Therapeutic Target in Inversion 16 Acute Myeloid Leukemia.Molecular cancer research : MCR · 2019Article
- Contrasting requirements during disease evolution identify EZH2 as a therapeutic target in AML.The Journal of experimental medicine · 2019Article
- Epigenetic Modifications in Acute Myeloid Leukemia: Prognosis, Treatment, and Heterogeneity.Frontiers in genetics · 2019Review
- C-terminal BRE overexpression in 11q23-rearranged and t(8;16) acute myeloid leukemia is caused by intragenic transcription initiation.Leukemia · 2018Article
- Preleukemia and Leukemia-Initiating Cell Activity in inv(16) Acute Myeloid Leukemia.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Acute myeloid leukemia subtype M4 with eosinophilia is associated with a chromosome 16 inversion that creates a fusion gene CBFB-MYH11. We have previously shown that CBFB-MYH11 is necessary but not sufficient for leukemogenesis. Here, we report the identification of genes that specifically cooperate with CBFB-MYH11 in leukemogenesis. Neonatal injection of Cbfb-MYH11 knock-in chimeric mice with retrovirus 4070A led to the development of acute myeloid leukemia in 2-5 months. Each leukemia sample contained one or a few viral insertions, suggesting that alteration of one gene could be sufficient to synergize with Cbfb-MYH11. The chromosomal position of 67 independent retroviral insertion sites (RISs) was determined, and 90% of the RISs mapped within 10 kb of a flanking gene. In total, 54 candidate genes were identified; six of them were common insertion sites (CISs). CIS genes included members of a zinc finger transcription factors family, Plag1 and Plagl2, with eight and two independent insertions, respectively. CIS genes also included Runx2, Myb, H2T24, and D6Mm5e. Comparison of the remaining 48 genes with single insertion sites with known leukemia-associated RISs indicated that 18 coincide with known RISs. To our knowledge, this retroviral genetic screen is the first to identify genes that cooperate with a fusion gene important for human myeloid leukemia.
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