ArticleProceedings of the National Academy of Sciences of the United States of America1996
Synergistic up-regulation of the myeloid-specific promoter for the macrophage colony-stimulating factor receptor by AML1 and the t(8;21) fusion protein may contribute to leukemogenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 132 citations in OpenAlex.
- Functional analysis of germline RUNX1 variants identified in individuals with suspected familial platelet disorder.Blood advances · 2026Article
- CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice.The Journal of clinical investigation · 2025Article
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- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- Runx1 is required for hematopoietic defects and leukemogenesis in Cbfb-MYH11 knock-in mice.Leukemia · 2015Article
- Differential requirements for HIV-1 Vif-mediated APOBEC3G degradation and RUNX1-mediated transcription by core binding factor beta.Journal of virology · 2013Article
- The C-terminus of CBFβ-SMMHC is required to induce embryonic hematopoietic defects and leukemogenesis.Blood · 2013Article
- Identification of benzodiazepine Ro5-3335 as an inhibitor of CBF leukemia through quantitative high throughput screen against RUNX1-CBFβ interaction.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Acute myeloid leukemia with the t(8;21) translocation: clinical consequences and biological implications.Journal of biomedicine & biotechnology · 2011Article
- The human SWI/SNF complex associates with RUNX1 to control transcription of hematopoietic target genes.Journal of cellular physiology · 2010Article
- Accelerated leukemogenesis by truncated CBF beta-SMMHC defective in high-affinity binding with RUNX1.Cancer cell · 2010Article
- A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia.Blood · 2010Article
- Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis.Leukemia · 2009Article
- The leukemogenic t(8;21) fusion protein AML1-ETO controls rRNA genes and associates with nucleolar-organizing regions at mitotic chromosomes.Journal of cell science · 2008Article
- AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets.PLoS genetics · 2008Article
- Review
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- Physical and functional interaction of Runt-related protein 1 with hypoxia-inducible factor-1alpha.Oncogene · 2008Article
- Transcriptional dysregulation mediated by RUNX1-RUNX1T1 in normal human progenitor cells and in acute myeloid leukaemia.Leukemia · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
AML1 is involved in the (8;21) translocation, associated with acute myelogenous leukemia (AML)-type M2, which results in the production of the AML1-ETO fusion protein: the amino-terminal 177 amino acids of AML1 and the carboxyl-terminal 575 amino acids of ETO. The mechanism by which AML1-ETO accomplishes leukemic transformation is unknown; however, AML1-ETO interferes with AML1 transactivation of such AML1 targets as the T-cell receptor beta enhancer and the granulocyte-macrophage colony-stimulating factor promoter. Herein, we explored the effect of AML1-ETO on regulation of a myeloid-specific AML1 target, the macrophage colony-stimulating factor (M-CSF) receptor promoter. We found that AML1-ETO and AML1 work synergistically to transactivate the M-CSF receptor promoter, thus exhibiting a different activity than previously described. Truncation mutants within the ETO portion of AML1-ETO revealed the region of ETO necessary for the cooperativity between AML1 and AML1-ETO lies between amino acids 347 and 540. Endogenous M-CSF receptor expression was examined in Kasumi-1 cells, derived from a patient with AML-M2 t(8;21) and the promonocytic cell line U937. Kasumi-1 cells exhibited a significantly higher level of M-CSF receptor expression than U937 cells. Bone marrow from patients with AML-M2 t(8;21) also exhibited a higher level of expression of M-CSF receptor compared with normal controls. The upregulation of M-CSF receptor expression by AML1-ETO may contribute to the development of a leukemic state in these patients.
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