ArticleBlood2013
Attenuation of AML1-ETO cellular dysregulation correlates with increased leukemogenic potential.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Decoding the Implications of Zinc in the Development and Therapy of Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Review
- Roles of Histone Deacetylases in Acute Myeloid Leukemia With Fusion Proteins.Frontiers in oncology · 2021Review
- RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019Review
- A tool compound targeting the core binding factor Runt domain to disrupt binding to CBFβ in leukemic cells.Leukemia & lymphoma · 2018Article
- Allogeneic hematopoietic stem cell transplantation for relapsed acute myeloid leukemia in ETO positive with reduced-intensity conditioning.Oncotarget · 2018Article
- A novel epigeneticEMBO molecular medicine · 2017Article
- Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia.Oncotarget · 2016Review
- TLE4 regulation of wnt-mediated inflammation underlies its role as a tumor suppressor in myeloid leukemia.Leukemia research · 2016Article
- Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- JMJD1C is required for the survival of acute myeloid leukemia by functioning as a coactivator for key transcription factors.Genes & development · 2015Article
- RUNX1-ETO induces a type I interferon response which negatively effects t(8;21)-induced increased self-renewal and leukemia development.Leukemia & lymphoma · 2014Article
- Leukaemia: Holding back.Nature reviews. Cancer · 2013Article
- Cooperation between RUNX1-ETO9a and novel transcriptional partner KLF6 in upregulation of Alox5 in acute myeloid leukemia.PLoS genetics · 2013Article
- The role of SON in splicing, development, and disease.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
AML1-ETO (RUNX1-ETO) fusion proteins are generated by the 8;21 translocation, commonly found in acute myeloid leukemia, which fuses the AML1 (RUNX1) and ETO (MTG8, RUNX1T1) genes. Previous studies have shown that AML1-ETO interferes with AML1 function but requires additional cooperating mutations to induce leukemia development. In mouse models, AML1-ETO forms lacking the C-terminus have been shown to have greatly enhanced leukemogenic potential. Here, we investigate the role of 2 AML1-ETO C-terminal-interacting proteins, N-CoR, a transcriptional corepressor, and SON, a splicing/transcription factor required for cell cycle progression, in AML1-ETO-induced leukemia development. AML1-ETO-W692A loses N-CoR binding at NHR4, displays attenuated transcriptional repression ability and decreased cellular dysregulation, and promotes leukemia in vivo. These results support the importance of the degree of dysregulation by AML1-ETO in cellular transformation and demonstrate that AML1-ETO-W692A can be used as an effective experimental model for determining which factors compromise the leukemogenic potential of AML1-ETO.
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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.