ArticleProceedings of the National Academy of Sciences of the United States of America2009
Transforming activity of AML1-ETO is independent of CBFbeta and ETO interaction but requires formation of homo-oligomeric complexes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Identification of non-charged 7.44 analogs interacting with the NHR2 domain of RUNX1-ETO with improved antiproliferative effect in RUNX-ETO positive cells.Scientific reports · 2025Article
- Oncogenic role of RARG rearrangements in acute myeloid leukemia resembling acute promyelocytic leukemia.Nature communications · 2025Article
- The selective prolyl hydroxylase inhibitor IOX5 stabilizes HIF-1α and compromises development and progression of acute myeloid leukemia.Nature cancer · 2024Article
- The RUNX1/RUNX1T1 network: translating insights into therapeutic options.Experimental hematology · 2021Review
- RUNX1-dependent mechanisms in biological control and dysregulation in cancer.Journal of cellular physiology · 2019Review
- 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
- Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.Leukemia · 2017Article
- Role of RUNX1 in hematological malignancies.Blood · 2017Review
- Emerging Roles of MTG16 in Cell-Fate Control of Hematopoietic Stem Cells and Cancer.Stem cells international · 2017Review
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- Critical role of retinoid/rexinoid signaling in mediating transformation and therapeutic response of NUP98-RARG leukemia.Leukemia · 2015Article
- A stable transcription factor complex nucleated by oligomeric AML1-ETO controls leukaemogenesis.Nature · 2013Article
- A role for RUNX1 in hematopoiesis and myeloid leukemia.International journal of hematology · 2013Review
- A novel application of furazolidone: anti-leukemic activity in acute myeloid leukemia.PloS one · 2013Article
- Interference with RUNX1/ETO leukemogenic function by cell-penetrating peptides targeting the NHR2 oligomerization domain.BioMed research international · 2013Article
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- The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.Science (New York, N.Y.) · 2011Article
- Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects.International journal of hematology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Although both heterodimeric subunits of core binding factors (AML1/RUNX1 and CBFbeta) essential for normal hematopoiesis are frequently mutated to form different chimeric fusion proteins in acute leukemia, the underlying molecular mechanisms and structural domains required for cellular transformation remain largely unknown. Despite the critical role of CBFbeta for wild-type AML1 function and its direct involvement in chromosomal translocation, we demonstrate that both the expression and interaction with CBFbeta are superfluous for AML1-ETO (AE)-mediated transformation of primary hematopoietic cells. Similarly, the hetero-oligomeric interaction with transcriptional repressor ETO family proteins and the highly conserved NHR1 domain in AE fusion are also dispensable for transforming activity. In contrast, AE-mediated transformation is critically dependent on the DNA binding and homo-oligomeric properties of the fusion. Abolishment of homo-oligomerization by a small-molecule inhibitor could specifically suppress AML1 fusion-mediated transformation of primary hematopoietic cells. Together, these results not only identify the essential molecular components but also potential avenues for therapeutic targeting of AE-mediated leukemogenesis.
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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.