ArticleCell reports2017
RUNX1-ETO and RUNX1-EVI1 Differentially Reprogram the Chromatin Landscape in t(8;21) and t(3;21) AML.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- EIF4A3-dependent nonsense-mediated decay buffers AML1-ETO9a dosage and modulates outcome in t(8;21) acute myeloid leukemia.Leukemia · 2026Article
- Article
- Rare acute myeloid leukemia harboring BCR/ABL1 (P210), AML1-MDS1/EVI1, and AML1/EAP: case report and literature review.Frontiers in oncology · 2026Article
- A system-level model reveals that transcriptional stochasticity is required for hematopoietic stem cell differentiation.NPJ systems biology and applications · 2024Article
- Targeting Menin in Acute Myeloid Leukemia: Therapeutic Advances and Future Directions.Cancers · 2024Review
- BloodChIP Xtra: an expanded database of comparative genome-wide transcription factor binding and gene-expression profiles in healthy human stem/progenitor subsets and leukemic cells.Nucleic acids research · 2024Article
- Chemical-genetics refines transcription factor regulatory circuits.Trends in cancer · 2024Review
- Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.Cell reports · 2023Article
- Article
- EVI1-mediated Programming of Normal and Malignant Hematopoiesis.HemaSphere · 2023Review
- A critical role of RUNX1 in governing megakaryocyte-primed hematopoietic stem cell differentiation.Blood advances · 2023Article
- Article
- The retinoic acid receptor co-factor NRIP1 is uniquely upregulated and represents a therapeutic target in acute myeloid leukemia with chromosome 3q rearrangements.Haematologica · 2022Article
- eRNAs Identify Immune Microenvironment Patterns and Provide a Novel Prognostic Tool in Acute Myeloid Leukemia.Frontiers in molecular biosciences · 2022Article
- Myeloid lncRNA LOUP mediates opposing regulatory effects of RUNX1 and RUNX1-ETO in t(8;21) AML.Blood · 2021Article
- Role of Enhancers in Development and Diseases.Epigenomes · 2021Review
- Review
- Identification of gene targets of mutant C/EBPα reveals a critical role for MSI2 in CEBPA-mutated AML.Leukemia · 2021Article
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is a heterogeneous disease caused by mutations in transcriptional regulator genes, but how different mutant regulators shape the chromatin landscape is unclear. Here, we compared the transcriptional networks of two types of AML with chromosomal translocations of the RUNX1 locus that fuse the RUNX1 DNA-binding domain to different regulators, the t(8;21) expressing RUNX1-ETO and the t(3;21) expressing RUNX1-EVI1. Despite containing the same DNA-binding domain, the two fusion proteins display distinct binding patterns, show differences in gene expression and chromatin landscape, and are dependent on different transcription factors. RUNX1-EVI1 directs a stem cell-like transcriptional network reliant on GATA2, whereas that of RUNX1-ETO-expressing cells is more mature and depends on RUNX1. However, both types of AML are dependent on the continuous expression of the fusion proteins. Our data provide a molecular explanation for the differences in clinical prognosis for these types of AML.
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Registered trials
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