ReviewOncogene2021
AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.
Review in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 52 citations in OpenAlex.
- RUNX1 upregulation and RUNX1-ETO depletion inhibits survival of t(8;21)-positive leukemia cells.Global medical genetics · 2026Article
- Novel noscapine derivative induces AML differentiation by dual-engaging DHODH and mitochondrial lipids to trigger a metabolic-epigenetic-transcriptional cascade.Acta pharmaceutica Sinica. B · 2026Article
- FOXO1 in cancer: context-dependent roles, microRNA regulation, and therapeutic opportunities.Discover oncology · 2026Review
- Oncogenic activation of EVC/EVC2 defines a therapeutically targetable subset of acute myeloid leukemia.Leukemia · 2026Article
- Lactate-binding protein DNMT3A in HRMECs promotes angiogenesis by upregulating VEGFA through HIF-1α lactylation.Genome biology · 2025Article
- t(8;21)AML patients with RUNX1e6::RUNX1T19a splice variant have poor prognosis.Annals of hematology · 2025Article
- WTAP-mediated mOncogene · 2025Article
- 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
- Homoharringtonine: mechanisms, clinical applications and research progress.Frontiers in oncology · 2025Review
- Article
- Fusion Genes in Myeloid Malignancies.Cancers · 2024Review
- Article
- PROteolysis-Targeting Chimeras (PROTACs) in leukemia: overview and future perspectives.MedComm · 2024Review
- A novel AML1-ETO/FTO positive feedback loop promotes leukemogenesis and Ara-C resistance via stabilizing IGFBP2 in t(8;21) acute myeloid leukemia.Experimental hematology & oncology · 2024Article
- From Genotype to Phenotype: How Enhancers Control Gene Expression and Cell Identity in Hematopoiesis.HemaSphere · 2023Review
- Article
- Review
- Preleukemic Fusion Genes Induced via Ionizing Radiation.International journal of molecular sciences · 2023Review
- Circular RNAs and Untranslated Regions in Acute Myeloid Leukemia.International journal of molecular sciences · 2023Review
- LYL1 facilitates AETFC assembly and gene activation by recruiting CARM1 in t(8;21) AML.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chromosomal translocation t(8;21) and the resulting oncofusion gene AML1/ETO have long served as a prototypical genetic lesion to model and understand leukemogenesis. In this review, we describe the wide-ranging role of AML1/ETO in AML leukemogenesis, with a particular focus on the aberrant epigenetic regulation of gene transcription driven by this AML-defining mutation. We begin by analyzing how structural changes secondary to distinct genomic breakpoints and splice changes, as well as posttranscriptional modifications, influence AML1/ETO protein function. Next, we characterize how AML1/ETO recruits chromatin-modifying enzymes to target genes and how the oncofusion protein alters chromatin marks, transcription factor binding, and gene expression. We explore the specific impact of these global changes in the epigenetic network facilitated by the AML1/ETO oncofusion on cellular processes and leukemic growth. Furthermore, we define the genetic landscape of AML1/ETO-positive AML, presenting the current literature concerning the incidence of cooperating mutations in genes such as KIT, FLT3, and NRAS. Finally, we outline how alterations in transcriptional regulation patterns create potential vulnerabilities that may be exploited by epigenetically active agents and other therapeutics.
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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.