ReviewFrontiers of medicine2012
AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.
Review in Frontiers of medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 72 citations in OpenAlex.
- Trial
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- Case Report: CD19 CAR-T therapy induces dual remission in AML-M2b patient with CNS-PTLD and relapse.Frontiers in immunology · 2025Article
- Article
- [Establishment of leukemia cell model with inducible AML1-ETO expression and its effect on fatty acid metabolism in leukemia cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- Measurable residual disease study through three different methods can anticipate relapse and guide pre-emptive therapy in childhood acute myeloid leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Targeting UHRF1-SAP30-MXD4 axis for leukemia initiating cell eradication in myeloid leukemia.Cell research · 2022Article
- UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8.International journal of hematology · 2022Article
- Improved Gene Fusion Detection in Childhood Cancer Diagnostics Using RNA Sequencing.JCO precision oncology · 2022Article
- Conservation and divergence in gene regulation between mouse and human immune cells deserves equal emphasis.Trends in immunology · 2021Review
- Studying leukemia stem cell properties and vulnerabilities with human iPSCs.Stem cell research · 2021Article
- RUNX1 and RUNX2 transcription factors function in opposing roles to regulate breast cancer stem cells.Journal of cellular physiology · 2020Article
- Fusion transcripts: Unexploited vulnerabilities in cancer?Wiley interdisciplinary reviews. RNA · 2020Review
- Homoharringtonine deregulatesProceedings of the National Academy of Sciences of the United States of America · 2019Article
- The Impact of the Cellular Origin in Acute Myeloid Leukemia: Learning From Mouse Models.HemaSphere · 2019Review
- Different roles of E proteins in t(8;21) leukemia: E2-2 compromises the function of AETFC and negatively regulates leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Article
- Suppression of Breast Cancer Stem Cells and Tumor Growth by the RUNX1 Transcription Factor.Molecular cancer research : MCR · 2018Article
- ASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion.Haematologica · 2018Article
- Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AML1-ETO fusion transcription factor is generated by the t(8;21) translocation, which is present in approximately 4%-12% of adult and 12%-30% of pediatric acute myeloid leukemia (AML) patients. Both human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary events. In this review, we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in vivo. We also discuss potential therapeutic strategies for t(8;21) positive AML that involve targeting the fusion protein itself, the proteins that bind to it, or the genes that it regulates. Recently published studies suggest that a targeted therapy for t(8;21) positive AML is feasible and may be coming sometime soon.
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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.