ArticleProceedings of the National Academy of Sciences of the United States of America2004
Stem cell expression of the AML1/ETO fusion protein induces a myeloproliferative disorder in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 89 citations in OpenAlex.
- Mutational cooperativity of RUNX1::RUNX1T1 isoform 9a and oncogenic NRAS in zebrafish myeloid leukaemia.Biology open · 2024Article
- Review
- Article
- Childhood hematopoietic stem cells constitute the permissive window for RUNX1-ETO leukemogenesis.International journal of hematology · 2023Review
- Aberrant cell state plasticity mediated by developmental reprogramming precedes colorectal cancer initiation.Science advances · 2023Article
- Review
- An update on the molecular pathogenesis and potential therapeutic targeting of AML with t(8;21)(q22;q22.1);RUNX1-RUNX1T1.Blood advances · 2020Review
- Novel and Rare Fusion Transcripts Involving Transcription Factors and Tumor Suppressor Genes in Acute Myeloid Leukemia.Cancers · 2019Article
- The Impact of the Cellular Origin in Acute Myeloid Leukemia: Learning From Mouse Models.HemaSphere · 2019Review
- Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.Leukemia · 2017Article
- VENTX induces expansion of primitive erythroid cells and contributes to the development of acute myeloid leukemia in mice.Oncotarget · 2016Article
- AML1/ETO accelerates cell migration and impairs cell-to-cell adhesion and homing of hematopoietic stem/progenitor cells.Scientific reports · 2016Article
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- MiR144/451 Expression Is Repressed by RUNX1 During Megakaryopoiesis and Disturbed by RUNX1/ETO.PLoS genetics · 2016Article
- Mouse models for core binding factor leukemia.Leukemia · 2015Review
- STAT activation status differentiates leukemogenic from non-leukemogenic stem cells in AML and is suppressed by arsenic in t(6;9)-positive AML.Genes & cancer · 2014Article
- Overview of therapy and strategies for optimizing outcomes in de novo pediatric acute myeloid leukemia.Paediatric drugs · 2014Review
- Instruction of haematopoietic lineage choices, evolution of transcriptional landscapes and cancer stem cell hierarchies derived from an AML1-ETO mouse model.EMBO molecular medicine · 2013Article
- A role for RUNX1 in hematopoiesis and myeloid leukemia.International journal of hematology · 2013Review
- Novel function of the unique N-terminal region of RUNX1c in B cell growth regulation.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The t(8;21)(q22;q22) translocation, present in 10-15% of acute myeloid leukemia (AML) cases, generates the AML1/ETO fusion protein. To study the role of AML1/ETO in the pathogenesis of AML, we used the Ly6A locus that encodes the well characterized hematopoietic stem cell marker, Sca1, to target expression of AML1/ETO to the hematopoietic stem cell compartment in mice. Whereas germ-line expression of AML1/ETO from the AML1 promoter results in embryonic lethality, heterozygous Sca1(+/AML1-ETO ires EGFP) (abbreviated Sca(+/AE)) mutant mice are born in Mendelian ratios with no apparent abnormalities in growth or fertility. Hematopoietic cells from Sca(+/AE) mice have markedly extended survival in vitro and increasing myeloid clonogenic progenitor output over time. Sca(+/AE) mice develop a spontaneous myeloproliferative disorder with a latency of 6 months and a penetrance of 82% at 14 months. These results reinforce the notion that the phenotype of murine transgenic models of human leukemia is critically dependent on the cellular compartment targeted by the transgene. This model should provide a useful platform to analyze the effect of AML1/ETO on hematopoiesis and its potential cooperation with other mutations in the pathogenesis of leukemia.
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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.