ReviewOncogene2004
Molecular mechanisms of leukemogenesis by AML1/EVI-1.
Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 75 citations in OpenAlex.
- ConcurrentOncoTargets and therapy · 2026Article
- MECOM/PRDM3 and PRDM16 Serve as Prognostic-Related Biomarkers and Are Correlated With Immune Cell Infiltration in Lung Adenocarcinoma.Frontiers in oncology · 2022Article
- Acute lymphoblastic leukemia-derived exosome inhibits cytotoxicity of natural killer cells by TGF-β signaling pathway.3 Biotech · 2021Article
- [Clinical analysis of myeloid neoplasms with t (3;21) (q26;q22)].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.Oncogene · 2016Article
- RUNX1-Evi-1 fusion gene inhibited differentiation and apoptosis in myelopoiesis: an in vivo study.BMC cancer · 2015Article
- An unusual case of splenomegaly and increased lactate dehydrogenase heralding acute myeloid leukemia with eosinophilia and RUNX1-MECOM fusion transcripts.Leukemia research reports · 2014Article
- Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects.PloS one · 2014Article
- Molecular cytogenetics as a clinical test for prognostic and predictive biomarkers in newly diagnosed ovarian cancer.Journal of ovarian research · 2013Article
- Chimeras taking shape: potential functions of proteins encoded by chimeric RNA transcripts.Genome research · 2012Article
- Novel domain combinations in proteins encoded by chimeric transcripts.Bioinformatics (Oxford, England) · 2012Article
- Ecotopic viral integration site 1 (EVI1) regulates multiple cellular processes important for cancer and is a synergistic partner for FOS protein in invasive tumors.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Review
- Berbamine inhibits proliferation and induces apoptosis of KU812 cells by increasing Smad3 activity.Journal of Zhejiang University. Science. B · 2011Article
- Unraveling the genetics of otitis media: from mouse to human and back again.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Review
- In vivo identification of regulators of cell invasion across basement membranes.Science signaling · 2010Article
- The TEL-AML1 leukemia fusion gene dysregulates the TGF-beta pathway in early B lineage progenitor cells.The Journal of clinical investigation · 2009Article
- Runx transcription factors in neuronal development.Neural development · 2008Review
- Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AML1/EVI-1 chimeric gene is generated by the t(3;21)(q26;q22) translocation and plays a pivotal role in progression of hematopoietic stem cell malignancies such as chronic myelocytic leukemia and myelodysplastic syndrome. In AML1/EVI-1, an N-terminal half of AML1 including a runt homology domain is fused to the entire zinc-finger EVI-1 protein. AML1 is essential for hematopoietic cell development in fetal liver and its lineage-specific differentiation in adult. In contrast, EVI-1 is barely expressed in normal hematopoietic cells, but it is overexpressed in chronic myelocytic leukemia in blastic crisis and myelodysplastic syndrome-derived leukemia. There are at least four mechanisms identified in AML1/EVI-1 fusion protein that possibly lead into malignant transformation of hematopoietic stem cells. Firstly, AML1/EVI-1 exerts dominant-negative effects over AML1-induced transcriptional activation. Although target genes repressed by AML1/EVI-1 are still not known, binding competition to a specific DNA sequence and histone deacetylase recruitment through a co-repressor CtBP in EVI-1 part are conceivable underlying mechanisms for the dominant-negative effects. Secondly, AML1/EVI-1 interferes with TGF beta signaling and antagonizes the growth-inhibitory effects of TGF beta. The first zinc-finger domain of EVI-1 associates with Smad3, a TGF beta signal transducer, and represses its transcriptional activity by recruiting histone deacetylase through CtBP that interacts with EVI-1. Thirdly, AML1/EVI-1 blocks JNK activity and prevents stress-induced apoptosis. AML1/EVI-1 associates with JNK through the first zinc-finger domain of EVI-1 and disturbs the association between JNK and its substrates. Lastly, AML1/EVI-1 enhances AP-1 activity by activating the c-Fos promoter depending on the second zinc-finger domain of EVI-1, and promotes cell proliferation. All these functions cooperatively contribute to the malignant transformation of the hematopoietic stem cells by AML1/EVI-1.
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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.