ArticleJournal of leukocyte biology2009
Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes.
Article in Journal of leukocyte biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Orthogonal proteogenomic analysis identifies the druggable PA2G4-MYC axis in 3q26 AML.Nature communications · 2024Article
- EVI1 in Leukemia and Solid Tumors.Cancers · 2020Review
- Multimodal Lentiviral Vectors for Pharmacologically Controlled Switching Between Constitutive Single Gene Expression and Tetracycline-Regulated Multiple Gene Collaboration.Human gene therapy methods · 2017Article
- EVI1 Interferes with Myeloid Maturation via Transcriptional Repression of Cebpa, via Binding to Two Far Downstream Regulatory Elements.The Journal of biological chemistry · 2016Article
- PLZF Controls the Development of Fetal-Derived IL-17+Vγ6+ γδ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- EVI1 promotes tumor growth via transcriptional repression of MS4A3.Journal of hematology & oncology · 2015Article
- Article
- The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.Cell cycle (Georgetown, Tex.) · 2014Article
- Signal transduction inhibitors in treatment of myelodysplastic syndromes.Journal of hematology & oncology · 2013Review
- Selection for Evi1 activation in myelomonocytic leukemia induced by hyperactive signaling through wild-type NRas.Oncogene · 2013Article
- Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells.Leukemia · 2013Article
- EVI1 inhibits apoptosis induced by antileukemic drugs via upregulation of CDKN1A/p21/WAF in human myeloid cells.PloS one · 2013Article
- EVI1 and MDS1/EVI1 expression during primary human hematopoietic progenitor cell differentiation into various myeloid lineages.Anticancer research · 2012Article
- Overexpression of EVI1 interferes with cytokinesis and leads to accumulation of cells with supernumerary centrosomes in G0/1 phase.Cell cycle (Georgetown, Tex.) · 2012Article
- Article
- Acetylation of the proto-oncogene EVI1 abrogates Bcl-xL promoter binding and induces apoptosis.PloS one · 2011Article
- Tetracycline regulator expression alters the transcriptional program of mammalian cells.PloS one · 2010Article
- Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response.The FEBS journal · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The oncogene EVI1 has been implicated in the etiology of AML and MDS. Although AML cells are characterized by accelerated proliferation and differentiation arrest, MDS cells hyperproliferate when immature but fail to differentiate later and die instead. In agreement with its roles in AML and in immature MDS cells, EVI1 was found to stimulate cell proliferation and inhibit differentiation in several experimental systems. In contrast, the variant protein MDS1/EVI1 caused the opposite effect in some of these assays. In the present study, we expressed EVI1 and MDS1/EVI1 in a tetracycline-regulable manner in the human myeloid cell line U937. Induction of either of these proteins caused cells to accumulate in the G(0)/G(1)-phase of the cell cycle and moderately increased the rate of spontaneous apoptosis. However, when EVI1- or MDS1/EVI1-expressing cells were induced to differentiate, they massively succumbed to apoptosis, as reflected by the accumulation of phosphatidylserine in the outer leaflet of the plasma membrane and increased rates of DNA fragmentation. In summary, these data show that inducible expression of EVI1 in U937 cells causes phenotypes that may be relevant for its role in MDS and provides a basis for further investigation of its contribution to this fatal disease.
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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.