ArticleMolecular and cellular biology1992
Expression of the Evi-1 zinc finger gene in 32Dc13 myeloid cells blocks granulocytic differentiation in response to granulocyte colony-stimulating factor.
Article in Molecular and cellular biology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 116 citations in OpenAlex.
- BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML.Leukemia · 2026Article
- PRC2-mediated apoptosis evasion is a therapeutic target of MDS/AML harboring inv(3)/t(3;3) and monosomy 7.HemaSphere · 2025Article
- Evi1 governs Kdm6b-mediated histone demethylation to regulate the Laptm4b-driven mTOR pathway in hematopoietic progenitor cells.The Journal of clinical investigation · 2024Article
- Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression.Leukemia · 2024Article
- EVI1 dysregulation: impact on biology and therapy of myeloid malignancies.Blood cancer journal · 2021Review
- Article
- PRDM16s transforms megakaryocyte-erythroid progenitors into myeloid leukemia-initiating cells.Blood · 2019Article
- [Clinical features and prognostic analysis of 10 hematological malignancies with inv (3) /t (3;3)].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018Article
- EVI1 Interferes with Myeloid Maturation via Transcriptional Repression of Cebpa, via Binding to Two Far Downstream Regulatory Elements.The Journal of biological chemistry · 2016Article
- Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms.Nature communications · 2015Article
- EVI1 promotes tumor growth via transcriptional repression of MS4A3.Journal of hematology & oncology · 2015Article
- The closely related rare and severe acute myeloid leukemias carrying EVI1 or PRDM16 rearrangements share singular biological features.Haematologica · 2015Article
- A novel acquired inv(2)(p23.3q24.3) with concurrent submicroscopic deletions at 2p23.3, 2p22.1, 2q24.3 and 1p13.2 in a patient with chronic thrombocytopenia and anemia.Molecular cytogenetics · 2015Article
- Stem cell origin of myelodysplastic syndromes.Oncogene · 2014Review
- The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid.Cell cycle (Georgetown, Tex.) · 2014Article
- EVI1 splice variants modulate functional responses in ovarian cancer cells.Molecular oncology · 2013Article
- Critical role of miR-9 in myelopoiesis and EVI1-induced leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- Methylation and silencing of miRNA-124 by EVI1 and self-renewal exhaustion of hematopoietic stem cells in murine myelodysplastic syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Hematopoietic immortalizing function of the NKL-subclass homeobox gene TLX1.Genes, chromosomes & cancer · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Expression of the Evi-1 gene is frequently activated in murine myeloid leukemias by retroviral insertions immediately 5' or 90 kb 5' of the gene. The Evi-1 gene product is a nuclear, DNA-binding zinc finger protein of 145 kDa. On the basis of the properties of the myeloid cell lines in which the Evi-1 gene is activated, it has been hypothesized that its expression blocks normal differentiation. To explore this proposed role, we have constructed a retrovirus vector containing the gene and examined its effects on an interleukin-3-dependent myeloid cell line that differentiates in response to granulocyte colony-stimulating factor (G-CSF). Expression of the Evi-1 gene in these cells did not alter the normal growth factor requirements of the cells. However, expression of the Evi-1 gene blocked the ability of the cells to express myeloperoxidase and to terminally differentiate to granulocytes in response to G-CSF. This effect was not due to altered expression of the G-CSF receptor or to changes in the initial responses of the cells to G-CSF. These results support the hypothesis that the inappropriate expression of the Evi-1 gene in myeloid cells interferes with the ability of the cells to terminally differentiate.
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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.