ReviewCancer science2009
Pathogenetic significance of ecotropic viral integration site-1 in hematological malignancies.
Review in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed.
- MECOM promotes leukemia progression and inhibits mast cell differentiation through functional competition with GATA2.Leukemia · 2026Article
- The dynamic effect of genetic variation on the in vivo ER stress transcriptional response in different tissues.G3 (Bethesda, Md.) · 2022Article
- MECOM promotes supporting cell proliferation and differentiation in cochlea.Journal of otology · 2022Article
- Hematopoietic Stem Cell Factors: Their Functional Role in Self-Renewal and Clinical Aspects.Frontiers in cell and developmental biology · 2022Review
- HighFrontiers in oncology · 2021Article
- Myeloid leukemia with high EVI1 expression is sensitive to 5-aza-2'-deoxycytidine by targeting miR-9.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Identification of novelCold Spring Harbor molecular case studies · 2018Review
- Functional features of EVI1 and EVI1Δ324 isoforms of MECOM gene in genome-wide transcription regulation and oncogenicity.Oncogene · 2016Article
- The regulatory interaction of EVI1 with the TCL1A oncogene impacts cell survival and clinical outcome in CLL.Leukemia · 2015Article
- Chronic neutrophilic leukemia with overexpression of EVI-1, and concurrentOncology letters · 2015Article
- EVI1 oncogene promotes KRAS pathway through suppression of microRNA-96 in pancreatic carcinogenesis.Oncogene · 2014Article
- Molecular characterization of the rare translocation t(3;10)(q26;q21) in an acute myeloid leukemia patient.Molecular cytogenetics · 2014Article
- Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects.PloS one · 2014Article
- EVI1 oncoprotein interacts with a large and complex network of proteins and integrates signals through protein phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- TGF-β-induced apoptosis of B-cell lymphoma Ramos cells through reduction of MS4A1/CD20.Oncogene · 2013Article
- Microenvironment-Dependent Phenotypic Changes in a SCID Mouse Model for Malignant Mesothelioma.Frontiers in oncology · 2013Article
- Ecotropic viral integration site 1, stem cell self-renewal and leukemogenesis.Cancer science · 2012Review
- 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
- Evi1 is essential for hematopoietic stem cell self-renewal, and its expression marks hematopoietic cells with long-term multilineage repopulating activity.The Journal of experimental medicine · 2011Article
- HIF-VEGF pathways are critical for chronic otitis media in Junbo and Jeff mouse mutants.PLoS genetics · 2011Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ecotropic viral integration site-1 (Evi-1) gene was first identified as a common locus of retroviral integration in murine leukemia models. In humans, EVI-1 is located on chromosome 3q26, and rearrangements on chromosome 3q26 often activate EVI-1 expression in hematological malignancies. Overexpression of EVI-1 also occurs with high frequency in leukemia patients without 3q26 abnormalities, and importantly, high EVI-1 expression is an independent negative prognostic indicator irrespective of the presence of 3q26 rearrangements. Recent gene targeting studies in mice revealed that Evi-1 is preferentially expressed in hematopoietic stem cells and plays an essential role in proliferation and maintenance of hematopoietic stem cells. In addition, intense attention has been focused on the EVI-1 gene complex as retrovirus integration sites because transcription-activating integrations into the EVI-1 locus confer survival and self-renewing ability to hematopoietic cells. The experimental results using animal models suggest that activation of Evi-1 in hematopoietic cells leads to clonal expansion or dysplastic hematopoiesis, whereas onset of full-blown leukemia requires cooperative genetic events. EVI-1 possesses diverse functions as an oncoprotein, including suppression of transforming growth factor-beta-mediated growth inhibition, upregulation of GATA2, inhibition of the Jun kinase pathway, and stimulation of cell growth via activator protein-1. In this article, we summarize current knowledge regarding the biochemical properties and biological functions of EVI-1 in normal and malignant hematopoiesis, with specific focus on its pathogenetic significance in hematological malignancies.
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