ArticleLeukemia2013
EVI-1 modulates leukemogenic potential and apoptosis sensitivity in human acute lymphoblastic leukemia.
Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- REDD1/DDIT4 counteracts endoplasmic reticulum stress-induced apoptosis by controlling the expression of death receptor TRAILR2/DR5 in cancer cells.Cell death & disease · 2026Article
- SPINK2 silencing suppresses leukemic proliferation and restores myeloid commitment via MECOM downregulation in acute myeloid leukaemia.Cell death discovery · 2026Article
- BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML.Leukemia · 2026Article
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- LowFrontiers in medicine · 2025Article
- EVI1-mediated Programming of Normal and Malignant Hematopoiesis.HemaSphere · 2023Review
- MECOM Deficiency: from Bone Marrow Failure to Impaired B-Cell Development.Journal of clinical immunology · 2023Review
- MECOM promotes supporting cell proliferation and differentiation in cochlea.Journal of otology · 2022Article
- MECOM permits pancreatic acinar cell dedifferentiation avoiding cell death under stress conditions.Cell death and differentiation · 2021Article
- Syngeneic leukemia models using lentiviral transgenics.Cell death & disease · 2021Article
- EVI1 phosphorylation at S436 regulates interactions with CtBP1 and DNMT3A and promotes self-renewal.Cell death & disease · 2020Article
- EVI1 in Leukemia and Solid Tumors.Cancers · 2020Review
- EVI1 as a Marker for Lymph Node Metastasis in HNSCC.International journal of molecular sciences · 2020Article
- EVI1 carboxy-terminal phosphorylation is ATM-mediated and sustains transcriptional modulation and self-renewal via enhanced CtBP1 association.Nucleic acids research · 2018Article
- Long-term observation reveals high-frequency engraftment of human acute myeloid leukemia in immunodeficient mice.Haematologica · 2017Article
- Article
- Evi1 regulates Notch activation to induce zebrafish hematopoietic stem cell emergence.The EMBO journal · 2016Article
- Pediatric chronic myeloid leukemia with inv(3)(q21q26.2) and T lymphoblastic transformation: a case report.Biomarker research · 2016Article
- The regulatory interaction of EVI1 with the TCL1A oncogene impacts cell survival and clinical outcome in CLL.Leukemia · 2015Article
- Expression of stage-specific embryonic antigen-4 (SSEA-4) defines spontaneous loss of epithelial phenotype in human solid tumor cells.Glycobiology · 2015Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional regulator ecotropic viral integration site-1 (EVI-1) has mainly been studied for its role in myeloid malignancies, in which high EVI-1 levels are associated with particularly aggressive disease. The role of EVI-1 in lymphoid cells, however, is largely unknown. Here we show that EVI-1 is indeed expressed in lymphoid malignancies such as acute lymphoblastic leukemia (ALL) and a subset of chronic lymphocytic leukemia. Expression data from pediatric ALL further suggest that high EVI-1 levels are associated with poor prognosis. Suppression of EVI-1 expression by RNA interference reduces cell growth and enhances apoptosis sensitivity in response to various stimuli in lymphoblastic leukemia cells. At the molecular level, EVI-1 modulates expression of several apoptosis-related genes (such as BCL2, BCL-x, XIAP, NOXA, PUMA, TRAIL-R1). Furthermore, EVI-1 knockdown strongly impairs in vivo engraftment of lymphoblastic leukemia cells upon transplantation in immune-permissive NOD/SCID/IL2Rγ(null) mice, conferring a survival benefit when compared with mice transplanted with control cells. Thus, our data show that EVI-1 is expressed not only in myeloid but also in lymphoid leukemias, and contributes to the leukemogenic potential and apoptosis resistance of ALL cells.
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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.