ArticleBlood2012
EVI1 is critical for the pathogenesis of a subset of MLL-AF9-rearranged AMLs.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed, 83 citations in OpenAlex.
- Genetic deletion of JAM-C in preleukemic cells rewires leukemic stem cell gene expression program in AML.Blood advances · 2024Trial
- High expression of myocyte enhancer factor 2C (MEF2C) is associated with adverse-risk features and poor outcome in pediatric acute myeloid leukemia: a report from the Children's Oncology Group.Journal of hematology & oncology · 2015Trial
- Comprehensive Molecular Characterization of High-Grade Endometrial Cancer in an Ancestrally Diverse Cohort.bioRxiv : the preprint server for biology · 2026Article
- All-trans retinoic acid combined with the VAH regimen for EVI1-positive acute myeloid leukemia: a case report with a brief literature review.Frontiers in oncology · 2026Article
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome.Nature communications · 2025Article
- Article
- Genomic landscape and clonal architecture in pediatric myeloid neoplasms with chromosome 7 deletions.Blood neoplasia · 2025Article
- HMX3 is a critical vulnerability in MECOM-negative KMT2A::MLLT3 acute myelomonocytic leukemia.Leukemia · 2025Article
- Article
- OncogeneScience advances · 2024Article
- MECOM Deficiency: from Bone Marrow Failure to Impaired B-Cell Development.Journal of clinical immunology · 2023Review
- Recruitment of MLL1 complex is essential for SETBP1 to induce myeloid transformation.iScience · 2022Article
- Article
- High Metabolic Dependence on Oxidative Phosphorylation Drives Sensitivity to Metformin Treatment inCancers · 2022Article
- Identification of therapeutic targets of the hijacked super-enhancer complex in EVI1-rearranged leukemia.Leukemia · 2021Article
- ZNF521 Enhances MLL-AF9-Dependent Hematopoietic Stem Cell Transformation in Acute Myeloid Leukemias by Altering the Gene Expression Landscape.International journal of molecular sciences · 2021Article
- Review
- EVI1 dysregulation: impact on biology and therapy of myeloid malignancies.Blood cancer journal · 2021Review
- Comprehensive diagnostics of acute myeloid leukemia by whole transcriptome RNA sequencing.Leukemia · 2021Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
Abstract
The proto-oncogene EVI1 (ecotropic viral integration site-1), located on chromosome band 3q26, is aberrantly expressed in human acute myeloid leukemia (AML) with 3q26 rearrangements. In the current study, we showed, in a large AML cohort carrying 11q23 translocations, that ∼ 43% of all mixed lineage leukemia (MLL)-rearranged leukemias are EVI1(pos). High EVI1 expression occurs in AMLs expressing the MLL-AF6, -AF9, -AF10, -ENL, or -ELL fusion genes. In addition, we present evidence that EVI1(pos) MLL-rearranged AMLs differ molecularly, morphologically, and immunophenotypically from EVI1(neg) MLL-rearranged leukemias. In mouse bone marrow cells transduced with MLL-AF9, we show that MLL-AF9 fusion protein maintains Evi1 expression on transformation of Evi1(pos) HSCs. MLL-AF9 does not activate Evi1 expression in MLL-AF9-transformed granulocyte macrophage progenitors (GMPs) that were initially Evi1(neg). Moreover, shRNA-mediated knockdown of Evi1 in an Evi1(pos) MLL-AF9 mouse model inhibits leukemia growth both in vitro and in vivo, suggesting that Evi1 provides a growth-promoting signal. Using the Evi1(pos) MLL-AF9 mouse leukemia model, we demonstrate increased sensitivity to chemotherapeutic agents on reduction of Evi1 expression. We conclude that EVI1 is a critical player in tumor growth in a subset of MLL-rearranged AMLs.
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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.