ReviewBlood cancer journal2021
EVI1 dysregulation: impact on biology and therapy of myeloid malignancies.
Review in Blood cancer journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
42 citing papers in PubMed, 57 citations in OpenAlex.
- Tandem Double Inversion Resolves the Structural Paradox Underlying Recurrent KAT6A::NCOA2 Fusion in Acute Myeloid Leukemia.Genes, chromosomes & cancer · 2026Article
- Mesenchymal Stem Cell-Derived Extracellular Vesicles Attenuate Diabetic β-Cell Apoptosis and Dedifferentiation by Delivering miR-4436.Tissue engineering and regenerative medicine · 2026Article
- Dynamics and master transcription factors dependence of intestinal super-enhancers during differentiation and oncogenesis.Nucleic acids research · 2026Article
- MECOM Function Is Critical for AR-Driven Treatment-Resistant Prostate Cancer.Cancer research · 2026Article
- REDD1/DDIT4 counteracts endoplasmic reticulum stress-induced apoptosis by controlling the expression of death receptor TRAILR2/DR5 in cancer cells.Cell death & disease · 2026Article
- BET inhibitor-based combinations targeting novel dependencies in MECOM-rearranged (r) AML.Leukemia · 2026Article
- Highly effective combination of BRG1/BRM inhibitor with BET inhibitor or decitabine for high-risk MECOM-rearranged AML.HemaSphere · 2026Article
- Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome.Nature communications · 2025Article
- MECOM fusion partner and bone marrow blast percentage influence outcomes of patients with MECOM rearranged acute myeloid leukaemia.British journal of haematology · 2025Article
- Review
- BRD4 and MYB inhibition overcomes venetoclax resistance in EVI1-rearranged acute myeloid leukemia.Scientific reports · 2025Article
- Short Inverted Repeats as Mutational Hotspots and Putative Drivers of Genome Instability in Osteosarcoma.Genes · 2025Article
- HMX3 is a critical vulnerability in MECOM-negative KMT2A::MLLT3 acute myelomonocytic leukemia.Leukemia · 2025Article
- Case Report: Decitabine and venetoclax sequentially followed by FLAG-Ida and venetoclax with immediate allogeneic stem cell transplantation in newly diagnosed acute myeloid leukemia with chromosome 3 inversion/Frontiers in oncology · 2025Article
- Evi1 governs Kdm6b-mediated histone demethylation to regulate the Laptm4b-driven mTOR pathway in hematopoietic progenitor cells.The Journal of clinical investigation · 2024Article
- Clinical significance of dynamic monitoring of EVI1 gene expression in pediatric acute myeloid leukemia.BMC pediatrics · 2024Article
- MECOM Locus classical transcript isoforms affect tumor immune microenvironment and different targets in ovarian cancer.Journal of ovarian research · 2024Article
- The microprotein HDSP promotes gastric cancer progression through activating the MECOM-SPINK1-EGFR signaling axis.Nature communications · 2024Article
- Neuronal activity stimulates a genetic program to rapidly generate synapses during development.Nature neuroscience · 2024Article
- An activity-regulated transcriptional program directly drives synaptogenesis.Nature neuroscience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ecotropic viral integration site 1 (Evi1) was discovered in 1988 as a common site of ecotropic viral integration resulting in myeloid malignancies in mice. EVI1 is an oncogenic zinc-finger transcription factor whose overexpression contributes to disease progression and an aggressive phenotype, correlating with poor clinical outcome in myeloid malignancies. Despite progress in understanding the biology of EVI1 dysregulation, significant improvements in therapeutic outcome remain elusive. Here, we highlight advances in understanding EVI1 biology and discuss how this new knowledge informs development of novel therapeutic interventions. EVI1 is overexpression is correlated with poor outcome in some epithelial cancers. However, the focus of this review is the genetic lesions, biology, and current therapeutics of myeloid malignancies overexpressing EVI1.
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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.