ArticleNature communications2018
EVI1 overexpression reprograms hematopoiesis via upregulation of Spi1 transcription.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 57 citations in OpenAlex.
- Glycosylation orchestrates megakaryocytic fate of hematopoietic stem cells via Wnt-MUC13 signaling.Nature communications · 2026Article
- Mesenchymal Stem Cell-Derived Extracellular Vesicles Attenuate Diabetic β-Cell Apoptosis and Dedifferentiation by Delivering miR-4436.Tissue engineering and regenerative medicine · 2026Article
- Genome-wide screening identifies ZFP91 as a key regulator of EVI1 in myeloid leukemia.Oncogene · 2026Article
- TGF-β in hematologic malignancies: molecular functions and clinical applications.Frontiers in immunology · 2026Review
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Article
- Review
- Deconvoluting clonal and cellular architecture in IDH-mutant acute myeloid leukemia.Cell stem cell · 2025Article
- Article
- LowFrontiers in medicine · 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
- Uncovering uncharacterized binding of transcription factors from ATAC-seq footprinting data.Scientific reports · 2024Article
- Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression.Leukemia · 2024Article
- Chromatin priming elements direct tissue-specific gene activity before hematopoietic specification.Life science alliance · 2024Article
- Identification of Potential Crucial Biomarkers in STEMI Through Integrated Bioinformatic Analysis.Arquivos brasileiros de cardiologia · 2024Article
- EVI1-mediated Programming of Normal and Malignant Hematopoiesis.HemaSphere · 2023Review
- Characteristics and clinical outcomes of patients with acute myeloid leukemia with inv(3)(q21q26.2) or t(3;3)(q21;q26.2).Haematologica · 2023Article
- Lateral thinking in syndromic congenital cardiovascular disease.Disease models & mechanisms · 2023Article
- 3q26.2/Cancers · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Inv(3q26) and t(3:3)(q21;q26) are specific to poor-prognosis myeloid malignancies, and result in marked overexpression of EVI1, a zinc-finger transcription factor and myeloid-specific oncoprotein. Despite extensive study, the mechanism by which EVI1 contributes to myeloid malignancy remains unclear. Here we describe a new mouse model that mimics the transcriptional effects of 3q26 rearrangement. We show that EVI1 overexpression causes global distortion of hematopoiesis, with suppression of erythropoiesis and lymphopoiesis, and marked premalignant expansion of myelopoiesis that eventually results in leukemic transformation. We show that myeloid skewing is dependent on DNA binding by EVI1, which upregulates Spi1, encoding master myeloid regulator PU.1. We show that EVI1 binds to the -14 kb upstream regulatory element (-14kbURE) at Spi1; knockdown of Spi1 dampens the myeloid skewing. Furthermore, deletion of the -14kbURE at Spi1 abrogates the effects of EVI1 on hematopoietic stem cells. These findings support a novel mechanism of leukemogenesis through EVI1 overexpression.
Indexed as
Identifiers
What OpenQuestion holds
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.