ReviewCancer science2012
Ecotropic viral integration site 1, stem cell self-renewal and leukemogenesis.
Review in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 50 citations in OpenAlex.
- SPINK2 in hematopoiesis and cancer: Biology and clinical implications.Cell death discovery · 2026Review
- A novel MECOM gene variant causes severe thrombocytopenia in a neonate: a case report and review of the literature.Journal of medical case reports · 2025Review
- Rare Hematologic Malignancies and Pre-Leukemic Entities in Children and Adolescents Young Adults.Cancers · 2024Review
- Atypical CML: diagnosis and treatment.Hematology. American Society of Hematology. Education Program · 2023Article
- Predictive genomic biomarkers of therapeutic effects in renal cell carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Expanded phenotypic and hematologic abnormalities beyond bone marrow failure in MECOM-associated syndromes.American journal of medical genetics. Part A · 2023Article
- Perinatal-lethal nonimmune fetal hydrops attributed toCold Spring Harbor molecular case studies · 2023Article
- Phenotypic heterogeneity in individuals with MECOM variants in 2 families.Blood advances · 2022Article
- Chronic myeloid leukemia stem cells: targeting therapeutic implications.Stem cell research & therapy · 2021Review
- Molecular Pathogenesis ofFrontiers in oncology · 2021Review
- HighFrontiers in oncology · 2021Article
- A SARS-CoV-2 host infection model network based on genomic human Transcription Factors (TFs) depletion.Heliyon · 2020Article
- EVI1 in Leukemia and Solid Tumors.Cancers · 2020Review
- Role of miR-96/EVI1/miR-449a Axis in the Nasopharyngeal Carcinoma Cell Migration and Tumor Sphere Formation.International journal of molecular sciences · 2020Article
- Genetic classification and confirmation of inherited platelet disorders: current status in Korea.Clinical and experimental pediatrics · 2020Article
- Article
- EVI1 as a Marker for Lymph Node Metastasis in HNSCC.International journal of molecular sciences · 2020Article
- Hematopoietic transformation in the absence of MLL1/KMT2A: distinctions in target gene reactivation.Cell cycle (Georgetown, Tex.) · 2019Article
- A critical role of epigenetic inactivation of miR-9 in EVI1Molecular cancer · 2019Article
- Chronic myelogenous leukemia, a still unsolved problem: pitfalls and new therapeutic possibilities.Drug design, development and therapy · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has become evident that acute myeloid leukemia (AML) is organized as a cellular hierarchy initiated and maintained by a subset of self-renewing leukemia stem cells. Recent gene expression profile analysis of human leukemia stem cells and hematopoietic stem cell (HSC) populations identified a key transcriptional program shared by leukemia stem cells and HSC, which is associated with adverse outcomes in AML patients. One molecule that has been established as a pivotal regulator in fine-tuning of stem cell properties as well as a potent oncogenic determinant is ecotropic viral integration site 1 (EVI1). EVI1 is a transcription factor that has stem cell-specific expression pattern and is essential for the regulation of HSC self-renewal. This gene is notorious for its involvement in AML, as its activation confers extremely poor prognosis in patients with AML. Molecular analysis has identified a variety of gene products that are involved in HSC regulation as downstream targets or interacting proteins of EVI1. Thus, exploration of the molecular pathogenesis underlying EVI1-related leukemogenesis provides insight into how shared stemness transcriptional programs contribute to leukemia progression and therapeutic resistance in AML. Here, we review the current knowledge regarding the role of EVI1 in HSC self-renewal and leukemogenesis and highlight the relationship between stem cell self-renewal properties and adverse outcome in myeloid malignancies.
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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.