Evidence map›Paper›PMID 23212151›Full record

ArticleLeukemia2013

Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells.

O S Kustikova, A Schwarzer, M Stahlhut, M H Brugman, T Neumann, M Yang, Z Li, A Schambach, N Heinz, S Gerdes and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
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  6. Review
  7. Gene therapy for the leukodystrophies: From preclinical animal studies to clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  8. Article
  9. Review
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  11. Article
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  13. Predicting genotoxicity of viral vectors for stem cell gene therapy using gene expression-based machine learning.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
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  15. Article
  16. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

O S KustikovaInstitute of Experimental Hematology, Hannover Medical School, Carl-Neuberg-Strasse 1, Hannover, Germany.
A Schwarzer
M Stahlhut
M H Brugman
T Neumann
M Yang
Z Li
A Schambach
N Heinz
S Gerdes
I Roeder
T C Ha
D Steinemann
B Schlegelberger
C Baum
Medizinische Hochschule Hannover · DEUniversity Hospital Carl Gustav Carus · DELeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor Evi1 has an outstanding role in the formation and transformation of hematopoietic cells. Its activation by chromosomal rearrangement induces a myelodysplastic syndrome with progression to acute myeloid leukemia of poor prognosis. Similarly, retroviral insertion-mediated upregulation confers a competitive advantage to transplanted hematopoietic cells, triggering clonal dominance or even leukemia. To study the molecular and functional response of primary murine hematopoietic progenitor cells to the activation of Evi1, we established an inducible lentiviral expression system. EVI1 had a biphasic effect with initial growth inhibition and retarded myeloid differentiation linked to enhanced survival of myeloblasts in long-term cultures. Gene expression microarray analysis revealed that within 24 h EVI1 upregulated 'stemness' genes characteristic for long-term hematopoietic stem cells (Aldh1a1, Abca1, Cdkn1b, Cdkn1c, Epcam, among others) but downregulated genes involved in DNA replication (Cyclins and their kinases, among others) and DNA repair (including Brca1, Brca2, Rad51). Cell cycle analysis demonstrated EVI1's anti-proliferative effect to be strictly dose-dependent with accumulation of cells in G0/G1, but preservation of a small fraction of long-term proliferating cells. Although confined to cultured cells, our study contributes to new hypotheses addressing the mechanisms and molecular targets involved in preleukemic clonal dominance or leukemic transformation by Evi1.

Indexed as

Cell CycleAnimalsCell DifferentiationCell LineCell SurvivalDNA-Binding ProteinsGranulocyte Precursor CellsHematopoietic Stem CellsHumansMDS1 and EVI1 Complex Locus ProteinMiceMice, Inbred C57BLProto-OncogenesTranscription FactorsDNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanTranscription Factors

Identifiers

PMID23212151
OpenAlexW2074426771

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.