Evidence map›Paper›PMID 22308434›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Ecotopic viral integration site 1 (EVI1) regulates multiple cellular processes important for cancer and is a synergistic partner for FOS protein in invasive tumors.

Emilie A Bard-Chapeau, Justin Jeyakani, Chung H Kok, Julius Muller, Belinda Q Chua, Jayantha Gunaratne, Arsen Batagov, Piroon Jenjaroenpun, Vladimir A Kuznetsov, Chia-Lin Wei and 4 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Gynecologic oncology reports · 2025
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  8. eLife · 2025
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  13. Review
  14. Article
  15. Perinatal-lethal nonimmune fetal hydrops attributed toCold Spring Harbor molecular case studies · 2023
    Article
  16. Article
  17. Article
  18. Review
  19. International journal of molecular sciences · 2022
    Article
  20. Article
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

14 authors at 6 institutions in 3 countries.

Emilie A Bard-ChapeauInstitute of Molecular and Cell Biology, Singapore 138673.
Justin Jeyakani
Chung H Kok
Julius Muller
Belinda Q Chua
Jayantha Gunaratne
Arsen Batagov
Piroon Jenjaroenpun
Vladimir A Kuznetsov
Chia-Lin Wei
Richard J D'Andrea
Guillaume Bourque
Nancy A Jenkins
Neal G Copeland
Institute of Molecular and Cell Biology · SGBioinformatics Institute · SGGenome Institute of Singapore · SGHouston Methodist · USSouth Australia Pathology · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ecotropic viral integration site 1 (EVI1) is an oncogenic dual domain zinc finger transcription factor that plays an essential role in the regulation of hematopoietic stem cell renewal, and its overexpression in myeloid leukemia and epithelial cancers is associated with poor patient survival. Despite the discovery of EVI1 in 1988 and its emerging role as a dominant oncogene in various types of cancer, few EVI1 target genes are known. This lack of knowledge has precluded a clear understanding of exactly how EVI1 contributes to cancer. Using a combination of ChIP-Seq and microarray studies in human ovarian carcinoma cells, we show that the two zinc finger domains of EVI1 bind to DNA independently and regulate different sets of target genes. Strikingly, an enriched fraction of EVI1 target genes are cancer genes or genes associated with cancer. We also show that more than 25% of EVI1-occupied genes contain linked EVI1 and activator protein (AP)1 DNA binding sites, and this finding provides evidence for a synergistic cooperative interaction between EVI1 and the AP1 family member FOS in the regulation of cell adhesion, proliferation, and colony formation. An increased number of dual EVI1/AP1 target genes are also differentially regulated in late-stage ovarian carcinomas, further confirming the importance of the functional cooperation between EVI1 and FOS. Collectively, our data indicate that EVI1 is a multipurpose transcription factor that synergizes with FOS in invasive tumors.

Indexed as

Binding SitesCell AdhesionChromatin ImmunoprecipitationDNADNA-Binding ProteinsEpithelial CellsGene Expression RegulationHeLa CellsHumansMDS1 and EVI1 Complex Locus ProteinNeoplasm InvasivenessNeoplasmsProtein BindingProto-Oncogene Proteins c-fosProto-OncogenesTranscription FactorsDNADNA-Binding ProteinsMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanProto-Oncogene Proteins c-fosTranscription Factors

Identifiers

PMID22308434
PMCPMC3277513
OpenAlexW2009085603

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.