Evidence map›Paper›PMID 27533460›Full record

ArticleOncotarget2016

The putative tumor suppressor gene EphA7 is a novel BMI-1 target.

Gaëlle Prost, Sebastian Braun, Falk Hertwig, Marcus Winkler, Lucas Jagemann, Sara Nolbrant, Isabelle V Leefa, Nils Offen, Kenichi Miharada, Stefan Lang and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 19% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Medulloblastoma genomics in the modern molecular era.Brain pathology (Zurich, Switzerland) · 2020
    Review
  3. Article
  4. 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

12 authors at 2 institutions in 2 countries.

Gaëlle ProstLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Sebastian BraunLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Falk HertwigLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Marcus WinklerLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Lucas JagemannLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Sara NolbrantLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Isabelle V LeefaLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Nils OffenLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Kenichi MiharadaLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Stefan LangLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Isabella ArtnerLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Ulrike A NuberLund Strategic Center for Stem Cell Biology, Lund University, 22184 Lund, Sweden.
Lund University · SETechnical University of Darmstadt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bmi1 was originally identified as a gene that contributes to the development of mouse lymphoma by inhibiting MYC-induced apoptosis through repression of Ink4a and Arf. It codes for the Polycomb group protein BMI-1 and acts primarily as a transcriptional repressor via chromatin modifications. Although it binds to a large number of genomic regions, the direct BMI-1 target genes described so far do not explain the full spectrum of BMI-1-mediated effects. Here we identify the putative tumor suppressor gene EphA7 as a novel direct BMI-1 target in neural cells and lymphocytes. EphA7 silencing has been reported in several different human tumor types including lymphomas, and our data suggest BMI1 overexpression as a novel mechanism leading to EphA7 inactivation via H3K27 trimethylation and DNA methylation.

Indexed as

Gene Expression RegulationGenes, Tumor SuppressorAnimalsB-LymphocytesCell Culture TechniquesCell NucleusCell ProliferationCells, CulturedCerebellumDNA MethylationDown-RegulationHistonesImmunohistochemistryKi-67 AntigenLateral VentriclesMiceBmi1 protein, mouseepha7 receptor, mouseHistonesKi-67 AntigenPolycomb Repressive Complex 1Proto-Oncogene ProteinsReceptor, EphA7Bmi1DNA methylationEphA7neural stem cells

Identifiers

PMID27533460
PMCPMC5295425
OpenAlexW2517782044

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.