Evidence map›Paper›PMID 26050622›Full record

ReviewOncogene2016

Context-dependent actions of Polycomb repressors in cancer.

M Koppens, M van Lohuizen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.7field-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

54 citing papers in PubMed, 93 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
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  6. Article
  7. Ezh2 promotes mammary tumor initiation through epigenetic regulation of the Wnt and mTORC1 signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Review
  9. Review
  10. Review
  11. Polycomb-mediated genome architecture enables long-range spreading of H3K27 methylation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

2 authors at 2 institutions in 1 country.

M KoppensDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
M van LohuizenDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Oncode Institute · NLThe Netherlands Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycomb Group (PcG) proteins form Polycomb Repressive Complexes (PRCs) that function as epigenetic repressors of gene expression. The large variety of PcG proteins, in addition to the high number of paralogs, allows for the formation of diverse PRCs with different properties, providing fine-tuned control over cell specification. Initially identified as being oncogenes, a small number of PcG genes are involved in tumor development in part through the repression of the CDKN2A locus. Therefore, enhanced PcG-mediated repression has long been assumed to be cancer promoting. However, recent data have revealed that for some cancers, PcG proteins act as tumor suppressors, indicating that this traditional view is oversimplified. In this review, we present an overview of the roles of PcG genes in oncogenesis and how the nature of their role is context dependent.

Indexed as

Cell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p16Epigenetic RepressionHumansNeoplasmsPolycomb Repressive Complex 1Polycomb Repressive Complex 2Transcription, GeneticTumor Suppressor ProteinsCyclin-Dependent Kinase Inhibitor p16Polycomb Repressive Complex 1Polycomb Repressive Complex 2Tumor Suppressor Proteins

Identifiers

PMID26050622
OpenAlexW1563429683

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.