Evidence map›Paper›PMID 32650416›Full record

ReviewCells2020

EZH2 in Myeloid Malignancies.

Jenny Rinke, Andrew Chase, Nicholas C P Cross, Andreas Hochhaus, Thomas Ernst

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. EZH2 Inhibition and Myeloid Risk: A Feature of On-Target Biology.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Review
  3. Review
  4. Review
  5. Epigenetic regulation of EZH2 by ncRNAs: mechanisms and oncogenic implications.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Humanized mouse models in MDS.Cell death & disease · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Novel targeted therapies in chronic myeloid leukemia.Pharmaceutical science advances · 2024
    Review
  17. Review
  18. Review
  19. The prognostic and therapeutic potential of HO-1 in leukemia and MDS.Cell communication and signaling : CCS · 2023
    Review
  20. Expression of Enhancer of Zeste Homolog 2 (EZH2) Gene in Acute Myeloid Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2023
    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

5 authors at 3 institutions in 2 countries.

Jenny RinkeKlinik für Innere Medizin II, Universitätsklinikum Jena, 07743 Jena, Germany.
Andrew ChaseSchool of Medicine, University of Southampton, Southampton SO17 1BJ, UK.
Nicholas C P CrossSchool of Medicine, University of Southampton, Southampton SO17 1BJ, UK.
Andreas HochhausKlinik für Innere Medizin II, Universitätsklinikum Jena, 07743 Jena, Germany.
Thomas ErnstKlinik für Innere Medizin II, Universitätsklinikum Jena, 07743 Jena, Germany.
Jena University Hospital · DEUniversity of Southampton · GBWessex Regional Genetics Laboratory · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our understanding of the significance of epigenetic dysregulation in the pathogenesis of myeloid malignancies has greatly advanced in the past decade. Enhancer of Zeste Homolog 2 (EZH2) is the catalytic core component of the Polycomb Repressive Complex 2 (PRC2), which is responsible for gene silencing through trimethylation of H3K27. EZH2 dysregulation is highly tumorigenic and has been observed in various cancers, with EZH2 acting as an oncogene or a tumor-suppressor depending on cellular context. While loss-of-function mutations of EZH2 frequently affect patients with myelodysplastic/myeloproliferative neoplasms, myelodysplastic syndrome and myelofibrosis, cases of chronic myeloid leukemia (CML) seem to be largely characterized by EZH2 overexpression. A variety of other factors frequently aberrant in myeloid leukemia can affect PRC2 function and disease pathogenesis, including Additional Sex Combs Like 1 (

Indexed as

AnimalsEnhancer of Zeste Homolog 2 ProteinHumansMutationMyeloproliferative DisordersPolycomb Repressive Complex 2Repressor ProteinsASXL1 protein, humanEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanPolycomb Repressive Complex 2Repressor ProteinsASXL1CMLEZH2MDSMPNmutationsmyeloid malignanciesPRC2

Identifiers

PMID32650416
PMCPMC7407223
OpenAlexW3041401016

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.