Evidence map›Paper›PMID 35915507›Full record

ReviewClinical epigenetics2022

Therapeutic potential of inhibiting histone 3 lysine 27 demethylases: a review of the literature.

Jeries Abu-Hanna, Jigisha A Patel, Evangelos Anastasakis, Richard Cohen, Lucie H Clapp, Marilena Loizidou, Mohammad M R Eddama

Open access · goldAbstract readReview
In one paragraph

Review in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.9field-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

36 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  4. Review
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Deletion of the X-chromosomal geneScience translational medicine · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025
    Review
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

7 authors at 2 institutions in 1 country.

Jeries Abu-HannaDivision of Surgery and Interventional Science, Research Department of Surgical Biotechnology, University College London, GI Services, Ground Floor, 250 Euston Road, London, NW1 2PG, UK.
Jigisha A PatelDivision of Surgery and Interventional Science, Research Department of Surgical Biotechnology, University College London, GI Services, Ground Floor, 250 Euston Road, London, NW1 2PG, UK.
Evangelos AnastasakisUCL Medical School, University College London, London, UK.
Richard CohenDivision of Surgery and Interventional Science, Research Department of Surgical Biotechnology, University College London, GI Services, Ground Floor, 250 Euston Road, London, NW1 2PG, UK.
Lucie H ClappInstitute of Cardiovascular Science, University College London, London, UK.
Marilena LoizidouDivision of Surgery and Interventional Science, Research Department of Surgical Biotechnology, University College London, GI Services, Ground Floor, 250 Euston Road, London, NW1 2PG, UK.
Mohammad M R EddamaDivision of Surgery and Interventional Science, Research Department of Surgical Biotechnology, University College London, GI Services, Ground Floor, 250 Euston Road, London, NW1 2PG, UK. m.eddama.12@ucl.ac.uk.ORCID 0000-0002-4582-0788
University College London · GBUniversity College Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone 3 lysine 27 (H3K27) demethylation constitutes an important epigenetic mechanism of gene activation. It is mediated by the Jumonji C domain-containing lysine demethylases KDM6A and KDM6B, both of which have been implicated in a wide myriad of diseases, including blood and solid tumours, autoimmune and inflammatory disorders, and infectious diseases. Here, we review and summarise the pre-clinical evidence, both in vitro and in vivo, in support of the therapeutic potential of inhibiting H3K27-targeting demethylases, with a focus on the small-molecule inhibitor GSK-J4. In malignancies, KDM6A/B inhibition possesses the ability to inhibit proliferation, induce apoptosis, promote differentiation, and heighten sensitivity to currently employed chemotherapeutics. KDM6A/B inhibition also comprises a potent anti-inflammatory approach in inflammatory and autoimmune disorders associated with inappropriately exuberant inflammatory and autoimmune responses, restoring immunological homeostasis to inflamed tissues. With respect to infectious diseases, KDM6A/B inhibition can suppress the growth of infectious pathogens and attenuate the immunopathology precipitated by these pathogens. The pre-clinical in vitro and in vivo data, summarised in this review, suggest that inhibiting H3K27 demethylases holds immense therapeutic potential in many diseases.

Indexed as

HistonesNeoplasmsDNA MethylationEpigenesis, GeneticHistone DemethylasesHumansJumonji Domain-Containing Histone DemethylasesLysineHistone DemethylasesHistonesJumonji Domain-Containing Histone DemethylasesKDM6B protein, humanLysineAutoimmune diseasesCancerEpigeneticsGSK-J4H3K27Histone lysine demethylaseInfectious diseasesInflammationJMJD3KDM6AKDM6BUTX

Identifiers

PMID35915507
PMCPMC9344682
OpenAlexW4289262076

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.