Evidence map›Paper›PMID 33391954›Full record

ReviewCureus2020

Advances in Epigenetic Cancer Therapeutics.

Christopher Hillyar, Kathrine S Rallis, Jajini Varghese

Open access · diamondAbstract readReview
In one paragraph

Review in Cureus, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Cold and hot tumors: from molecular mechanisms to targeted therapy.Signal transduction and targeted therapy · 2024
    Review
  7. Article
  8. Article
  9. The Epigenetics of Migraine.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Epigenetic alterations in canine mammary cancer.Genetics and molecular biology · 2022
    Article
  18. Article
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Christopher HillyarOncology, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, GBR.
Kathrine S RallisOncology, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, GBR.
Jajini VargheseBreast and Plastic Surgery, University College London Institute of Surgery and Interventional Science & Royal Free NHS Trust, London, GBR.
University College London · GBRoyal Free London NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer has traditionally been hailed a genetic disease, dictated by successive genetic aberrations which alter gene expression. Yet, recent advances in molecular sequencing technologies, enabling the characterisation of cancer patient phenotypes on a large scale, have highlighted epigenetic changes as a hallmark of cancer. Epigenetic modifications, including DNA methylation and demethylation and histone modifications, have been found to play a key role in the pathogenesis of a wide variety of cancers through the regulation of chromatin state, gene expression and other nuclear events. Targeting epigenetic aberrations offers remarkable promise as a potential anti-cancer therapy given the reversible nature of epigenetic changes. Hence, epigenetic therapy has emerged as a rapidly advancing field of cancer research. A plethora of epigenetic therapies which inhibit enzymes of post-translational histone modifications, so-called 'writers', 'erasers' and 'readers', have been developed, with several epigenetic inhibitor agents approved for use in routine clinical practice. Epigenetic therapeutics inhibit the methylation or demethylation and acetylation or deacetylation of DNA and histone proteins. Their targets include writers (DNA methyltransferases [DNMT], histone acetyltransferases [HAT] and histone deacetylases [HDAC]) and erasers (histone demethylases [HDM] and histone methylases [HMT]). With new epigenetic mechanisms increasingly being elucidated, a vast array of targets and therapeutics have been brought to the fore. This review discusses recent advances in cancer epigenetics with a focus on molecular targets and mechanisms of action of epigenetic cancer therapeutics.

Indexed as

cancerdna methylationepigeneticshistone acetyltransferasehistone deacetylasehistone demethylasehistone methyltransferasehistone modificationsinhibitors

Identifiers

PMID33391954
PMCPMC7772155
OpenAlexW3107092934

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.