Evidence map›Paper›PMID 26441991›Full record

ReviewFrontiers in immunology2015

Functional Role of G9a Histone Methyltransferase in Cancer.

Francesco Casciello, Karolina Windloch, Frank Gannon, Jason S Lee

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

137 citing papers in PubMed, 242 citations in OpenAlex.

  1. Article
  2. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  3. Article
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  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Adenosine Kinase: An Epigenetic Modulator and Drug Target.Journal of inherited metabolic disease · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

77 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Francesco CascielloControl of Gene Expression Laboratory, QIMR Berghofer Medical Research Institute , Herston, QLD , Australia ; School of Natural Sciences, Griffith University , Nathan, QLD , Australia.
Karolina WindlochControl of Gene Expression Laboratory, QIMR Berghofer Medical Research Institute , Herston, QLD , Australia.
Frank GannonControl of Gene Expression Laboratory, QIMR Berghofer Medical Research Institute , Herston, QLD , Australia.
Jason S LeeControl of Gene Expression Laboratory, QIMR Berghofer Medical Research Institute , Herston, QLD , Australia ; Faculty of Health, School of Biomedical Sciences, Queensland University of Technology , Kelvin Grove, QLD , Australia ; School of Chemistry and Molecular Biosciences, University of Queensland , Brisbane, QLD , Australia.
QIMR Berghofer Medical Research Institute · AUGriffith University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-translational modifications of DNA and histones are epigenetic mechanisms, which affect the chromatin structure, ultimately leading to gene expression changes. A number of different epigenetic enzymes are actively involved in the addition or the removal of various covalent modifications, which include acetylation, methylation, phosphorylation, ubiquitination, and sumoylation. Deregulation of these processes is a hallmark of cancer. For instance, G9a, a histone methyltransferase responsible for histone H3 lysine 9 (H3K9) mono- and dimethylation, has been observed to be upregulated in different types of cancer and its overexpression has been associated with poor prognosis. Key roles played by these enzymes in various diseases have led to the hypothesis that these molecules represent valuable targets for future therapies. Several small molecule inhibitors have been developed to specifically block the epigenetic activity of these enzymes, representing promising therapeutic tools in the treatment of human malignancies, such as cancer. In this review, the role of one of these epigenetic enzymes, G9a, is discussed, focusing on its functional role in regulating gene expression as well as its implications in cancer initiation and progression. We also discuss important findings from recent studies using epigenetic inhibitors in cell systems in vitro as well as experimental tumor growth and metastasis assays in vivo.

Indexed as

cancerepigenetic regulationG9ahistone methylationmetastasistumor growth

Identifiers

PMID26441991
PMCPMC4585248
OpenAlexW1920711459

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.