Evidence map›Paper›PMID 40653802›Full record

ArticleEpigenomics2025

Bifaceted functions of histone methyltransferases.

Jawad Akhtar, Vassiliki Saloura

Abstract read
In one paragraph

Article in Epigenomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

2 authors.

Jawad AkhtarThoracic and GI Malignancies Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Vassiliki SalouraThoracic and GI Malignancies Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.

Funding

The Role of WHSC1L1 in Squamous Cell Carcinoma of the Head and NeckZIABC011831 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SALOURA, VASSILIKI · 2018 to 2025
$7.6M
Intramural NIH HHS ZIA BC011831
6 · The paper itself

Abstract

In this perspective, Akhtar et al provide a brief overview of Enhancer of Zeste Homolog 2 (EZH2) and SET and MYND-domain containing 3 (SMYD3) as histone methyltransferases that function both as activators and repressors of gene transcription in cancer. The importance of deciphering the mechanisms underlying this bifaceted function toward thoughtful pharmacologic interventions is underlined and protein or mRNA degradation are highlighted as the most biologically rational pharmaceutical platforms to target these bifaceted histone methyltransferases.

Indexed as

Histone-Lysine N-MethyltransferaseNeoplasmsPolycomb Repressive Complex 2Enhancer of Zeste Homolog 2 ProteinHistone MethyltransferasesHistonesHumansEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesPolycomb Repressive Complex 2Cancer epigeneticschromatin modificationsdual transcriptional functionepigenetic mechanismsgene expression

Identifiers

PMID40653802
PMCPMC12369619

What OpenQuestion holds

Textmetadata
LicenceTDM
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.