Evidence map›Paper›PMID 38602535›Full record

ReviewCellular and molecular life sciences : CMLS2024

Epigenomic insights into common human disease pathology.

Christopher G Bell

Open access · goldAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.8field-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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  10. Review
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  13. Review
  14. DNA methylation as a contributor to dysregulation ofbioRxiv : the preprint server for biology · 2025
    Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
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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

1 author at 1 institution in 1 country.

Christopher G BellWilliam Harvey Research Institute, Barts & The London Faculty of Medicine, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK. c.bell@qmul.ac.uk.ORCID http://orcid.org/0000-0003-4601-1242
Queen Mary University of London · GB

Funding

Barts Charity G-002372BrightFocus Foundation 60349147Impetus Grant from the Norn Group & Hevolution Foundation Round 2
6 · The paper itself

Abstract

The epigenome-the chemical modifications and chromatin-related packaging of the genome-enables the same genetic template to be activated or repressed in different cellular settings. This multi-layered mechanism facilitates cell-type specific function by setting the local sequence and 3D interactive activity level. Gene transcription is further modulated through the interplay with transcription factors and co-regulators. The human body requires this epigenomic apparatus to be precisely installed throughout development and then adequately maintained during the lifespan. The causal role of the epigenome in human pathology, beyond imprinting disorders and specific tumour suppressor genes, was further brought into the spotlight by large-scale sequencing projects identifying that mutations in epigenomic machinery genes could be critical drivers in both cancer and developmental disorders. Abrogation of this cellular mechanism is providing new molecular insights into pathogenesis. However, deciphering the full breadth and implications of these epigenomic changes remains challenging. Knowledge is accruing regarding disease mechanisms and clinical biomarkers, through pathogenically relevant and surrogate tissue analyses, respectively. Advances include consortia generated cell-type specific reference epigenomes, high-throughput DNA methylome association studies, as well as insights into ageing-related diseases from biological 'clocks' constructed by machine learning algorithms. Also, 3rd-generation sequencing is beginning to disentangle the complexity of genetic and DNA modification haplotypes. Cell-free DNA methylation as a cancer biomarker has clear clinical utility and further potential to assess organ damage across many disorders. Finally, molecular understanding of disease aetiology brings with it the opportunity for exact therapeutic alteration of the epigenome through CRISPR-activation or inhibition.

Indexed as

Cell-Free Nucleic AcidsEpigenomicsAlgorithmsBiological ClocksBiomarkers, TumorHumansBiomarkers, TumorCell-Free Nucleic AcidsAgeingAgeing-related diseaseChromatinCommon diseaseDNA methylationEWAS

Identifiers

PMID38602535
PMCPMC11008083
OpenAlexW4394726425

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.