Evidence map›Paper›PMID 38775978›Full record

ArticleArchives of dermatological research2024

Signatures of epigenetic, biological and mitotic age acceleration and telomere shortening are associated with arsenic-induced skin lesions.

Richie Jeremian, Yuliya Lytvyn, Rayyan Fotovati, Kaiyang Li, Muskaan Sachdeva, Nawar Tarafdar, Jorge R Georgakopoulos, Vincent Piguet, Ivan V Litvinov, Jensen Yeung

Abstract readLetter
PubMed Publisher
In one paragraph

Article in Archives of dermatological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

10 authors.

Richie JeremianFaculty of Medicine and Health Sciences, McGill University, 1001 Decarie Boulevard, Montréal, QC, H4A 3J1, Canada. richie.jeremian@mail.mcgill.ca.ORCID http://orcid.org/0000-0001-9258-6296
Yuliya LytvynDivision of Dermatology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.ORCID http://orcid.org/0000-0003-1805-9994
Rayyan FotovatiFaculty of Medicine and Health Sciences, McGill University, 1001 Decarie Boulevard, Montréal, QC, H4A 3J1, Canada.
Kaiyang LiFaculty of Medicine and Health Sciences, McGill University, 1001 Decarie Boulevard, Montréal, QC, H4A 3J1, Canada.ORCID http://orcid.org/0000-0001-8557-166X
Muskaan SachdevaDivision of Dermatology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.ORCID http://orcid.org/0000-0002-2252-5663
Nawar TarafdarSchulich School of Medicine and Dentistry, Western University, London, ON, Canada.
Jorge R GeorgakopoulosDivision of Dermatology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.
Vincent PiguetDivision of Dermatology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.ORCID http://orcid.org/0000-0001-6079-4517
Ivan V LitvinovResearch Institute of the McGill University Health Centre (RI-MUHC), Montréal, Canada.ORCID http://orcid.org/0000-0003-0562-4675
Jensen YeungDivision of Dermatology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.ORCID http://orcid.org/0000-0002-7318-5515

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic arsenic exposure is a global health hazard significantly associated with the development of deleterious cutaneous changes and increased keratinocyte cancer risk. Although arsenic exposure is associated with broad-scale cellular and molecular changes, gaps exist in understanding how these changes impact the skin and facilitate malignant transformation. Recently developed epigenetic "clocks" can accurately predict chronological, biological and mitotic age, as well as telomere length, on the basis of tissue DNA methylation state. Deviations of predicted from expected age (epigenetic age dysregulation) have been associated with numerous complex diseases, increased all-cause mortality and higher cancer risk. We investigated the ability of these algorithms to detect molecular changes associated with chronic arsenic exposure in the context of associated skin lesions. To accomplish this, we utilized a multi-algorithmic approach incorporating seven "clocks" (Horvath, Skin&Blood, PhenoAge, PCPhenoAge, GrimAge, DNAmTL and epiTOC2) to analyze peripheral blood of pediatric and adult cohorts of arsenic-exposed (n = 84) and arsenic-naïve (n = 33) individuals, among whom n = 18 were affected by skin lesions. Arsenic-exposed adults with skin lesions exhibited accelerated epigenetic (Skin&Blood: + 7.0 years [95% CI 3.7; 10.2], q = 6.8 × 10

Indexed as

ArsenicDNA MethylationEpigenesis, GeneticTelomere ShorteningAdolescentAdultChildFemaleHumansMaleMiddle AgedMitosisSkinSkin DiseasesSkin NeoplasmsYoung AdultArsenicArsenic exposureEpigenetic age accelerationSkin lesionsTelomere length

Identifiers

PMID38775978

What Socratic holds

Textmetadata
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 Socratic graph.