Evidence map›Paper›PMID 38030093›Full record

ArticleToxicology and applied pharmacology2024

Defining high confidence targets of differential CpG methylation in response to in utero arsenic exposure and implications for cancer risk.

Tabitha Lumour-Mensah, Bernardo Lemos

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  4. 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 at 2 institutions in 1 country.

Tabitha Lumour-MensahDepartment of Environmental Health, Harvard School of Public Health, Boston, MA, United States of America.
Bernardo LemosDepartment of Environmental Health, Harvard School of Public Health, Boston, MA, United States of America; R. Ken Coit College of Pharmacy, The University of Arizona, Tucson, AZ, United States of America. Electronic address: blemos@pharmacy.arizona.edu.
Harvard University · USUniversity of Arizona · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Training Program in Environmental EpidemiologyT32ES007069 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI LADEN, FRANCINE · 1985 to 2024
$13.9M
Novel markers of exposure and pathways of response to ChromiumR01ES027981 · NIEHS · UNIVERSITY OF ARIZONA · PI LEMOS, BERNARDO · 2018 to 2022
$2.0M
NIEHS NIH HHS P30 ES006694NIEHS NIH HHS R01 ES027981NIEHS NIH HHS T32 ES007069
6 · The paper itself

Abstract

Arsenic is a relatively abundant metalloid that impacts DNA methylation and has been implicated in various adverse health outcomes including several cancers and diabetes. However, uncertainty remains about the identity of genomic CpGs that are sensitive to arsenic exposure, in utero or otherwise. Here we identified a high confidence set of CpG sites whose methylation is sensitive to in utero arsenic exposure. To do so, we analyzed methylation of infant CpGs as a function of maternal urinary arsenic in cord blood and placenta from geographically and ancestrally distinct human populations. Independent analyses of these distinct populations were followed by combination of results across sexes and populations/tissue types. Following these analyses, we concluded that both sex and tissue type are important drivers of heterogeneity in methylation response at several CpGs. We also identified 17 high confidence CpGs that were hypermethylated across sex, tissue type and population; 11 of these were located within protein coding genes. This pattern is consistent with hypotheses that arsenic increases cancer risk by inducing the hypermethylation of genic regions. This study represents an opportunity to understand consistent, reproducible patterns of epigenomic responses after in utero arsenic exposure and may aid towards novel biomarkers or signatures of arsenic exposure. Identifying arsenic-responsive sites can also contribute to our understanding of the biological mechanisms by which arsenic exposure can affect biological function and increase risk of cancer and other age-related diseases.

Indexed as

ArsenicNeoplasmsCpG IslandsDNA MethylationFemaleFetal BloodHumansMaternal ExposurePlacentaPregnancyArsenicArsenicDNA MethylationFetal ExposureP-Value CombinationSex-Specific Trends

Identifiers

PMID38030093
PMCPMC10889851
OpenAlexW4389038603

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.