Evidence map›Paper›PMID 20682481›Full record

ReviewEnvironmental health perspectives2011

An emerging role for epigenetic dysregulation in arsenic toxicity and carcinogenesis.

Xuefeng Ren, Cliona M McHale, Christine F Skibola, Allan H Smith, Martyn T Smith, Luoping Zhang

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 5 pooled it
13.5field-weighted citation impact, top 1% 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

157 citing papers in PubMed, 5 syntheses or guidelines pooled it, 357 citations in OpenAlex.

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  15. Single-Cell Multiome Impact of Prenatal Heavy Metal Exposure on Early Airway Development.American journal of respiratory cell and molecular biology · 2026
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97 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

6 authors at 2 institutions in 1 country.

Xuefeng RenDivision of Environmental Health Sciences, School of Public Health, University of California–Berkeley, Berkeley, California 94720, USA. xfr@berkeley.edu
Cliona M McHale
Christine F Skibola
Allan H Smith
Martyn T Smith
Luoping Zhang
Center for Environmental Health · USUniversity of California, Berkeley · US

Funding

Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MORELLO-FROSCH, RACHEL ADELE · 1987 to 2025
$74.6M
NIEHS NIH HHS P42 ES004705
6 · The paper itself

Abstract

backgroundExposure to arsenic, an established human carcinogen, through consumption of highly contaminated drinking water is a worldwide public health concern. Several mechanisms by which arsenical compounds induce tumorigenesis have been proposed, including oxidative stress, genotoxic damage, and chromosomal abnormalities. Recent studies have suggested that epigenetic mechanisms may also mediate toxicity and carcinogenicity resulting from arsenic exposure.

objectiveWe examined the evidence supporting the roles of the three major epigenetic mechanisms-DNA methylation, histone modification, and microRNA (miRNA) expression-in arsenic toxicity and, in particular, carcinogenicity. We also investigated future research directions necessary to clarify epigenetic and other mechanisms in humans. DATA SOURCES AND SYNTHESIS: We conducted a PubMed search of arsenic exposure and epigenetic modification through April 2010 and summarized the in vitro and in vivo research findings, from both our group and others, on arsenic-associated epigenetic alteration and its potential role in toxicity and carcinogenicity.

conclusionsArsenic exposure has been shown to alter methylation levels of both global DNA and gene promoters; histone acetylation, methylation, and phosphorylation; and miRNA expression, in studies analyzing mainly a limited number of epigenetic end points. Systematic epigenomic studies in human populations exposed to arsenic or in patients with arsenic-associated cancer have not yet been performed. Such studies would help to elucidate the relationship between arsenic exposure, epigenetic dysregulation, and carcinogenesis and are becoming feasible because of recent technological advancements.

Indexed as

ArsenicCarcinogenicity TestsCarcinogens, EnvironmentalDNA DamageDNA MethylationDose-Response Relationship, DrugEnvironmental ExposureEpigenesis, GeneticHistonesHumansMicroRNAsOxidative StressArsenicCarcinogens, EnvironmentalHistonesMicroRNAs

Identifiers

PMID20682481
PMCPMC3018488
OpenAlexW2064844197

What OpenQuestion holds

Textmetadata
LicenceCC0
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.