Evidence map›Paper›PMID 28179585›Full record

ReviewOncotarget2017

Oncogenomic disruptions in arsenic-induced carcinogenesis.

Adam P Sage, Brenda C Minatel, Kevin W Ng, Greg L Stewart, Trevor J B Dummer, Wan L Lam, Victor D Martinez

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2017. 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
4.1field-weighted citation impact, top 6% 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, 67 citations in OpenAlex.

  1. Persistent effects of early-life arsenic exposure inEnvironmental science. Processes & impacts · 2026
    Article
  2. E-Cigarette effects on oral health: A molecular perspective.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. The Role of Non-Coding RNAs in Chromosomal Instability in Cancer.The Journal of pharmacology and experimental therapeutics · 2023
    Review
  8. Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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  16. Review
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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

7 authors at 2 institutions in 1 country.

Adam P SageDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
Brenda C MinatelDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
Kevin W NgDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
Greg L StewartDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
Trevor J B DummerCentre of Excellence in Cancer Prevention, School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada.
Wan L LamDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
Victor D MartinezDepartment of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
Occupational Cancer Research Centre · CACanadian Centre for Applied Research in Cancer Control · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic exposure to arsenic affects more than 200 million people worldwide, and has been associated with many adverse health effects, including cancer in several organs. There is accumulating evidence that arsenic biotransformation, a step in the elimination of arsenic from the human body, can induce changes at a genetic and epigenetic level, leading to carcinogenesis. At the genetic level, arsenic interferes with key cellular processes such as DNA damage-repair and chromosomal structure, leading to genomic instability. At the epigenetic level, arsenic places a high demand on the cellular methyl pool, leading to global hypomethylation and hypermethylation of specific gene promoters. These arsenic-associated DNA alterations result in the deregulation of both oncogenic and tumour-suppressive genes. Furthermore, recent reports have implicated aberrant expression of non-coding RNAs and the consequential disruption of signaling pathways in the context of arsenic-induced carcinogenesis. This article provides an overview of the oncogenomic anomalies associated with arsenic exposure and conveys the importance of non-coding RNAs in the arsenic-induced carcinogenic process.

Indexed as

AnimalsArsenicCarcinogenesisChromosome AberrationsEpigenesis, GeneticGene Expression RegulationGenetic Predisposition to DiseaseGenetic VariationGenomic InstabilityHumansNeoplasmsRNA InterferenceRNA, UntranslatedArsenicRNA, Untranslatedarseniccancerepigeneticsgeneticsnon-coding RNA

Identifiers

PMID28179585
PMCPMC5421966
OpenAlexW2586823048

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.