Evidence map›Paper›PMID 35297370›Full record

ArticleBiomedical journal2021

Joint effects of genomic markers and urinary methylation capacity associated with inorganic arsenic metabolism on the occurrence of cancers among residents in arseniasis-endemic areas: A cohort subset with average fifteen-year follow-up.

Pei-Ju Liao, Kuang-Hung Hsu, Hung-Yi Chiou, Chien-Jen Chen, Chih-Hung Lee

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomedical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Metabolic Derangement by Arsenic: a Review of the Mechanisms.Biological trace element research · 2024
    Review
  4. Article
  5. 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

5 authors at 5 institutions in 1 country.

Pei-Ju LiaoDepartment of Health Care Administration, Oriental Institute of Technology, New Taipei City, Taiwan.
Kuang-Hung HsuHealthy Aging Research Center, Chang Gung University, Taoyuan, Taiwan; Laboratory for Epidemiology, Department of Health Care Management, Chang Gung University, Taoyuan, Taiwan; Department of Emergency Medicine, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan; Department of Urology, Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan; Research Center for Food and Cosmetic Safety, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan; Department of Safety, Health and Environmental Engineering, Ming Chi University of Technology, New Taipei City, Taiwan. Electronic address: khsu@mail.cgu.edu.tw.
Hung-Yi ChiouDepartment of Public Health, Taipei Medical University, Taipei, Taiwan.
Chien-Jen ChenGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Chih-Hung LeeDepartment of Dermatology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan. Electronic address: dermlee@gmail.com.
Asia Eastern University of Science and Technology · TWGenomics Research Center, Academia Sinica · TWKaohsiung Chang Gung Memorial Hospital · TWMing Chi University of Technology · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic exposure to inorganic arsenic results in many cancers in susceptible persons. The metabolism of inorganic arsenic and genomic susceptibility are thought to be associated with cancer occurrence.

methodsThis study aims to examine the interaction of genomic susceptibility markers and urinary methylation capacity indicators involved in inorganic arsenic metabolism with all-cancer occurrence. This study conducted a follow-up on 96 residents to determine their urinary inorganic arsenic metabolites and genomic assay from an arseniasis area. Among them, 24 cancer developed. Multivariable Cox proportional hazards model was used to determine and estimate the candidate independent variables for cancer development.

resultsThe residents with high inorganic arsenic exposure, high primary methylation index (PMI; MMA/InAs) (but lower secondary methylation index (SMI)), and non-heterogeneity type of genomic markers, including GSTO1, AS3MT, and MPO, tend to develop cancers. Subjects with higher PMI are at higher risk of developing cancers (HR = 1.66; 95% CI = 1.30-2.12). Cancer occurrence was greater among the CC type of GSTO1 (HR = 3.33; 95% CI = 1.11-10.00), CC type of AS3MT (HR = 19.21; 95% CI = 1.16-318.80), and AA type of MPO (HR = 13.40; 95% CI = 1.26-142.40). After adjusting confounders, a mutually moderating effect was revealed between genomic markers and methylation capacity on cancer occurrence.

conclusionsThis study found the hypermethylation responses to inorganic arsenic exposure and an array of genomic markers may increase the susceptibility of a wide range of organ cancers. The findings indicated a high-risk arsenic-exposed population to develop cancers. The phenotype of arsenic metabolism and genomic polymorphism suggested a potential preventive strategy for arsenic carcinogenesis.

Indexed as

ArsenicArsenicalsNeoplasmsFollow-Up StudiesGenomicsGlutathione TransferaseHumansMethylationMethyltransferasesArsenicArsenicalsAS3MT protein, humanGlutathione TransferaseGSTO1 protein, humanMethyltransferasesCancersGenomic markersInorganic arsenicInorganic arsenic metabolismUnderground water

Identifiers

PMID35297370
PMCPMC9068568
OpenAlexW3106009274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.