ArticleEnvironmental health : a global access science source2017
Association between genome-wide copy number variation and arsenic-induced skin lesions: a prospective study.
Article in Environmental health : a global access science source, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Systematic review on gene-sun exposure interactions in skin cancer.Molecular genetics & genomic medicine · 2023Pooled it
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- Molecular and cell phenotype programs in oral epithelial cells directed by co-exposure to arsenic and smokeless tobacco.bioRxiv : the preprint server for biology · 2024Article
- Article
- Unraveling the genetics of arsenic toxicity with cellular morphology QTL.PLoS genetics · 2024Article
- Cell morphology QTL reveal gene by environment interactions in a genetically diverse cell population.bioRxiv : the preprint server for biology · 2023Article
- Article
- Article
- KRAS-retroviral fusion transcripts and gene amplification in arsenic-transformed, human prostate CAsE-PE cancer cells.Toxicology and applied pharmacology · 2020Article
- Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation.Frontiers in public health · 2020Review
- Early-Life Arsenic Exposure, Nutritional Status, and Adult Diabetes Risk.Current diabetes reports · 2019Review
- Observational
- Molecular and cell phenotype programs in oral epithelial cells directed by co-exposure to arsenic and smokeless tobacco.BioFactors (Oxford, England)Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundExposure to arsenic in drinking water is a global health problem and arsenic-induced skin lesions are hallmark of chronic arsenic toxicity. We and others have reported germline genetic variations as risk factors for such skin lesions. The role of copy number variation (CNV) in the germline DNA in this regard is unknown.
methodsFrom a large prospectively followed-up cohort, exposed to arsenic, we randomly selected 2171 subjects without arsenic-induced skin lesions at enrollment and genotyped their whole blood DNA samples on Illumina Cyto12v2.1 SNP chips to generate DNA copy number. Participants were followed up every 2 years for a total of 8 years, especially for the development of skin lesions. In Cox regression models, each CNV segment was used as a predictor, accounting for other potential covariates, for incidence of skin lesions.
resultThe presence of genomic deletion(s) in a number of genes (OR5J2, GOLGA6L7P, APBA2, GALNTL5, VN1R31P, PHKG1P2, SGCZ, ZNF658) and lincRNA genes (RP11-76I14.1, CTC-535 M15.2, RP11-73B2.2) were associated with higher risk [HR between 1.67 (CI 1.3-2.1) and 2.15 (CI 1.5-2.9) for different CNVs] for development of skin lesions independent of gender, age, and arsenic exposure. Some deletions had stronger effect in a specific gender (ZNF658 in males, SGCZ in females) and some had stronger effect in higher arsenic exposure (lincRNA CTD-3179P9.1) suggesting a possible gene-environment interaction.
conclusionThis first genome-wide CNV study in a prospectively followed-up large cohort, exposed to arsenic, suggests that DNA deletion in several genes and lincRNA genes may predispose an individual to a higher risk of development of arsenic-induced skin lesions.
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