ArticleSpringerPlus2013
Human GMDS gene fragment hypermethylation in chronic high level of arsenic exposure with and without arsenic induced cancer.
Article in SpringerPlus, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Review
- Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation.Frontiers in public health · 2020Review
- Decreased Expression of Long Non-Coding RNA GMDS Divergent Transcript (GMDS-DT) is a Potential Biomarker for Poor Prognosis of Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Sex-specific associations of arsenic exposure with global DNA methylation and hydroxymethylation in leukocytes: results from two studies in Bangladesh.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2015Article
- Gene-specific differential DNA methylation and chronic arsenic exposure in an epigenome-wide association study of adults in Bangladesh.Environmental health perspectives · 2015Article
- Inactivation ofToxicology reports · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arsenic, though a poor mutagen, is an accepted environmental carcinogen. Perturbation of DNA methylation pattern leading to aberrant gene expression has been hypothesized as the mechanism for arsenic induced carcinogenesis. We had earlier demonstrated the hypermethylation of promoter region of p53 and p16 genes in persons exposed to different doses of arsenic. Till now no genomic hot spot has been identified which is frequently hypermethylated or hypomethylated in persons chronically exposed to environmental arsenic. In the present work, we have identified one hypermethylated sequence by methyl-sensitive arbitrarily primed polymerase chain reaction in the peripheral blood leukocyte DNA of chronically arsenic exposed persons with and without arsenic induced skin cancer. The sequence is from GMDS gene responsible for fucose metabolism. Southern hybridization of the sequence to the amplification products of methyl sensitive restriction enzyme digested genome of persons exposed to different doses of arsenic indicated that methylation increased in a dose dependent manner.
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What OpenQuestion holds
Registered trials
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.