Evidence map›Paper›PMID 24934723›Full record

ArticleJournal of cancer research and clinical oncology2014

Aberrant methylation of the MSH3 promoter and distal enhancer in esophageal cancer patients exposed to first-hand tobacco smoke.

Matjaz Vogelsang, Juliano D Paccez, Georgia Schäfer, Kevin Dzobo, Luiz F Zerbini, M Iqbal Parker

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Esophageal cancer genetics in South Africa.Clinical and experimental gastroenterology · 2019
    Review
  7. Article
  8. Article
  9. Expression and methylation of circulating microRNA-510 in essential hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2017
    Article
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  12. 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

6 authors at 1 institution in 1 country.

Matjaz VogelsangInternational Centre for Genetic Engineering and Biotechnology (ICGEB), Cape Town Component, UCT Medical Campus, Anzio Road, Observatory, Cape Town, 7925, South Africa.
Juliano D Paccez
Georgia Schäfer
Kevin Dzobo
Luiz F Zerbini
M Iqbal Parker
International Centre for Genetic Engineering and Biotechnology · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePolymorphisms in MSH3 gene confer risk of esophageal cancer when in combination with tobacco smoke exposure. The purpose of this study was to investigate the methylation status of MSH3 gene in esophageal cancer patients in order to further elucidate possible role of MSH3 in esophageal tumorigenesis.

methodsWe applied nested methylation-specific polymerase chain reaction to investigate the methylation status of the MSH3 promoter in tumors and matching adjacent normal-looking tissues of 84 esophageal cancer patients from a high-risk South African population. The Cancer Genome Atlas data were used to examine DNA methylation profiles at 17 CpG sites located in the MSH3 locus.

resultsOverall, promoter methylation was detected in 91.9 % of tumors, which was significantly higher compared to 76.0 % in adjacent normal-looking esophageal tissues (P = 0.008). When samples were grouped according to different demographics (including age, gender and ethnicity) and smoking status of patients, methylation frequencies were found to be significantly higher in tumor tissues of Black subjects (P = 0.024), patients of 55-65 years of age (P = 0.032), males (P = 0.037) and tobacco smokers (P = 0.015). Furthermore, methylation of the MSH3 promoter was significantly more frequent in tumor samples from smokers compared to tumor samples from non-smokers [odds ratio (OR) = 31.9, P = 0.031]. The TCGA data confirmed significantly higher DNA methylation level at the MSH3 promoter region in tumors (P = 0.0024). In addition, we found evidence of an aberrantly methylated putative MSH3-associated distal enhancer element.

conclusionOur results suggest that methylation of MSH3 together with exposure to tobacco smoke is involved in esophageal carcinogenesis. Due to the active role of the MSH3 protein in modulating chemosensitivity of cells, methylation of MSH3 should further be examined in association with the outcome of esophageal cancer treatment using anticancer drugs.

Indexed as

DNA MethylationAgedCarcinoma, Squamous CellDNA-Binding ProteinsEnhancer Elements, GeneticEsophageal NeoplasmsFemaleGenetic Association StudiesHumansMaleMiddle AgedMutS Homolog 3 ProteinPromoter Regions, GeneticSequence Analysis, DNASmokingDNA-Binding ProteinsMSH3 protein, humanMutS Homolog 3 Protein

Identifiers

PMID24934723
PMCPMC11824020
OpenAlexW1984750939

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Registered trials

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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.