Evidence map›Paper›PMID 31483011›Full record

ArticleSao Paulo medical journal = Revista paulista de medicina2019

Methylation status of the PPP1R13L promoter region among lung cancer patients and healthy controls. Analytical cross-sectional study.

Jiaoyang Yin, Yegang Ma, Ulla Vogel, Chunhong Wang, Ying Zhang, Huiwen Wang

Open access · diamondAbstract read
In one paragraph

Article in Sao Paulo medical journal = Revista paulista de medicina, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

6 authors at 3 institutions in 2 countries.

Jiaoyang YinPhD. Professor, Key Laboratory of Environment and Population Health of Liaoning Education Ministry, Shenyang Medical College, Shenyang, China.ORCID http://orcid.org/0000-0002-2510-3693
Yegang MaMD. Professor/Chief Physician of Thoracic Surgery, Department of Thoracic Surgery, Liaoning Cancer Hospital, Shenyang, China.ORCID http://orcid.org/0000-0002-6973-6177
Ulla VogelPhD. Professor, National Research Centre for the Working Environment, Copenhagen DK-2100, Denmark.ORCID http://orcid.org/0000-0001-6807-1524
Chunhong WangMSc. Associate Professor, Key Laboratory of Environment and Population Health of Liaoning Education Ministry, Shenyang Medical College, Shenyang, China.ORCID http://orcid.org/0000-0002-5083-3962
Ying ZhangPhD. Associate Professor, Key Laboratory of Environment and Population Health of Liaoning Education Ministry, Shenyang Medical College, Shenyang, China.ORCID http://orcid.org/0000-0002-0193-939X
Huiwen WangMSc. Professor, Key Laboratory of Environment and Population Health of Liaoning Education Ministry, Shenyang Medical College, Shenyang, China.ORCID http://orcid.org/0000-0002-8699-7555
Shenyang Medical College · CNLiaoning Cancer Hospital & Institute · CNNational Research Centre for the Working Environment · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is evidence that genetic predisposition and epigenetic alteration (e.g. DNA methylation) play major roles in lung cancer. In our genetic epidemiological studies, rs1970764 in oncogene PPP1R13L was most consistently associated with lung cancer risk. Here, we explored the role of PPP1R13L methylation in lung cancer development. DESIGN AND

settingAnalytical cross-sectional study (45 lung cancer cases and 45 controls), conducted in China.

methodsWe investigated the DNA methylation status of 2,160 cytosine-phosphate-guanine (CpG) sites in the PPP1R13L promoter region using the EpiTYPER assay of the Sequenom MassARRAY platform.

resultsIn the whole study group, the methylation levels of CpG-6, CpG-9, CpG-20 and CpG-21 were significantly lower and those of CpG-16 were significantly higher in cases than in controls. Among smokers, the methylation levels at five CpG sites (CpG-6, CpG-11, CpG-15, CpG-20 and CpG-21) were statistically significantly lower among cases. Among men, the methylation levels at four CpG sites (CpG-11, CpG-15, CpG-20 and CpG-21) were significantly lower among cases. Regarding smokers, the methylation levels at CpG-7.8 and CpG-21 among cases and at CpG-22 among controls were significantly lower, compared with nonsmokers. The frequency of positivity for methylation was not significantly different between lung cancer cases and controls (68.22% for cases and 71.87% for controls; P = 0.119).

conclusionOur study on a Chinese population suggests that lung cancer patients have aberrant methylation status (hypomethylation tended to be more frequent) in peripheral blood leukocytes at several CpG sites in the PPP1R13L promoter region and that exposure to smoking may influence methylation status.

Indexed as

AgedCase-Control StudiesCross-Sectional StudiesDNA MethylationFemaleGenetic Predisposition to DiseaseHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMaleMiddle AgedPromoter Regions, GeneticRepressor ProteinsIntracellular Signaling Peptides and ProteinsPPP1R13L protein, humanRepressor Proteins

Identifiers

PMID31483011
PMCPMC9744005
OpenAlexW2970610521

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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.