Evidence map›Paper›PMID 25746376›Full record

ArticleAtherosclerosis2015

Interaction effects between Paraoxonase 1 variants and cigarette smoking on risk of coronary heart disease in a Singaporean Chinese population.

Yi Han, Rajkumar Dorajoo, Tingjing Ke, Burger Ayala, Xuling Chang, Chiea-Chuen Khor, Rob M van Dam, Jian-Min Yuan, Woon-Puay Koh, Jianjun Liu and 3 more

Abstract read
In one paragraph

Article in Atherosclerosis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 5 pooled it
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 5 syntheses or guidelines pooled it, 23 citations in OpenAlex.

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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

13 authors at 5 institutions in 3 countries.

Yi HanDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Khoo Teck Puat - National University Children's Medical Institute, National University Health System, Singapore.
Rajkumar DorajooGenome Institute of Singapore, Agency for Science, Technology and Research, Singapore, Singapore.
Tingjing KeDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Khoo Teck Puat - National University Children's Medical Institute, National University Health System, Singapore.
Burger AyalaDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Khoo Teck Puat - National University Children's Medical Institute, National University Health System, Singapore; School of Public Health and Community Medicine, Hebrew University of Jerusalem, Israel.
Xuling ChangDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Khoo Teck Puat - National University Children's Medical Institute, National University Health System, Singapore.
Chiea-Chuen KhorGenome Institute of Singapore, Agency for Science, Technology and Research, Singapore, Singapore.
Rob M van DamSaw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore.
Jian-Min YuanDepartment of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.
Woon-Puay KohSaw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore; Duke-NUS Graduate Medical School Singapore, Singapore.
Jianjun LiuGenome Institute of Singapore, Agency for Science, Technology and Research, Singapore, Singapore; Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore.
Daniel Y T GohDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Khoo Teck Puat - National University Children's Medical Institute, National University Health System, Singapore.
Yechiel FriedlanderSchool of Public Health and Community Medicine, Hebrew University of Jerusalem, Israel. Electronic address: yechielf@ekmd.huji.ac.il.
Chew-Kiat HengDepartment of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Khoo Teck Puat - National University Children's Medical Institute, National University Health System, Singapore. Electronic address: paehck@nus.edu.sg.
National University Health System · SGAgency for Science, Technology and Research · SGHebrew University of Jerusalem · ILNational University of Singapore · SGUPMC Hillman Cancer Center · US

Funding

Cancer epidemiology cohorts in Shanghai and Singapore UM1CA182876 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YUAN, JIAN-MIN · 2014 to 2018
$4.3M
NCI NIH HHS UM1 CA182876
6 · The paper itself

Abstract

objectiveParaoxonase 1 (PON1) plays an important role in reducing the risk of coronary heart disease (CHD). Smoking is known to reduce PON1 activity. We aimed to investigate the effects of interactions between PON1 variants and smoking on CHD in the Singaporean Chinese population.

methodsIn a case-control study nested within Singapore Chinese Health Study (N=1914), subjects with and without CHD were classified into never-smokers and ever-smokers (ever smoked at least one cigarette a day for 1 year or longer). Associations at four independent SNPs at the PON1 locus (rs3735590, rs3917550, rs662, rs3917481) with CHD were evaluated using logistic regression, before/after stratification on smoking status. Interactions between smoking and PON1 variants were analyzed with likelihood ratio tests, by including the SNP*smoking interaction term in regression analyses.

resultsThe T allele at the coding SNP, rs662, was associated with higher risk of CHD in ever-smokers only (OR=1.35, 95% CI 1.08-1.68; adjusted P=0.036). At the miR-SNP, rs3735590, carrying at least one copy of minor allele T was associated with increased risk of CHD in a dominant manner in never-smokers only (OR=1.53, 95% CI 1.11-2.11; adjusted P=0.036). Significant interactions between two PON1 SNPs and smoking in relation to CHD risk were identified (adjusted P=0.012 for rs662; adjusted P=0.044 for rs3735590). These associations remained significant after adjustment for known CHD risk factors and upon correction for multiple tests.

conclusionsTwo PON1 SNPs, rs662 and rs3735590, were found to significantly interact with cigarette smoking to modulate the risk of CHD in the Singaporean Chinese population.

Indexed as

Gene-Environment InteractionPolymorphism, Single NucleotideAgedAryldialkylphosphataseAsian PeopleCase-Control StudiesChinaChi-Square DistributionCoronary DiseaseFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHumansLogistic ModelsMaleAryldialkylphosphatasePON1 protein, humanCigarette smokingCoronary heart diseaseInteractionmiR-SNPParaoxonase 1Singaporean ChineseSingle nucleotide polymorphism (SNP)

Identifiers

PMID25746376
PMCPMC4501379
OpenAlexW2013977207

What OpenQuestion holds

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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.