Evidence map›Paper›PMID 25372592›Full record

ArticlePloS one2014

Exonic variants associated with development of aspirin exacerbated respiratory diseases.

Seung-Woo Shin, Byung Lae Park, HunSoo Chang, Jong Sook Park, Da-Jeong Bae, Hyun-Ji Song, Inseon S Choi, Mi-Kyeong Kim, Hea-Sim Park, Lyoung Hyo Kim and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Biomolecules · 2020
    Article
  6. Article
  7. Review
  8. Article
  9. Genetic and Epigenetic Components of Aspirin-Exacerbated Respiratory Disease.Immunology and allergy clinics of North America · 2016
    Review
  10. Review
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

14 authors at 6 institutions in 1 country.

Seung-Woo ShinGenome Research Center for Allergy and Respiratory Diseases, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea.
Byung Lae ParkDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea.
HunSoo ChangGenome Research Center for Allergy and Respiratory Diseases, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea; Department of Interdisciplinary Program in Biomedical Science Major Graduate School of Soonchunhyang University, Asan, Republic of Korea.
Jong Sook ParkGenome Research Center for Allergy and Respiratory Diseases, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea.
Da-Jeong BaeDepartment of Interdisciplinary Program in Biomedical Science Major Graduate School of Soonchunhyang University, Asan, Republic of Korea.
Hyun-Ji SongDepartment of Interdisciplinary Program in Biomedical Science Major Graduate School of Soonchunhyang University, Asan, Republic of Korea.
Inseon S ChoiDepartment of Allergy, Chonnam National University Medical School and Research Institute of Medical Sciences, Gwangju, Republic of Korea.
Mi-Kyeong KimDivision of Allergy, Department of Internal Medicine, Chungbuk National University, Cheongju, Republic of Korea.
Hea-Sim ParkDepartment of Allergy & Clinical Immunology, Ajou University Hospital, Suwoon, Republic of Korea.
Lyoung Hyo KimDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea; Department of Life Science, Sogang University, Seoul, Republic of Korea.
Suhg NamgoongDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea; Department of Life Science, Sogang University, Seoul, Republic of Korea.
Ji On KimDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea; Department of Life Science, Sogang University, Seoul, Republic of Korea.
Hyoung Doo ShinDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea; Department of Life Science, Sogang University, Seoul, Republic of Korea.
Choon-Sik ParkGenome Research Center for Allergy and Respiratory Diseases, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea.
Soonchunhyang University · KRSogang University · KRSNP Genetics (South Korea) · KRAjou University Hospital · KRChonnam National University · KRChungbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aspirin-exacerbated respiratory disease (AERD) is one phenotype of asthma, often occurring in the form of a severe and sudden attack. Due to the time-consuming nature and difficulty of oral aspirin challenge (OAC) for AERD diagnosis, non-invasive biomarkers have been sought. The aim of this study was to identify AERD-associated exonic SNPs and examine the diagnostic potential of a combination of these candidate SNPs to predict AERD. DNA from 165 AERD patients, 397 subjects with aspirin-tolerant asthma (ATA), and 398 normal controls were subjected to an Exome BeadChip assay containing 240K SNPs. 1,023 models (210-1) were generated from combinations of the top 10 SNPs, selected by the p-values in association with AERD. The area under the curve (AUC) of the receiver operating characteristic (ROC) curves was calculated for each model. SNP Function Portal and PolyPhen-2 were used to validate the functional significance of candidate SNPs. An exonic SNP, exm537513 in HLA-DPB1, showed the lowest p-value (p = 3.40×10-8) in its association with AERD risk. From the top 10 SNPs, a combination model of 7 SNPs (exm537513, exm83523, exm1884673, exm538564, exm2264237, exm396794, and exm791954) showed the best AUC of 0.75 (asymptotic p-value of 7.94×10-21), with 34% sensitivity and 93% specificity to discriminate AERD from ATA. Amino acid changes due to exm83523 in CHIA were predicted to be "probably damaging" to the structure and function of the protein, with a high score of '1'. A combination model of seven SNPs may provide a useful, non-invasive genetic marker combination for predicting AERD.

Indexed as

ExonsGenetic Predisposition to DiseaseGenetic VariationAdolescentAdultAgedAsthma, Aspirin-InducedDisease ProgressionFemaleGenetic Association StudiesGenome-Wide Association StudyGenotypeHumansMaleMiddle AgedPolymorphism, Single Nucleotide

Identifiers

PMID25372592
PMCPMC4221198
OpenAlexW1971266362

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.