Evidence map›Paper›PMID 25707394›Full record

ArticleThe pharmacogenomics journal2015

Development of a genetic marker set to diagnose aspirin-exacerbated respiratory disease in a genome-wide association study.

H S Chang, S W Shin, T H Lee, D J Bae, J S Park, Y H Kim, S T Uh, B W Choi, M K Kim, I S Choi and 3 more

Abstract read
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In one paragraph

Article in The pharmacogenomics journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Olfaction and sinonasal symptoms in patients with CRSwNP and AERD and without AERD: a cross-sectional and longitudinal study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017
    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

13 authors.

H S ChangDepartment of Medical Bioscience, Graduate School, Soonchunhyang University, Asan, Republic of Korea.
S W ShinAsthma Genome Research Center, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea.
T H LeeDepartment of Medical Bioscience, Graduate School, Soonchunhyang University, Asan, Republic of Korea.
D J BaeDepartment of Medical Bioscience, Graduate School, Soonchunhyang University, Asan, Republic of Korea.
J S Park1] Asthma Genome Research Center, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea [2] Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea.
Y H KimDivision of Allergy and Respiratory Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Republic of Korea.
S T UhDivision of Allergy and Respiratory Medicine, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea.
B W ChoiDepartment of Internal Medicine, Chung-Ang University Yongsan Hospital, Seoul, Republic of Korea.
M K KimDivision of Internal Medicine, Chungbuk National University, Cheongju, Republic of Korea.
I S ChoiDepartment of Allergy, Chonnam National University, Gwangju, Republic of Korea.
B L ParkDepartment of Genetic Epidemiology, SNP Genetics Incorporation, Seoul, Republic of Korea.
H D Shin1] Department of Genetic Epidemiology, SNP Genetics Incorporation, Seoul, Republic of Korea [2] Department of Life Science, Sogang University, Seoul, Republic of Korea.
C S Park1] Asthma Genome Research Center, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea [2] Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We developed a genetic marker set of single nucleotide polymorphisms (SNPs) by summing risk scores of 14 SNPs showing a significant association with aspirin-exacerbated respiratory disease (AERD) from our previous 660 W genome-wide association data. The summed scores were higher in the AERD than in the aspirin-tolerant asthma (ATA) group (P=8.58 × 10(-37)), and were correlated with the percent decrease in forced expiratory volume in 1 s after aspirin challenge (r(2)=0.150, P=5.84 × 10(-30)). The area under the curve of the scores for AERD in the receiver operating characteristic curve was 0.821. The best cutoff value of the summed risk scores was 1.01328 (P=1.38 × 10(-32)). The sensitivity and specificity of the best scores were 64.7% and 85.0%, respectively, with 42.1% positive and 93.4% negative predictive values. The summed risk score may be used as a genetic marker with good discriminative power for distinguishing AERD from ATA.

Indexed as

Genome-Wide Association StudyAdultAgedAlgorithmsArea Under CurveAsthma, Aspirin-InducedFemaleForced Expiratory VolumeGenetic MarkersHumansMaleMiddle AgedPolymorphism, Single NucleotidePredictive Value of TestsRespiratory Function TestsRisk AssessmentGenetic Markers

Identifiers

PMID25707394

What OpenQuestion holds

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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.