ArticlePloS one2010
Genome-wide and follow-up studies identify CEP68 gene variants associated with risk of aspirin-intolerant asthma.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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.
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.
Who cites it
32 citing papers in PubMed, 76 citations in OpenAlex.
- Centrosome linker protein CEP68 modulates cellular stress responses via nuclear condensate formation and HSP27 interaction.iScience · 2026Article
- Clues of HLAs, metabolic SNPs, and epigenetic factors in T cell-mediated drug hypersensitivity reactions.Heliyon · 2024Review
- Article
- Genome-Wide Association Study of Korean Asthmatics: A Comparison With UK Asthmatics.Allergy, asthma & immunology research · 2021Article
- Pharmacogenetics in Primary Headache Disorders.Frontiers in pharmacology · 2021Review
- Pharmacogenomics of Hypersensitivity to Non-steroidal Anti-inflammatory Drugs.Frontiers in genetics · 2021Review
- Review on Databases and Bioinformatic Approaches on Pharmacogenomics of Adverse Drug Reactions.Pharmacogenomics and personalized medicine · 2021Review
- Polymorphisms in CEP68 gene associated with risk of immediate selective reactions to non-steroidal anti-inflammatory drugs.The pharmacogenomics journal · 2019Article
- Lessons Learned From GWAS of Asthma.Allergy, asthma & immunology research · 2019Review
- Clinical Implications of Single Nucleotide Polymorphisms in Diagnosis of Asthma and its Subtypes.Yonsei medical journal · 2019Review
- Association analysis of ILVBL gene polymorphisms with aspirin-exacerbated respiratory disease in asthma.BMC pulmonary medicine · 2017Article
- Pharmacogenomics of off-target adverse drug reactions.British journal of clinical pharmacology · 2017Review
- Genetic and Epigenetic Components of Aspirin-Exacerbated Respiratory Disease.Immunology and allergy clinics of North America · 2016Review
- Aspirin-exacerbated respiratory disease: pathophysiological insights and clinical advances.Journal of asthma and allergy · 2016Review
- Development of a genetic marker set to diagnose aspirin-exacerbated respiratory disease in a genome-wide association study.The pharmacogenomics journal · 2015Article
- Does aspirin-induced oxidative stress cause asthma exacerbation?Archives of medical science : AMS · 2015Article
- Phenotypes, Risk Factors, and Mechanisms of Adult-Onset Asthma.Mediators of inflammation · 2015Review
- Polymorphisms of ATF6B Are Potentially Associated With FEV1 Decline by Aspirin Provocation in Asthmatics.Allergy, asthma & immunology research · 2014Article
- Article
- Exonic variants associated with development of aspirin exacerbated respiratory diseases.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aspirin-intolerant asthma (AIA) is a rare condition that is characterized by the development of bronchoconstriction in asthmatic patients after ingestion of non-steroidal anti-inflammatory drugs including aspirin. However, the underlying mechanisms of AIA occurrence are still not fully understood. To identify the genetic variations associated with aspirin intolerance in asthmatics, the first stage of genome-wide association study with 109,365 single nucleotide polymorphisms (SNPs) was undertaken in a Korean AIA (n = 80) cohort and aspirin-tolerant asthma (ATA, n = 100) subjects as controls. For the second stage of follow-up study, 150 common SNPs from 11 candidate genes were genotyped in 163 AIA patients including intermediate AIA (AIA-I) subjects and 429 ATA controls. Among 11 candidate genes, multivariate logistic analyses showed that SNPs of CEP68 gene showed the most significant association with aspirin intolerance (P values of co-dominant for CEP68, 6.0×10(-5) to 4.0×10(-5)). All seven SNPs of the CEP68 gene showed linkage disequilibrium (LD), and the haplotype of CEP68_ht4 (T-G-A-A-A-C-G) showed a highly significant association with aspirin intolerance (OR= 2.63; 95% CI= 1.64-4.21; P = 6.0×10(-5)). Moreover, the nonsynonymous CEP68 rs7572857G>A variant that replaces glycine with serine showed a higher decline of forced expiratory volume in 1s (FEV(1)) by aspirin provocation than other variants (P = 3.0×10(-5)). Our findings imply that CEP68 could be a susceptible gene for aspirin intolerance in asthmatics, suggesting that the nonsynonymous Gly74Ser could affect the polarity of the protein structure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.