Evidence map›Paper›PMID 21543791›Full record

ReviewProceedings of the American Thoracic Society2011

Genetic studies of the etiology of asthma.

Kathleen C Barnes

Abstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. New findings showing how DNA methylation influences diseases.World journal of biological chemistry · 2019
    Article
  6. Article
  7. The association between caesarean section and childhood asthma: an updated systematic review and meta-analysis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Review
  8. Article
  9. Balkan journal of medical genetics : BJMG · 2018
    Article
  10. Article
  11. Transferability of genome-wide associated loci for asthma in African Americans.The Journal of asthma : official journal of the Association for the Care of Asthma · 2017
    Article
  12. Review
  13. Article
  14. Review
  15. Allergic diseases: the price of civilisational progress.Postepy dermatologii i alergologii · 2014
    Review
  16. Asthma: Gln27Glu and Arg16Gly polymorphisms of the beta2-adrenergic receptor gene as risk factors.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2014
    Article
  17. Review
  18. Severe asthma in childhood: recent advances in phenotyping and pathogenesis.Current opinion in allergy and clinical immunology · 2012
    Review
  19. 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

1 author.

Kathleen C BarnesThe Johns Hopkins Asthma & Allergy Center, Baltimore, MD 21224, USA. kbarnes@jhmi.edu

Funding

Genome-Wide Association Studies of Asthma in Populations of African DescentR01HL087699 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BARNES, KATHLEEN C · 2006 to 2008
$5.8M
NHLBI NIH HHS R01 HL087699
6 · The paper itself

Abstract

Asthma is a heterogeneous disease for which a strong genetic basis is firmly established. Although the generally accepted definition includes three domains of symptoms (variable airway obstruction, airway hyper-responsiveness, and airway inflammation), there is general agreement that, rather than being a single disease entity, asthma consists of related, overlapping syndromes. A considerable proportion of asthma is IgE-mediated, but the observation that not all individuals with asthma are atopic adds to the heterogeneity. Although a genetic basis for asthma is undeniable, elucidation of polymorphisms that are "causal" is greatly hampered by variability in the clinical phenotype, which is likely due to the multiple molecular mechanisms underlying the complex pathological processes involved in disease development and progression. One objective of this review is to consider progress that has been made to date in gene discovery in the field of asthma, with a focus on the evolution of molecular genetic methods that have led to the discoveries thus far, and with a particular focus on the major advances owed to the published genome-wide association studies (GWAS) on asthma to date. A second objective is to consider a Darwinian approach toward understanding the genetic underpinnings of asthma, including evidence supporting a modified Hygiene Hypothesis, which suggests that there are co-associations between asthma risk polymorphisms and polymorphisms associated with another IgE-mediated disease, schistosomiasis. The overall conclusion is that the huge research efforts and expense committed to asthma genetics have changed the perception about disease etiology in general and the functional relevance of the asthma genes identified thus far in particular.

Indexed as

AsthmaGenetic PleiotropyGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPolymorphism, Genetic

Identifiers

PMID21543791
PMCPMC3131830

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.