Evidence map›Paper›PMID 23897914›Full record

ArticlePediatrics2013

A genome-wide association study (GWAS) for bronchopulmonary dysplasia.

Hui Wang, Krystal R St Julien, David K Stevenson, Thomas J Hoffmann, John S Witte, Laura C Lazzeroni, Mark A Krasnow, Cecele C Quaintance, John W Oehlert, Laura L Jelliffe-Pawlowski and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pediatrics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
10.0field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. The Role of Heme Oxygenase-1 Promoter Polymorphisms in Perinatal Disease.International journal of environmental research and public health · 2021
    Pooled it
  3. Trial
  4. Ancestry and genetic associations with bronchopulmonary dysplasia in preterm infants.American journal of physiology. Lung cellular and molecular physiology · 2018
    Trial
  5. Review
  6. Article
  7. Toward precision for bronchopulmonary dysplasia: Moving past current definitions.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Review
  8. Article
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10 more citing papers are in PubMed but not listed here.

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 1 country.

Hui WangDepartment of Pediatrics, and cHoward Hughes Medical Institute, Stanford University School of Medicine, Palo Alto, California 94305, USA.
Krystal R St Julien
David K Stevenson
Thomas J Hoffmann
John S Witte
Laura C Lazzeroni
Mark A Krasnow
Cecele C Quaintance
John W Oehlert
Laura L Jelliffe-Pawlowski
Jeffrey B Gould
Gary M Shaw
Hugh M O'Brodovich
Pediatrics and Genetics · USUniversity of California, San Francisco · USCalifornia Department of Public Health · USHoward Hughes Medical Institute · USStanford University · US

Funding

Genomic Influences on Bronchopulmonary Dysplasia-A Population-Based StudyRC2HL101748 · NHLBI · STANFORD UNIVERSITY · PI OBRODOVICH, HUGH · 2009 to 2010
$3.5M
Howard Hughes Medical InstituteNHLBI NIH HHS RC2 HL101748
6 · The paper itself

Abstract

objectiveTwin studies suggest that heritability of moderate-severe bronchopulmonary dysplasia (BPD) is 53% to 79%, we conducted a genome-wide association study (GWAS) to identify genetic variants associated with the risk for BPD.

methodsThe discovery GWAS was completed on 1726 very low birth weight infants (gestational age = 25(0)-29(6/7) weeks) who had a minimum of 3 days of intermittent positive pressure ventilation and were in the hospital at 36 weeks' postmenstrual age. At 36 weeks' postmenstrual age, moderate-severe BPD cases (n = 899) were defined as requiring continuous supplemental oxygen, whereas controls (n = 827) inhaled room air. An additional 795 comparable infants (371 cases, 424 controls) were a replication population. Genomic DNA from case and control newborn screening bloodspots was used for the GWAS. The replication study interrogated single-nucleotide polymorphisms (SNPs) identified in the discovery GWAS and those within the HumanExome beadchip.

resultsGenotyping using genomic DNA was successful. We did not identify SNPs associated with BPD at the genome-wide significance level (5 × 10(-8)) and no SNP identified in previous studies reached statistical significance (Bonferroni-corrected P value threshold .0018). Pathway analyses were not informative.

conclusionsWe did not identify genomic loci or pathways that account for the previously described heritability for BPD. Potential explanations include causal mutations that are genetic variants and were not assayed or are mapped to many distributed loci, inadequate sample size, race ethnicity of our study population, or case-control differences investigated are not attributable to underlying common genetic variation.

Indexed as

Genome-Wide Association StudyInfant, Very Low Birth WeightBronchopulmonary DysplasiaCaliforniaExomeFemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeGestational AgeHumansInfantInfant, NewbornMaleModels, GeneticPhenotypechronic lung diseasegenetic predisposition to diseasegenome-wide association study (GWAS)prematurevery low birth weight infant

Identifiers

PMID23897914
PMCPMC3727675
OpenAlexW2149664848

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.