Evidence map›Paper›PMID 42316380›Full record

ArticleBMC genomic data2026

A candidate-variant association study of self-reported asthma in mothers of the Cebu Longitudinal Health and Nutrition Survey (CLHNS) cohort.

Alvin E Lirio, Jing Chen, Paulita Duazo, Nanette Lee, Linda Adair, Martin D Tobin, Catherine John, Anna L Guyatt

Abstract read
In one paragraph

Article in BMC genomic data, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Alvin E LirioDivision of Public Health and Epidemiology, University of Leicester, Leicester, UK.
Jing ChenDivision of Public Health and Epidemiology, University of Leicester, Leicester, UK.
Paulita DuazoUSC Office of Population Studies, University of San Carlos, Cebu City, Philippines.
Nanette LeeUSC Office of Population Studies, University of San Carlos, Cebu City, Philippines.
Linda AdairUNC Chapel Hill Genetics Department, Chapel Hill, USA.
Martin D TobinDivision of Public Health and Epidemiology, University of Leicester, Leicester, UK.
Catherine JohnDivision of Public Health and Epidemiology, University of Leicester, Leicester, UK. catherine.john@leicester.ac.uk.
Anna L GuyattDivision of Public Health and Epidemiology, University of Leicester, Leicester, UK. anna.guyatt@le.ac.uk.

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
NIEHS NIH HHS P30 ES010126Wellcome Trust Discovery Award 225221/Z/22/Z
6 · The paper itself

Abstract

backgroundAsthma is an obstructive respiratory disease with greatest morbidity in low- and middle-income countries: 15% of the Filipino population are estimated to have asthma, half of whom have inadequately controlled disease. There are many known genetic associations with asthma, but lack of representation across ancestries means that understudied populations do not yet stand to benefit equally from genomic research. We performed the first genetic association study of asthma in a Filipino population. We performed a candidate-variant association study in 1,678 unrelated mothers (129 with self-reported asthma) of the Cebu Longitudinal Health and Nutrition Survey (CLHNS). Using the largest published multi-ancestry asthma GWAS (Global Biobank Meta-Analysis Initiative, GBMI), we selected sentinel single-nucleotide polymorphisms (SNPs) associated in the multi-ancestry analysis (P < 5 × 10

resultsTwenty-seven SNPs were analysed. Only one intronic variant in SMAD3 was associated with asthma at a Bonferroni-corrected threshold (rs17293632, OR 1.80, 95%CI 1.28-2.54, P = 0.0008). SMAD3 is involved in TGF-β signalling, related to airway remodelling in asthma. The GRS was associated with increased odds of asthma (OR per weighted allele increase 1.07 [95%CI 1.01-1.14], P = 0.022). Five of the 37 top signals in the EAS GWAS were associated in our study, although none of these five signals reached a Bonferroni p-value threshold of P = 1.35 × 10

conclusionsDespite the small sample size, we detected a known SNP-asthma association in CLHNS using a candidate-variant approach, and demonstrated the value of aggregating variants into GRS when power is limited (using confidently ascribed weights from large GWAS). However, we were underpowered to undertake a GWAS, and thus to discover novel associations. Commitment by the genomics field as a whole to cohort development and investment in understudied populations will be key to addressing inequity in asthma genetic research. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

AsthmaMothersPolymorphism, Single NucleotideAdultFemaleGenetic Predisposition to DiseaseGenetic Risk ScoreGenome-Wide Association StudyHumansLongitudinal StudiesMiddle AgedNutrition SurveysPhilippinesSelf ReportSmad3 ProteinSmad3 ProteinSMAD3 protein, humanAsthmaCandidate-variant association studyFilipinoGenetic risk scores

Identifiers

PMID42316380
PMCPMC13308225

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.