Evidence map›Paper›PMID 25608829›Full record

ArticleJournal of human genetics2015

Identification of FAM13A gene associated with the ratio of FEV1 to FVC in Korean population by genome-wide association studies including gene-environment interactions.

Soriul Kim, Hyun Kim, Namhan Cho, Seung Ku Lee, Bok-Ghee Han, Jae Woong Sull, Sun Ha Jee, Chol Shin

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In one paragraph

Article in Journal of human genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Residential Green and Blue Space, the Natural Environment, Genetic Susceptibility, and Incident COPD.International journal of chronic obstructive pulmonary disease · 2026
    Article
  4. Article
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Review
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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 at 5 institutions in 1 country.

Soriul Kim1] Institute of Human Genomic Study, Ansan Hospital, Korea University, Ansan, Republic of Korea [2] Department of Public Health, Graduate School, Yonsei University, Seoul, Republic of Korea.
Hyun KimInstitute of Human Genomic Study, Ansan Hospital, Korea University, Ansan, Republic of Korea.
Namhan ChoDepartment of Preventive Medicine, Ajou University School of Medicine, Suwon, Republic of Korea.
Seung Ku LeeInstitute of Human Genomic Study, Ansan Hospital, Korea University, Ansan, Republic of Korea.
Bok-Ghee HanCenter for Genome Science, National Institute of Health, Cheongwon, Republic of Korea.
Jae Woong SullDepartment of Bio-Medical Laboratory Science, College of Health Science, Eulji University, Sungnam, Republic of Korea.
Sun Ha JeeDepartment of Epidemiology and Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, Republic of Korea.
Chol Shin1] Institute of Human Genomic Study, Ansan Hospital, Korea University, Ansan, Republic of Korea [2] Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Korea University Ansan Hospital, Ansan, Republic of Korea.
Korea University · KRAjou University · KREulji University · KRKorea National Institute of Health · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a complex, multifactorial disease. Although smoking is a main risk factor for obstructive impairment, not all smokers develop this critical disease. We conducted a genome-wide association study to identify the association between genetic variants and pulmonary function and also examined how these variants relate to lung impairment in accordance with smoking behaviors. Using two community-based cohorts, the Ansan cohort (n=4319) and the Ansung cohort (n=3674), in the Korean Genome Epidemiology Study, we analyzed the association between genetic variants (single-nucleotide polymorphisms and haplotypes) and the ratio of FEV1 to FVC (FEV1/FVC) using multivariate linear regression models. Similar analyses were conducted after stratification by smoking status. Four genome-wide significant signals in the FAM13A gene (the strongest signal at rs2609264, P=1.76 × 10(-7) in a combined set) were associated with FEV1/FVC. For the association with ratio, the effect size in the CTGA haplotype (risk haplotype) was -0.57% (s.e., 0.11; P=2.10 × 10(-7)) as compared with the TCAG haplotype (reference haplotype) in a combined set. There was also a significant interaction of FAM13A haplotypes with heavy smoking on FEV1/FVC (P for interaction=0.028). We confirmed the previously reported association of FAM13A in 4q22.1 with pulmonary function. The FAM13A haplotypes also interacted with heavy smoking to affect the risk of reduced pulmonary function.

Indexed as

Gene-Environment InteractionAdultAsian PeopleBase SequenceCohort StudiesForced Expiratory VolumeGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyGTPase-Activating ProteinsHaplotypesHumansLinear ModelsMiddle AgedMultivariate AnalysisPolymorphism, Single NucleotideFAM13A protein, humanGTPase-Activating Proteins

Identifiers

PMID25608829
OpenAlexW1964498035

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.