Evidence map›Paper›PMID 24289273›Full record

ArticleEnvironmental health : a global access science source2013

Gene-environment interaction effects on lung function- a genome-wide association study within the Framingham heart study.

Shu-Yi Liao, Xihong Lin, David C Christiani

Open access · goldAbstract read
In one paragraph

Article in Environmental health : a global access science source, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

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  11. Occupational exposures and longitudinal lung function decline.American journal of industrial medicine · 2015
    Article
  12. Article
  13. Article
  14. The Cumulative Effect of Gene-Gene Interactions BetweenInternational journal of chronic obstructive pulmonary disease
    Article
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

3 authors at 1 institution in 1 country.

Shu-Yi Liao
Xihong Lin
David C ChristianiHarvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA. dchris@hsph.harvard.edu.
Harvard University · US

Funding

Statistical Methods for Analysis of Massive Genetic and Genomic Data in Cancer ResearchR35CA197449 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI XIHONG LIN · 2015 to 2026
$10.9M
The Spread of Health Behaviors in the Framingham Heart Study Social NetworkP01AG031093 · NIA · YALE UNIVERSITY · PI MCGUIRE, THOMAS G. · 2008 to 2012
$10.7M
Statistical Methods for Correlated and High-Dimensional Biomedical DataR37CA076404 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI LIN, XIHONG · 2007 to 2014
$2.5M
SLEEP AND ENTRAINMENT OF SCN FUNCTIONR01HL064278 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI STROHL, KINGMAN PERKINS · 1999 to 2002
$871k
THE FRAMINGHAM HEART STUDY-N01HC25195-268025195-268025195N01HC025195 · HC · TRUSTEES OF BOSTON UNIVERSITY · PI WOLF, PHILIP A · 2002 to 2006
–
NCI NIH HHS R35 CA197449NCI NIH HHS R37 CA076404NHLBI NIH HHS N01-HC-25195NHLBI NIH HHS N02-HL-64278NIA NIH HHS P01 AG 031093
6 · The paper itself

Abstract

backgroundPrevious studies in occupational exposure and lung function have focused only on the main effect of occupational exposure or genetics on lung function. Some disease-susceptible genes may be missed due to their low marginal effects, despite potential involvement in the disease process through interactions with the environment. Through comprehensive genome-wide gene-environment interaction studies, we can uncover these susceptibility genes. Our objective in this study was to explore gene by occupational exposure interaction effects on lung function using both the individual SNPs approach and the genetic network approach.

methodsThe study population comprised the Offspring Cohort and the Third Generation from the Framingham Heart Study. We used forced expiratory volume in one second (FEV1) and ratio of FEV1 to forced vital capacity (FVC) as outcomes. Occupational exposures were classified using a population-specific job exposure matrix. We performed genome-wide gene-environment interaction analysis, using the Affymetrix 550 K mapping array for genotyping. A linear regression-based generalized estimating equation was applied to account for within-family relatedness. Network analysis was conducted using results from single-nucleotide polymorphism (SNP)-level analyses and from gene expression study results.

resultsThere were 4,785 participants in total. SNP-level analysis and network analysis identified SNP rs9931086 (P(interaction) =1.16 × 10(-7)) in gene SLC38A8, which may significantly modify the effects of occupational exposure on FEV1. Genes identified from the network analysis included CTLA-4, HDAC, and PPAR-alpha.

conclusionsOur study implies that SNP rs9931086 in SLC38A8 and genes CTLA-4, HDAC, and PPAR-alpha, which are related to inflammatory processes, may modify the effect of occupational exposure on lung function.

Indexed as

Gene-Environment InteractionGenome-Wide Association StudyOccupational ExposurePolymorphism, Single NucleotideAdultAgedBostonDustFemaleForced Expiratory VolumeGene Regulatory NetworksHumansLungMaleMiddle AgedVital CapacityDust

Identifiers

PMID24289273
PMCPMC3882096
OpenAlexW2110780798

What OpenQuestion holds

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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.