Evidence map›Paper›PMID 28738859›Full record

ArticleRespiratory research2017

Genes and pathways underlying susceptibility to impaired lung function in the context of environmental tobacco smoke exposure.

K de Jong, J M Vonk, M Imboden, L Lahousse, A Hofman, G G Brusselle, N M Probst-Hensch, D S Postma, H M Boezen

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2017. 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
0.9field-weighted citation impact, top 26% 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, 19 citations in OpenAlex.

  1. Article
  2. Observational
  3. Oxidative medicine and cellular longevity · 2021
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Precision medicine in COPD: where are we and where do we need to go?European respiratory review : an official journal of the European Respiratory Society · 2018
    Review
  10. Review
  11. 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

9 authors at 4 institutions in 3 countries.

K de JongDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, the Netherlands.ORCID 0000-0002-3948-1046
J M VonkDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, the Netherlands.
M ImbodenSwiss Tropical and Public Health Institute, Basel, Switzerland.
L LahousseDepartment of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands.
A HofmanDepartment of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands.
G G BrusselleDepartment of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands.
N M Probst-HenschSwiss Tropical and Public Health Institute, Basel, Switzerland.
D S PostmaGroningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
H M BoezenDepartment of Epidemiology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, the Netherlands. h.m.boezen@umcg.nl.
University Medical Center Groningen · NLGhent University Hospital · BESwiss Tropical and Public Health Institute · CHErasmus MC · NL

Funding

Wellcome Trust
6 · The paper itself

Abstract

backgroundStudies aiming to assess genetic susceptibility for impaired lung function levels upon exposure to environmental tobacco smoke (ETS) have thus far focused on candidate-genes selected based on a-priori knowledge of potentially relevant biological pathways, such as glutathione S-transferases and ADAM33. By using a hypothesis-free approach, we aimed to identify novel susceptibility loci, and additionally explored biological pathways potentially underlying this susceptibility to impaired lung function in the context of ETS exposure.

methodsGenome-wide interactions of single nucleotide polymorphism (SNP) by ETS exposure (0 versus ≥1 h/day) in relation to the level of forced expiratory volume in one second (FEV

resultsFourty Five SNP-by-ETS exposure interactions with p-values <10

conclusionThis unique, first genome-wide gene-by-ETS interaction study on the level of FEV

Indexed as

Genetic LociPolymorphism, Single NucleotideAdolescentAdultAgedAged, 80 and overApoptosisFemaleForced Expiratory VolumeGene Regulatory NetworksGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLungLung DiseasesMalep38 Mitogen-Activated Protein KinasesTobacco Smoke PollutionTumor Necrosis FactorsEnvironmental tobacco smoke pollutionForced expiratory volumeSingle nucleotide polymorphism

Identifiers

PMID28738859
PMCPMC5525356
OpenAlexW2737658844

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.