Evidence map›Paper›PMID 17894889›Full record

ArticleGenome biology2007

Reversible and permanent effects of tobacco smoke exposure on airway epithelial gene expression.

Jennifer Beane, Paola Sebastiani, Gang Liu, Jerome S Brody, Marc E Lenburg, Avrum Spira

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

133 citing papers in PubMed, 1 synthesis or guideline pooled it, 253 citations in OpenAlex.

  1. Epigenetic Signatures of Cigarette Smoking.Circulation. Cardiovascular genetics · 2016
    Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Airway Spatial Transcriptomics in Smoking.medRxiv : the preprint server for health sciences · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Serial Sampling of the Small Airway Epithelium to Identify Persistent Smoking-dysregulated Genes.American journal of respiratory and critical care medicine · 2023
    Article
  20. Article

73 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

6 authors at 3 institutions in 1 country.

Jennifer BeaneBioinformatics Program, Boston University, Cummington Street, Boston, MA 02215, USA. jbeane@bu.edu
Paola Sebastiani
Gang Liu
Jerome S Brody
Marc E Lenburg
Avrum Spira
Boston Medical Center · USBoston University · USUniversity Medical Center · US

Funding

A non-invasive gene-expression biomarker of airway response to tobacco exposureU01ES016035 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SPIRA, AVRUM E · 2007 to 2010
$2.9M
Airway gene expression in smokers: an early diagnostic biomarker for lung cancerR01CA124640 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SPIRA, AVRUM E · 2007 to 2011
$1.5M
NCI NIH HHS R01 CA124640NCI NIH HHS R01CA124640NCI NIH HHS R21CA10650NIEHS NIH HHS U01 ES016035
6 · The paper itself

Abstract

backgroundTobacco use remains the leading preventable cause of death in the US. The risk of dying from smoking-related diseases remains elevated for former smokers years after quitting. The identification of irreversible effects of tobacco smoke on airway gene expression may provide insights into the causes of this elevated risk.

resultsUsing oligonucleotide microarrays, we measured gene expression in large airway epithelial cells obtained via bronchoscopy from never, current, and former smokers (n = 104). Linear models identified 175 genes differentially expressed between current and never smokers, and classified these as irreversible (n = 28), slowly reversible (n = 6), or rapidly reversible (n = 139) based on their expression in former smokers. A greater percentage of irreversible and slowly reversible genes were down-regulated by smoking, suggesting possible mechanisms for persistent changes, such as allelic loss at 16q13. Similarities with airway epithelium gene expression changes caused by other environmental exposures suggest that common mechanisms are involved in the response to tobacco smoke. Finally, using irreversible genes, we built a biomarker of ever exposure to tobacco smoke capable of classifying an independent set of former and current smokers with 81% and 100% accuracy, respectively.

conclusionWe have categorized smoking-related changes in airway gene expression by their degree of reversibility upon smoking cessation. Our findings provide insights into the mechanisms leading to reversible and persistent effects of tobacco smoke that may explain former smokers increased risk for developing tobacco-induced lung disease and provide novel targets for chemoprophylaxis. Airway gene expression may also serve as a sensitive biomarker to identify individuals with past exposure to tobacco smoke.

Indexed as

Gene Expression RegulationSmokeAdultAgedBiomarkersEpitheliumHumansMiddle AgedNicotianaOligonucleotide Array Sequence AnalysisReproducibility of ResultsRespiratory SystemSmokingTobacco Smoke PollutionTracheaBiomarkersSmokeTobacco Smoke Pollution

Identifiers

PMID17894889
PMCPMC2375039
OpenAlexW2127711365

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.