Evidence map›Paper›PMID 17727719›Full record

ArticleBMC genomics2007

Effect of active smoking on the human bronchial epithelium transcriptome.

Raj Chari, Kim M Lonergan, Raymond T Ng, Calum MacAulay, Wan L Lam, Stephen Lam

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 93 citations in OpenAlex.

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  10. The Airway Transcriptome as a Biomarker for Early Lung Cancer Detection.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Review
  11. Review
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  13. Detecting the Presence and Progression of Premalignant Lung Lesions via Airway Gene Expression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Raj ChariDepartment of Cancer Genetics and Developmental Biology, British Columbia Cancer Research Centre, Vancouver, BC, Canada. rchari@bccrc.ca
Kim M Lonergan
Raymond T Ng
Calum MacAulay
Wan L Lam
Stephen Lam
Canadian Centre for Applied Research in Cancer Control · CAUniversity of British Columbia · CA

Funding

Whole genome array CGH of progressing oral dysplasiaR01DE015965 · NIDCR · BRITISH COLUMBIA CANCER AGENCY · PI LAM, WAN L · 2004 to 2007
$1.1M
NIDCR NIH HHS R01 DE015965NIDCR NIH HHS R01 DE15965-01
6 · The paper itself

Abstract

backgroundLung cancer is the most common cause of cancer-related deaths. Tobacco smoke exposure is the strongest aetiological factor associated with lung cancer. In this study, using serial analysis of gene expression (SAGE), we comprehensively examined the effect of active smoking by comparing the transcriptomes of clinical specimens obtained from current, former and never smokers, and identified genes showing both reversible and irreversible expression changes upon smoking cessation.

resultsTwenty-four SAGE profiles of the bronchial epithelium of eight current, twelve former and four never smokers were generated and analyzed. In total, 3,111,471 SAGE tags representing over 110 thousand potentially unique transcripts were generated, comprising the largest human SAGE study to date. We identified 1,733 constitutively expressed genes in current, former and never smoker transcriptomes. We have also identified both reversible and irreversible gene expression changes upon cessation of smoking; reversible changes were frequently associated with either xenobiotic metabolism, nucleotide metabolism or mucus secretion. Increased expression of TFF3, CABYR, and ENTPD8 were found to be reversible upon smoking cessation. Expression of GSK3B, which regulates COX2 expression, was irreversibly decreased. MUC5AC expression was only partially reversed. Validation of select genes was performed using quantitative RT-PCR on a secondary cohort of nine current smokers, seven former smokers and six never smokers.

conclusionExpression levels of some of the genes related to tobacco smoking return to levels similar to never smokers upon cessation of smoking, while expression of others appears to be permanently altered despite prolonged smoking cessation. These irreversible changes may account for the persistent lung cancer risk despite smoking cessation.

Indexed as

Gene Expression ProfilingSmokingAgedAged, 80 and overBronchiEpitheliumFemaleHumansMaleMiddle AgedReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSmoking CessationRNA, Messenger

Identifiers

PMID17727719
PMCPMC2001199
OpenAlexW2080178255

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.