Evidence map›Paper›PMID 19138944›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2008

Impact of smoking cessation on global gene expression in the bronchial epithelium of chronic smokers.

Li Zhang, J Jack Lee, Hongli Tang, You-Hong Fan, Lianchun Xiao, Hening Ren, Jonathan Kurie, Rodolfo C Morice, Waun Ki Hong, Li Mao

Open access · bronzeAbstract readComparative StudyMulticenter Study
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 75 citations in OpenAlex.

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  15. Genotoxicity ofToxicology research · 2017
    Article
  16. Molecular Impact of Electronic Cigarette Aerosol Exposure in Human Bronchial Epithelium.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Article
  17. Article
  18. Article
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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

10 authors at 1 institution in 1 country.

Li ZhangDepartment of Bioinformatics. The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA. Lzhangli@mdanderson.org
J Jack Lee
Hongli Tang
You-Hong Fan
Lianchun Xiao
Hening Ren
Jonathan Kurie
Rodolfo C Morice
Waun Ki Hong
Li Mao
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRIAL OF CELECOXIB IN LUNG CANCER CHEMOPREVENTIONP01CA091844 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI HONG, WAUN KI · 2001 to 2005
$8.2M
NCI NIH HHS P01 CA091844NCI NIH HHS P01 CA91844NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Cigarette smoke is the major cause of lung cancer and can interact in complex ways with drugs for lung cancer prevention or therapy. Molecular genetic research promises to elucidate the biological mechanisms underlying divergent drug effects in smokers versus nonsmokers and to help in developing new approaches for controlling lung cancer. The present study compared global gene expression profiles (determined via Affymetrix microarray measurements in bronchial epithelial cells) between chronic smokers, former smokers, and never smokers. Smoking effects on global gene expression were determined from a combined analysis of three independent data sets. Differential expression between current and never smokers occurred in 591 of 13,902 measured genes (P < 0.01 and >2-fold change; pooled data)--a profound effect. In contrast, differential expression between current and former smokers occurred in only 145 of the measured genes (P < 0.01 and >2-fold change; pooled data). Nine of these 145 genes showed consistent and significant changes in each of the three data sets (P < 0.01 and >2-fold change), with eight being down-regulated in former smokers. Seven of the eight down-regulated genes, including CYP1B1 and three AKR genes, influence the metabolism of carcinogens and/or therapeutic/chemopreventive agents. Our data comparing former and current smokers allowed us to pinpoint the genes involved in smoking-drug interactions in lung cancer prevention and therapy. These findings have important implications for developing new targeted and dosing approaches for prevention and therapy in the lung and other sites, highlighting the importance of monitoring smoking status in patients receiving oncologic drug interventions.

Indexed as

Gene Expression RegulationSmoking CessationAgedBronchiChronic DiseaseCohort StudiesFemaleGene Expression ProfilingHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisRespiratory MucosaSmokingTime FactorsTobacco Use Disorder

Identifiers

PMID19138944
PMCPMC4181408
OpenAlexW2136779207

What OpenQuestion holds

Textmetadata
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.