Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Effect of active smoking on bronchial epithelial transcriptome (24 SAGE libraries)

ABSTRACT: 24 SAGE libraries comprising of 8 current smokers, 12 former smokers and 4 never smokers. Keywords: SAGE, gene expression, current, former, never, smokers Raw tag counts for each tag in each library are provided

ORGANISM(S): Homo sapiens

SUBMITTER: Raj Chari

PROVIDER: E-GEOD-5473 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Effect of active smoking on the human bronchial epithelium transcriptome.

Chari Raj R Lonergan Kim M KM Ng Raymond T RT MacAulay Calum C Lam Wan L WL Lam Stephen S

BMC genomics 20070829

<h4>Background</h4>Lung 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.< ...[more]

PMID: 17727719

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Project description:Tobacco smoking is responsible for over 90% of lung cancer cases, and yet the precise molecular alterations induced by smoking in lung that develop into cancer and impact survival have remained obscure. We performed gene expression analysis using HG-U133A Affymetrix chips on 135 fresh frozen tissue samples of adenocarcinoma and paired noninvolved lung tissue from current, former and never smokers, with biochemically validated smoking information. ANOVA analysis adjusted for potential confounders, multiple testing procedure, Gene Set Enrichment Analysis, and GO-functional classification were conducted for gene selection. Results were confirmed in independent adenocarcinoma and non-tumor tissues from two studies. We identified a gene expression signature characteristic of smoking that includes cell cycle genes, particularly those involved in the mitotic spindle formation (e.g., NEK2, TTK, PRC1). Expression of these genes strongly differentiated both smokers from non-smokers in lung tumors and early stage tumor tissue from non-tumor tissue (p<0.001 and fold-change>1.5, for each comparison), consistent with an important role for this pathway in lung carcinogenesis induced by smoking. These changes persisted many years after smoking cessation. NEK2 (p<0.001) and TTK (p=0.002) expression in the noninvolved lung tissue was also associated with a 3-fold increased risk of mortality from lung adenocarcinoma in smokers. Our work provides insight into the smoking-related mechanisms of lung neoplasia, and shows that the very mitotic genes known to be involved in cancer development are induced by smoking and affect survival. These genes are candidate targets for chemoprevention and treatment of lung cancer in smokers. Experiment Overall Design: Overall, 180 adenocarcinoma and non-tumor tissue samples were selected for the analyses, including duplicate or triplicate samples from 14 subjects for quality control. From the original 180 samples, 148 provided sufficient quantity of high-quality RNA for microarray analyses; 13 additional samples were excluded because of problematic assays. Normalization was conducted on the remaining 135 microarrays. After normalization, 13 samples were excluded because of low percentage of tumor cells in the tumor tissues. This report is based on 122 samples, of which 15 duplicates were averaged, resulting in 107 final expression values from 58 tumor and 49 non-tumor tissues from 20 never smokers, 26 former smokers, and 28 current smokers.

Dataset Information

Effect of active smoking on bronchial epithelial transcriptome (24 SAGE libraries)

Publications

Effect of active smoking on the human bronchial epithelium transcriptome.

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