GEO DataSets

Analysis of cigarette smoking-induced changes in bronchial epithelia, and reversibility of effects when smoking is discontinued. May provide insight to molecular events leading to chronic obstructive pulmonary disease (COPD) and lung cancer.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 other sets

Platform:

GPL96

Series:

GSE994

75 Samples

Download data: CEL

(Submitter supplied) A number of studies have shown that cigarette smoking produces a field defect, such that genetic mutations induced by smoking occur throughout the lung and its intra and extra-pulmonary airways. Based on this concept, we have begun this study, which has as its goal the definition of the normal airway transcriptome, an analysis of how that transcriptome is affected by cigarette smoke, and to explore the reversibility of altered gene expression when smoking has been discontinued. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS534

Platform:

GPL96

75 Samples

Download data: CEL

(Submitter supplied) Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Datasets:

GDS3054 GDS3309

Platforms:

GPL571 GPL96

25 Samples

Download data: CEL, CHP, EXP

Analysis of nasal epithelia from cigarette smokers. Cigarette smoke creates a field of injury in epithelial cells lining the respiratory tract. Results extend the concept of a smoking-induced field of injury beyond intrathoracic (bronchial) epithelia to extrathoracic epithelia that line the nose.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent sets

Platform:

GPL571

Series:

GSE8987

15 Samples

Download data: CEL, CHP, EXP

Analysis of buccal epithelia from cigarette smokers. Cigarette smoke creates a field of injury in epithelial cells lining the respiratory tract. Results extend the concept of a smoking-induced field of injury beyond intrathoracic (bronchial) epithelia to extrathoracic epithelia that line the mouth.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 agent sets

Platform:

GPL96

Series:

GSE8987

10 Samples

Download data: CEL, CHP, EXP

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Expression profiling by high throughput sequencing

Platforms:

GPL13447 GPL10999

21 Samples

Download data: BEDGRAPH, CEL, TXT

(Submitter supplied) mRNA expression was profiled from pooled bronchial airway epithelial cell brushings (n=3 patients/pool) obtained during bronchoscopy from healthy never (NS) and current smokers (S) and smokers with (C) and without (NC) lung cancer

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL10999

8 Samples

Download data: BEDGRAPH, GTF, TXT

(Submitter supplied) mRNA expression was assayed from bronchial epithelial cell samples from smokers with and without lung cancer. A subset of the samples (2 of the lung cancer samples and 3 of the no cancer samples) were pooled and underwent whole transcriptome sequencing. The goals were to compare whole transcriptome sequencing gene expression levels to gene expression levels derived from these samples run on the Affymetrix HGU133A 2.0 platform.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13447

13 Samples

Download data: CEL

(Submitter supplied) BACKGROUND: We have previously reported gene expression changes in the bronchial airway epithelium of active chronic smokers. In this study, we investigate the effects of Acute Smoke Exposure (ASE) from cigarettes on airway epithelial gene expression. METHODS: Bronchial airway epithelial cell brushings were collected via fiberoptic bronchoscopy from 63 individuals without recent exposure to cigarette smoke (> 2 days), at baseline and at 24 hours after smoking three cigarettes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17244

126 Samples

Download data: CEL

(Submitter supplied) RNA was obtained from histologically normal bronchial epithelium of never, former, and current smokers undergoing fiberoptic bronchoscopy. Statistical analysis of the gene expression data identified gene differentially expressed between current and never smokers and classified these genes as irreversible, slowly reversible, or rapidly reversible based on their behavior in former smokers Keywords: Disease state analysis

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL96

104 Samples

Download data: CEL

(Submitter supplied) Smokers weigh less and have less body fat than non-smokers, and increased body fat and weight gain are observed following smoking cessation. To assess a possible molecular mechanism underlying the inverse association between smoking and body weight, we hypothesized that smoking may induce the expression of a fat depleting gene in the airway epithelium, the cell population that takes the brunt of the stress of cigarette smoke. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL80 GPL96 GPL570

92 Samples

Download data: CEL, CHP

(Submitter supplied) The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

135 Samples

Download data: CEL, CHP

(Submitter supplied) 24 SAGE libraries comprising of 8 current smokers, 12 former smokers and 4 never smokers. Keywords: SAGE, gene expression, current, former, never, smokers

Organism:

Homo sapiens

Type:

Expression profiling by SAGE

Platform:

GPL4

24 Samples

Download data

(Submitter supplied) To investigate the biochemical and genetic alterations that occur in response to cigarette smoke exposure among airway epithelial cells from different sites in the lungs, we performed microarray-based analysis using small airway epithelial cells (SAEC) and normal human bronchial epithelial cells (NHBE) following 24 h of cigarette smoke extract (CSE). In microarray-based analysis, the small airway showed higher susceptibility to CS compared to the large airway, such as enhanced expression of inflammatory-related pathways including the TNF signaling pathway. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

8 Samples

Download data: TXT

(Submitter supplied) mRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy and nasal epithelial cells collected by brushing the inferior turbinate from healthy current and never smoker volunteers in order to determine the relationship between smoking-related gene expression changes in bronchial and nasal epithelium within the same individual.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL5175

73 Samples

Download data: CEL

(Submitter supplied) Background: While electronic cigarette (ECIG) use is rapidly rising, their safety profile remains uncertain. The effects of tobacco cigarette (TCIG) smoke on bronchial airway epithelial gene-expression have provided insights into tobacco-related disease pathogenesis. Understanding the impact of electronic cigarettes (ECIGs) on airway gene-expression could provide insights into their potential long-term health effects. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17556

45 Samples

Download data: CEL

(Submitter supplied) Objective: Cigarette smoking ameliorates ulcerative colitis (UC) and aggravates Crohn’s disease (CD). Cigarette smoke suppresses inflammation-induced apoptosis in intestinal epithelial cells (DLD-1), which may explain its protective effect in UC. Here, we performed transcriptome profiling of cigarette smoke extract (CSE)-exposed DLD-1 and Jurkat cells (T-lymphocytes) and related this to UC susceptibility genes with protective functions in the intestinal epithelium. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

36 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

133 Samples

Download data

(Submitter supplied) While lung cancer is the leading cause of cancer death in the US, we have a limited understanding of the earliest molecular events preceding the onset of disease. Prior work has demonstrated that cigarette smoke creates a molecular “field of injury” throughout the airway epithelium and that there are distinct alterations in the airway transcriptome among smokers who have lung cancer. Molecular characterization of this airway “field of injury” in current and former smokers with premalignant lesions (PMLs) could provide novel insights into the earliest molecular events associated with lung carcinogenesis and identify relatively accessible biomarkers to guide lung cancer detection and early intervention. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

51 Samples

Download data: TSV

(Submitter supplied) While lung cancer is the leading cause of cancer death in the US, we have a limited understanding of the earliest molecular events preceding the onset of disease. Prior work has demonstrated that cigarette smoke creates a molecular “field of injury” throughout the airway epithelium and that there are distinct alterations in the airway transcriptome among smokers who have lung cancer. Molecular characterization of this airway “field of injury” in current and former smokers with premalignant lesions (PMLs) could provide novel insights into the earliest molecular events associated with lung carcinogenesis and identify relatively accessible biomarkers to guide lung cancer detection and early intervention. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

82 Samples

Download data: TSV