GEO DataSets

(Submitter supplied) Aging involves multiple biologically complex processes characterized by a decline in cellular homeostasis over time leading to a loss and impairment of physiological integrity and function. Specific cellular hallmarks of aging include abnormal gene expression patterns, shortened telomeres and associated biological dysfunction. Like all organs, the lung demonstrates both physiological and structural changes with age that result in a progressive decrease in lung function in healthy individuals. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

58 Samples

Download data: CEL, CHP

(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) The aldokatoreductases (AKRs) represent a gene superfamily that code for monomeric, soluble NAD(P)H-dependent oxidoreductases that mediate elimination reactions. AKR1B10, an AKR that functions to eliminate retinals, has been observed to be upregulated in squamous metaplasma and non small cell lung cancer, and has been suggested as a diagnostic marker specific to tobacco-related carcinogenesis. In the context of the link of smoking and lung cancer and the enhanced expression of AKR1B10 expression in lung cancer, we hypothesize that enhanced expression of AKR1B10 may be initiated in healthy smokers, prior to the development of any evidence of lung cancer. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

161 Samples

Download data: CEL, CHP

(Submitter supplied) Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

121 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) 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) Lectins are proteins present on cell surfaces or as shed extracellular proteins that function in innate immune defense as phagocytic receptors to recognize specific bacterial cell wall components. Based on the knowledge that cigarette smoking is associated with increased risk of bacterial infection, we hypothesized that cigarette smoking may modulate the expression of lectin genes in the airway epithelium. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

87 Samples

Download data: CEL, CHP

(Submitter supplied) The first changes associated with smoking are in the small airway epithelium (SAE). Given that smoking alters SAE gene expression, but only a fraction of smokers develop chronic obstructive pulmonary disease (COPD), we hypothesized that assessment of SAE genome-wide gene expression would permit biologic phenotyping of the smoking response, and that a subset of healthy smokers would have a “COPD-like” SAE transcriptome. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

171 Samples

Download data: CEL, CHP

(Submitter supplied) Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages in Response to the In Vivo Oxidant Stress of Cigarette Smoking The oxidant burden of cigarette smoking induces lung cell dysfunction, and play a significant role in the pathogenesis of lung disease. Two cell populations directly exposed to the oxidants in cigarette smoke are the small airway epithelium and alveolar macrophages. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

98 Samples

Download data: CEL, CHP

(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:

GPL570 GPL80 GPL96

92 Samples

Download data: CEL, CHP

(Submitter supplied) Although smoking-induced lung disease tends to be more common in the upper lobe, it is not known if this results from the skewed distribution of inhaled cigarette smoke or increased susceptibility of the upper lobes to these disorders. The distribution of inhaled cigarette smoke within the lung is complex, depending on lung pressure-volume relationships, gravity, individual smoking habits and the properties of the individual components of cigarette smoke. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

22 Samples

Download data: CEL, CHP

(Submitter supplied) Background: Whereas cilia damage and reduced cilia beat frequency have been implicated as causative of reduced mucociliary clearance in smokers, theoretically mucociliary clearance could also be affected by cilia length. Based on models of mucociliary clearance predicting cilia length must exceed the 6 -7 μm airway surface fluid depth to generate force in the mucus layer, we hypothesized cilia height may be decreased in airway epithelium of normal smokers compared to nonsmokers. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

50 Samples

Download data: CEL, CHP

(Submitter supplied) Comparison of gene and protein expression in the large airway epithelium of never and current smokers. Keywords: gene expression array-based (RNA / in situ oligonucleotide)

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL96

8 Samples

Download data: CEL

(Submitter supplied) The small airway epithelium (SAE), the first site of smoking-induced lung pathology, exhibits genome-wide changes in gene expression in response to cigarette smoking. Based on the increasing evidence that the epigenome can respond to external stimuli in a rapid manner, we assessed the SAE of smokers for genome-wide DNA methylation changes compared to nonsmokers, and whether changes in SAE DNA methylation were linked to the transcriptional output of these cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array; Methylation profiling by genome tiling array

Platforms:

GPL16419 GPL570

75 Samples

Download data: CEL, CHP, PAIR

(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) Despite overwhelming data that cigarette smoking causes chronic obstructive pulmonary disease (COPD), only a minority of chronic smokers are affected, strongly suggesting that genetic factors modify susceptibility to this disease. We hypothesized that there are individual variations in the response to cigarette smoking, with variability among smokers in expression levels of protective / susceptibility genes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

54 Samples

Download data: CEL, CHP