GEO DataSets

Analysis of phenotypically normal 10th to 12th order small airway bronchial epithelia from cigarette smokers. Cigarette smoking is the most common cause of chronic obstructive pulmonary disease (COPD). Results provide insight into the early pathogenesis of COPD.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL96

Series:

GSE3320

11 Samples

Download data

(Submitter supplied) Modification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (HG-133 Plus 2.0 array) in phenotypically normal smokers (n=10, 33 ± 7 pack-yr) compared to matched non-smokers (n=12). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2486

Platform:

GPL570

22 Samples

Download data: CEL, CHP

(Submitter supplied) The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (Affymetrix HG-U133A array) in phenotypically normal smokers (n=6, 24 ± 4 pack-yr) compared to matched non-smokers (n=5). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS1304

Platform:

GPL96

11 Samples

Download data

Analysis of small airway epithelial cells of phenotypically normal smokers. The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. Results provide insight into how smoking modifies small airway structure and function.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL570

Series:

GSE4498

22 Samples

Download data: CEL, CHP

(Submitter supplied) To help define the genes associated with mucus synthesis and secretion in the human small airway epithelium, we hypothesized that comparison of the transcriptomes of the small airway epithelium of individuals that express high vs low levels of MUC5AC, a major secretory mucin and the major component of airway mucus, could be used as a probe to identify the genes related to human small airway mucus production / secretion. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

132 Samples

Download data: CEL, CHP, TXT

(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) 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

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

Organism:

Homo sapiens

Type:

Expression profiling by array

Platforms:

GPL96 GPL80 GPL570

124 Samples

Download data: CEL, CHP, EXP

(Submitter supplied) Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers The microarray data deposited here is from 9 HG-U133 Plus 2.0 GeneChips, from 4 normal non-smokers, and 5 phenotypic normal smokers, all large airways. These data are part of a study aimed at understanding how cigarette smoking modifies neuroendocrine cells, in which microarray analysis with TaqMan confirmation was used to assess airway epithelial samples obtained by fiberoptic bronchoscopy from 81 individuals (normal nonsmokers, normal smokers, smokers with early COPD and smokers with established COPD). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2491

Platform:

GPL570

9 Samples

Download data

(Submitter supplied) Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers The microarray data deposited here is from 39 HG-U133 Plus 2.0 GeneChips, from 12 normal non-smokers, 12 phenotypic normal smokers, 9 Early COPD and 6 COPD individuals, all small airways, all small airway. A subset of these samples have been already submitted under GEO Accession Number GSE 4498. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

39 Samples

Download data: CEL, CHP

(Submitter supplied) Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers The microarray data deposited here is from 11 HG-U133A GeneChips, from 5 normal non-smokers and 6 phenotypic normal smokers, large airways. Samples from the small airways of these individuals have been obtained and analyzed using the HG-U133A GeneChip; the small airway samples are in GEO Accession Number GSE 3320, and the data analysis is described in Harvey, B-G; Heguy, A.; Leopold, P.L.; Carolan, B.; Ferris, B. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2490

Platform:

GPL96

11 Samples

Download data

(Submitter supplied) Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers The microarray data deposited here is from 44 HuGeneFL GeneChips, from 9 normal non-smokers and 13 phenotypic normal smokers, large airways, 2 samples per individual, one from the right lung and one from the left lung. These samples were previously described in Hackett NR, Heguy A, Harvey BG, O'Connor TP, Luettich K, Flieder DB, Kaplan R, Crystal RG. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS2489

Platform:

GPL80

44 Samples

Download data

Analysis of large airway epithelial cells of phenotypically normal smokers. Lung cancer tumors exhibit neuroendocrine properties, and chronic smokers have increased numbers of neuroendocrine cells. Results provide insight into the effect of cigarette smoking on neuroendocrine cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL570

Series:

GSE5059

9 Samples

Download data

Analysis of large airway epithelial cells of phenotypically normal smokers. Lung cancer tumors exhibit neuroendocrine properties, and chronic smokers have increased numbers of neuroendocrine cells. Results provide insight into the effect of cigarette smoking on neuroendocrine cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL96

Series:

GSE5057

11 Samples

Download data

Analysis of large airway epithelial cells of phenotypically normal smokers. Lung cancer tumors exhibit neuroendocrine properties, and chronic smokers have increased numbers of neuroendocrine cells. Results provide insight into the effect of cigarette smoking on neuroendocrine cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL80

Series:

GSE5056

44 Samples

Download data

(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) 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) Cigarette smoking is the leading cause of the respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). While the pathogenesis of COPD is complex, there is abundant evidence that alveolar macrophages (AM) play an important role. Based on the concept that COPD is a slow-progressing disorder likely involving multiple mediators released by AM activated by cigarette smoke, the present study focuses on the identification of previously unrecognized genes that may be linked to early events in the molecular pathogenesis of COPD, as opposed to factors associated with the presence of disease. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS1436

Platform:

GPL80

10 Samples

Download data: CEL, EXP

Anlaysis of alveolar macrophages of 5 phenotypically normal smokers who consume ~20 packs cigarettes/year. Smoking is the leading cause of respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). Provides insight into early events in molecular pathogenesis of COPD.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 2 stress sets

Platform:

GPL80

Series:

GSE3212

10 Samples

Download data: CEL, EXP

(Submitter supplied) The toll-like receptors (TLRs) are important components of the respiratory epithelium host innate defense, enabling the airway surface to recognize and respond to a variety of insults in inhaled air. Based on the knowledge that smokers are more susceptible to pulmonary infection and the airway epithelium of smokers with chronic obstructive pulmonary disease (COPD) is characterized by bacterial colonization and acute exacerbation of airway infections, we assessed whether smoking alters the expression of TLRs in human small airway epithelium, the primary site of smoking-induced disease. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

169 Samples

Download data: CEL, CHP