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Homo sapiens

ABSTRACT: Airway epithelial cells from smokers with and without bronchial premalignant lesions

PROVIDER: PRJNA315161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3225260_1.fastq.gz	Fastqsanger.gz
	SRR3225260_2.fastq.gz	Fastqsanger.gz
	SRR3225270_1.fastq.gz	Fastqsanger.gz
	SRR3225270_2.fastq.gz	Fastqsanger.gz
	SRR3225280_1.fastq.gz	Fastqsanger.gz

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Antioxidant response gene expression in the bronchial airway epithelial cells of smokers at risk for lung cancer

Project description:Prior microarray studies of smokers at high risk for lung cancer have demonstrated that heterogeneity in bronchial airway epithelial cell gene expression response to smoking can serve as an early diagnostic biomarker for lung cancer. This study examines the relationship between gene expression variation and genetic variation in a central molecular pathway (NRF2-mediated antioxidant response) associated with smoking exposure and lung cancer. We assessed global gene expression in histologically normal airway epithelial cells obtained at bronchoscopy from smokers who developed lung cancer (SC, n=20), smokers without lung cancer (SNC, n=24), and never smokers (NS, n=8). Functional enrichment showed that the NRF2-mediated antioxidant response pathway differed significantly among these groups. Keywords: Global mRNA expression profiling 21 total arrays (20 unique patients) run on total RNA obtained from Bronchial Epithelium of Smokers with Lung Cancer 30 total arrays (24 unique patients) run on total RNA obtained from Bronchial Epithelium of Smokers without Lung Cancer 9 total arrays (8 unique patients) run on total RNA obtained from Bronchial Epithelium of Never Smokers

2010-09-30 | E-GEOD-19027 | biostudies-arrayexpress

Characterizing smoking-induced transcriptional heterogeneity in the human bronchial epithelium at single-cell resolution

Project description:The human bronchial epithelium is composed of multiple, distinct cell types that cooperate to defend against environmental insults. While studies have shown that smoking alters bronchial epithelial function and morphology, its precise effects on specific cell types and overall tissue composition are unclear. We used single-cell RNA sequencing to profile bronchial epithelial cells from six never- and six current smokers. Unsupervised analyses led to the characterization of a set of toxin metabolism genes that localized to smoker ciliated cells, tissue remodeling associated with a loss of club cells and extensive goblet cell hyperplasia, and a novel peri-goblet epithelial subpopulation in smokers that expressed a marker of bronchial premalignant lesions. Our data demonstrates that smoke exposure drives a complex landscape of cellular alterations that may prime the human bronchial epithelium for disease.

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Homo sapiens

Project description:Premalignant lesions of the bronchial epithelium

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mRNA-seq of Human Airway Epithelial Cells

2011-06-01 | GSE29006 | GEO

Airway epithelial cells obtained via bronchoscopy from high risk subjects with and without bronchial premalignant lesions

Project description:Airway epithelial cells obtained via bronchoscopy from high risk subjects with and without bronchial premalignant lesions

| PRJNA315447 | ENA

MicroRNA expression from bronchial epithelial cell samples of current and never smokers.

Project description:MicroRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy from healthy current and never smoker volunteers in order to determine the effect of cigarette smoke exposure on airway epithelial microRNA expression Keywords: Global microRNA expression profiling Bronchial epithelial cells were collected from current and never smokers via bronchoscopy. Low molecular weight RNA ( < 200 nucleotides) was isolated and hybridized to Invitrogen NCode microRNA microarrays to determine which microRNAs detected in bronchial epithelial cells were differentially expressed in the airways of smokers.

2009-01-28 | E-GEOD-14634 | biostudies-arrayexpress

Antioxidant response gene expression in the bronchial airway epithelial cells of smokers at risk for lung cancer

2010-10-01 | GSE19027 | GEO

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Project description: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 4 samples were sequened, each representing a pool of 3 patients. The phenotypes of the 4 samples were as follows: healthy non-smoker, healthy smoker, smoker without lung cancer and smoker with lung cancer.

2011-06-01 | E-GEOD-29006 | biostudies-arrayexpress

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Project description:Airway epithelial cells from high-risk subjects obtained via multiple bronchoscopy procedures to follow bronchial premalignant lesions as part of lung cancer screening

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Gene Expression Alterations in Bronchial Epithelium of Electronic Cigarette Users

Project description: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. Objectives: We sought to compare the bronchial airway gene-expression profiles of former TCIG smokers now using ECIGs with the profiles of former and current TCIG smokers. Methods: We performed gene-expression profiling of bronchial epithelial cells collected from TCIG smokers not using ECIGs (n=21), former smokers using ECIGs (n=15), and current TCIG smokers not using ECIGs (n=9). We then compared our findings with previous studies of the effects of TCIG use on bronchial epithelium, as well an in vitro model of ECIG exposure. Results: Amongst 3,165 genes whose expression varied between the three study groups (q < 0.05), we identified 468 genes significantly altered in ECIG users relative to former smokers (p < 0.05). 79 of these genes were up or down-regulated concordantly between ECIG and TCIG. We did not detect ECIG-associated gene expression changes in known pathways associated with TCIG usage. Genes downregulated in ECIG users are enriched among the genes most downregulated by exposure of airway epithelium to ECIG vapor in vitro. Conclusions: TCIG exposure was associated with a larger number of airway gene-expression changes than with ECIG exposures. ECIGs induce both distinct and shared patterns of gene expression relative to TCIGs in the bronchial airway epithelium.

2019-10-09 | GSE112073 | GEO

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