Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular characterisation of the multistep process of lung squamous carcinogenesis by gene expression profiling

ABSTRACT: We comprehensively characterized the gene expression alterations occurring during squamous lung cancer development. Fresh frozen human bronchial biopsies (N=122) at successive morphological stages of lung squamous carcinogenesis were obtained by fluorescence bronchoscopy and analyzed using gene expression microarrays. A total of 122 biopsies from 77 individuals, 35 former and 42 current smokers, were included. The 122 biopsies were distributed according to histology and fluorescence status as follows: 13 biopsies with normal histology and normofluorescent (8/5 biopsies from former/current smokers), 14 with normal histology and hypofluorescent (8/6), 15 hyperplasia (7/8), 15 metaplasia (5/10), 13 mild dysplasia (8/5), 13 moderate dysplasia (7/6), 12 severe dysplasia (2/10), 13 carcinoma in situ (5/8) and 14 squamous cell carcinoma (SCC, 5/9). In addition, normal bronchial biopsies from 16 never-smokers were collected and pooled for use as reference RNA.

ORGANISM(S): Homo sapiens

SUBMITTER: Celine Mascaux

PROVIDER: E-GEOD-33479 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome Analysis of Preinvasive and Invasive Early Squamous Carcinoma in Archival Laser Microdissected Samples

Project description:Preinvasive squamous cell cancer (PSCC) are local transformations of bronchial epithelia that are frequently observed in current or former smokers. Their different grades and sizes suggest a continuum of dysplastic change with increasing severity, which may culminate in invasive squamous cell carcinoma (ISCC). As a consequence of the difficulty in identifying and obtaining PSCC samples, the molecular pathology that underlies their histological variability remains largely unknown. To address this issue, we have measured gene expression in the distinct stages of this proposed model of squamous carcinogenesis, i.e. low- and high-grade PSCC, lymph node-negative and positive ISCC compared with matched normal bronchial epithelia, using Human Exon 1.0 ST arrays and RNA obtained from microdissected formalin-fixed and paraffin embedded (FFPE) biopsies.

2017-06-09 | E-MTAB-3950 | biostudies-arrayexpress

Transcription profiling of human airway epithelial cells to investigate the reversible and permanent effects of tobacco smoke exposure

Project description: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 Experiment Overall Design: Microarrays run on total RNA obtained from Bronchial Epithelium of Never Smokers (n=21), Former Smokers (n=31), and Current Smokers (n=52)

2008-06-16 | E-GEOD-7895 | biostudies-arrayexpress

Molecular characterisation of the multistep process of lung squamous carcinogenesis by gene expression profiling

Project description:We comprehensively characterized the gene expression alterations occurring during squamous lung cancer development. Fresh frozen human bronchial biopsies (N=122) at successive morphological stages of lung squamous carcinogenesis were obtained by fluorescence bronchoscopy and analyzed using gene expression microarrays.

2014-10-31 | GSE33479 | GEO

Reversible and Permanent effects of Tobacco Smoke Exposure on Airway Epithelial Gene Expression

2007-10-02 | GSE7895 | GEO

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

Bronchial airway gene expression reflects a COPD-associated field of injury that changes with disease severity and is reversible with therapy

Project description:RNA was isolated from bronchial brushings obtained from current and former smokers with and without COPD. mRNA expression was profiled using Affymetrix Human Gene 1.0 ST Arrays.

2013-03-22 | GSE37147 | GEO

Smoking modulates different secretory subpopulations expressing SARS-CoV-2 entry genes in the nasal and bronchial airways (BCLHS bronchial brushings)

2022-10-25 | GSE210272 | GEO

Bronchial Airway Gene Expression in Smokers with Lung or Head and Neck Cancer

Project description:Cigarette smoking is the major cause of cancers of the respiratory tract, including non-small cell lung cancer (NSCLC) and head and neck cancer (HNC). In order to better understand carcinogenesis of the lung and upper airways, we have compared the gene expression profiles of tumour-distant, histologically normal bronchial biopsy specimens obtained from current smokers with NSCLC or HNC (SC, considered as a single group), as well as non-smokers (NS) and smokers without cancer (SNC). RNA from a total of 97 biopsies was used for gene expression profiling (Affymetrix HG-U133 Plus 2.0 array). Differentially expressed genes were used to compare NS, SNC, and SC, and functional analysis was carried out using Ingenuity Pathway Analysis (IPA). Smoking-related cancer of the respiratory tract was found to affect the expression of genes encoding xenobiotic biotransformation proteins, as well as proteins associated with crucial inflammation/immunity pathways and other processes that protect the airway from the chemicals in cigarette smoke or contribute to carcinogenesis. Finally, we used the prediction analysis for microarray (PAM) method to identify gene signatures of cigarette smoking and cancer, and uncovered a 15-gene signature that distinguished between SNC and SC with an accuracy of 83%. Thus, gene profiling of histologically normal bronchial biopsy specimens provided insight into cigarette-induced carcinogenesis of the respiratory tract and gene-signatures of cancer in smokers.

2014-05-24 | E-MTAB-1690 | biostudies-arrayexpress

PI3K pathway activity in the normal airway of smokers with lung cancer, and in smokers with airway dysplasia

Project description:Cytologically normal airway epithelial samples were collected during bronchoscopy of current and former smokers. Subjects enrolled in this study were either under suspicion of having lung cancer, had dysplasia in their airway, or were a healthy current, former or never smoker. We supplemented existing GEO series (GSE4115 and GSE7895) with the samples in this study to explore PI3K pathway activity in the these cohorts. This study contains: 2 arrays from smokers with COPD (no lung cancer), 1 array from smoker without COPD (no lung cancer); 2 samples from patients with lung cancer, 2 samples from patients without lung cancer; 20 samples from 10 matched individuals with airway dysplasia before and after treatment with myo-inositol, 6 additional samples from individuals with airway dysplasia; 27 samples from mammary epithelial cells used in oncogenic pathway analysis that have either the PI3K pathway activated, the Np63 pathway activated, or are a GFP control.

2010-04-11 | E-GEOD-12815 | biostudies-arrayexpress

Clinical study of the effect of combined treatment of aspirin and zileuton on biomarkers of tobacco-related carcinogenesis in current smokers

Project description:A chemopreventive effect of aspirin (ASA) on lung cancer risk is supported by epidemiologic and preclinical studies. Zileuton, a 5-LOX inhibitor has single agent activity and adds to the activity of NSAIDs in preclinical models of tobacco carcinogenesis We hypothesized that COX inhibitor + 5-LOX inhibitor may be more effective than placebo in modulating nasal epithelium gene signatures of tobacco exposure and lung cancer. We conducted a randomized, double-blinded study of low dose ASA plus zileuton vs. double placebo in current smokers to compare modulating effects on nasal epithelium gene expression and arachidonic acid (AA) metabolism. Sixty-three participants were randomized to combined treatment of ASA (81 mg QD) and zileuton (Zyflo CR) two 600 mg extended release tablets BID or placebo pills for 12 weeks. Combined ASA plus zileuton had minimal effects on nasal gene expression of nasal or bronchial gene expression signatures associated with smoking, lung cancer and chronic obstructive pulmonary disease but did favorably modulate a bronchial gene signature of squamous dysplasia. Combined ASA plus zileuton suppressed urinary leukotriene (LTE4) (change of 89.867±68.35 from baseline to 32.25±23.25, p <0.001), a surrogate of 5-LOX mediated AA metabolism but did not suppress urinary prostaglandin E2 metabolite (PGEM), a surrogate of cyclooxygenase-mediated AA metabolism. In conclusion, combined COX and 5-LOX inhibition by combined low dose ASA with zileuton in smokers favorably modulated a bronchial squamous dysplasia gene expression signature in the nasal epithelium of current smokers but had minimal effects on other carcinogenesis gene signatures. This combination decreased 5-LOX but not COX-2 mediated AA metabolism. Nasal gene expression signature determination is a novel approach to biomarker analysis, giving an approximation of the pulmonary milieu without having to perform invasive tissue sampling.

2022-06-29 | GSE175616 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data