Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EGAS00001005450-sc-2024-07-23T09:57:46Z - samples

ABSTRACT: The complexity of tobacco smoke induced mutagenesis in head and neck cancer - copy number variants (Mutographs)

PROVIDER: EGAD00001015390 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

EGAS00001005450-sc-2024-07-23T10:04:47Z - samples

Project description:The complexity of tobacco smoke induced mutagenesis in head and neck cancer - sequence data (Mutographs)

| EGAD00001015386 | EGA

EGAS00001005450-sc-2024-07-23T09:47:45Z - samples

Project description:The complexity of tobacco smoke induced mutagenesis in head and neck cancer - filtered vcf files (Mutographs)

| EGAD00001015388 | EGA

EGAS00001005450-sc-2024-07-23T09:38:56Z - samples

Project description:The complexity of tobacco smoke induced mutagenesis in head and neck cancer - patient metadata files (Mutographs)

| EGAD00001015387 | EGA

EGAS00001005450-sc-2024-07-23T09:51:24Z - samples

Project description:The complexity of tobacco smoke induced mutagenesis in head and neck cancer - structural variation vcf files (Mutographs)

| EGAD00001015389 | EGA

Tobacco Smoke Induces Polycomb-mediated Repression of Dickkopf-1 in Lung Cancer Cells

Project description:Polycomb-mediated repression of Dkk-1 activates Wnt signaling and enhances tumorigenic potential of lung cancer cells following tobacco smoke exposure Keywords: tobacco Smoke, lung cancer, epigenetics

2009-04-10 | GSE13309 | GEO

Effects of Cigarette Smoke on the Human Oral Mucosal Transcriptome

Project description:40 current smokers and 40 age- and gender- matched never smokers underwent buccal biopsies.The study had four objectives: (a) to define the effects of smoking on the transcriptome of oral epithelial cells; (b) to determine if any of the effects of tobacco smoke on the transcriptome are gender-dependent; (c) to compare the effects of tobacco smoke exposure on the transcriptome in oral v. bronchial epithelium and (d) to identify agents with the potential to suppress the effects of tobacco smoke on the transcriptome. We used microarrays to provide new insights into the carcinogenic effects of tobacco smoke and offer insights that may prove useful in developing preventive strategies.

2010-02-15 | GSE17913 | GEO

Transcriptomic and barrier responses of human airway epithelial cells exposed to cannabis smoke with and without LABA/GC intervention

Project description:Purpose: Globally, many jurisdictions are legalizing or decriminalizing cannabis, creating a potential public health issue that would benefit from experimental evidence to inform policy, government regulations, and user practices. Tobacco smoke exposure science has created a body of knowledge that demonstrates the conclusive negative impacts on respiratory health; similar knowledge remains to be established for cannabis. To address this unmet need, we performed in vitro functional and transcriptomic experiments with a human airway epithelial cell line (Calu-3) exposed to cannabis smoke, with tobacco smoke as a positive control. Results: We demonstrate that cannabis smoke induced functional and transcriptional responses that overlapped with tobacco smoke. Ontology and pathway analysis revealed that cannabis smoke induced DNA replication and oxidative stress responses. Functionally, cannabis smoke impaired epithelial cell barrier function, antiviral responses, and increased inflammatory mediator production. Our study reveals striking similarities between cannabis and tobacco smoke exposure on impairing barrier function, suppressing antiviral pathways, potentiating of pro-inflammatory mediators, and inducing oncogenic and oxidative stress gene expression signatures. LABA/GC intervention in airway epithelial cells exposed to cannabis smoke reduces levels of pro-inflammatory (CXCL8) and antiviral (CXCL10) mediators, while transcriptomic signatures of neutrophil mediated immunity and oxidative stress remain elevated. Conclusions: Collectively our data suggest that cannabis smoke exposure is not innocuous and may possess many of the deleterious properties of tobacco smoke, warranting additional studies to support public policy, government regulations, and user practices.

2020-01-28 | GSE125259 | GEO

Molecular alterations elicited by chronic exposure to cigarette smoke and chewing tobacco in oral keratinocytes

Project description:Tobacco is mainly consumed in two different forms (smoking and chewing) that vary in their composition and methods of intake. Despite being the leading cause of oral cancer, the molecular mechanisms resulting in malignancy upon tobacco exposure are yet to be fully elucidated. We therefore sought to compare the molecular alterations in oral keratinocytes exposed to smoke and chewing tobacco. OKF6/TERT1 cells were exposed to cigarette smoke condensate or chewing tobacco for progressively increasing durations (2, 4, 6 and 8 months). We employed a TMT-based quantitative proteomics approach to investigate the adverse effects of chronic cigarette smoke or chewing tobacco exposure in oral keratinocytes. LC/MS3 analysis resulted in the quantification of 5,342 proteins and 2,821 proteins in cigarette smoke and chewing tobacco exposed cells, respectively. Upstream regulator analysis indicates the involvement of distinct regulators in CSC exposed cells compared to STE exposed cells. In addition, exome sequencing revealed discrete genetic alterations in cells exposed to each insult. Current analysis defines a clear distinction in the molecular dysregulation in oral cells in response to different tobacco-based insults. Some of the proteins dysregulated in cigarette smoke or chewing tobacco exposed cells may serve as potential early detection biomarkers which could aid in stratification of patients based on tobacco usage history.

2019-11-08 | PXD007127 | Pride

Effect of cigarette smoke on gene expression in mammary epithelial cells [gene expression]

Project description:Recent epidemiological studies demonstrate that both active and involuntary exposure to tobacco smoke increases the risk of breast cancer. Little is known, however, about the molecular mechanisms by which tobacco smoke contributes to breast carcinogenesis. To investigate these mechanisms we have analyzed gene expression and methylation in MCF 10A mammary epithelial cells chronically exposed to aqueous cigarette smoke extract (CSE).

2013-08-12 | GSE42667 | GEO