Project description:Polycomb-mediated repression of Dkk-1 activates Wnt signaling and enhances tumorigenic potential of lung cancer cells following tobacco smoke exposure Experiment Overall Design: microarray techniques were used to examine proliferation and gene expression in A549 and Calu-6 lung cancer cells cultured in normal media with or without tobacco smoke condensate (TSC)

2009-04-19 | E-GEOD-13309 | biostudies-arrayexpress

E-GEOD-15092

Project description:The effects of PTIP on Polycomb mediated repression in Drosophila Kc167 cells.

2014-10-08 | E-GEOD-15092 | ExpressionAtlas

Role of tobacco smoke on lung response to crystalline silica exposure in rats

Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of lung toxicity in response to crystalline silica exposure. Nevertheless, the precise role of tobacco smoke exposure on the lung response to tobacco smoke exposure and the underlying mechanisms remain largely elusive. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary toxicity and the underlying molecular mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in rats exposed to air, crystalline silica, tobacco smoke, or crystalline silica plus tobacco smoke. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by tobacco smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to tobacco smoke, silica or a combination of both compared with the air exposed control rats.

2024-12-31 | GSE149286 | GEO

Effect of tobacco smoke exposure cessation on lung response to crystalline silica exposure in rats

Project description:Our previous studies have shown that tobacco smoke exposure exacerbated the lung response to crystalline silica exposure in rats. The objective of the present study, a follow-up to our previous study, was to determine the effect of tobacco smoke exposure cessation on the lung response to crystalline silica exposure in the rats. Rats were exposed to air, crystalline silica (1 week followed by a 1 year progression/recovery period with no exposure), tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure), or crystalline silica (1 week) plus tobacco smoke (6 months of exposure followed by 6 months of recovery with no exposure). Lung toxicity was determined at the end of the 1-year progression/recovery period in all 4 groups of the rats. Silica exposure resulted in significant lung toxicity which was further exacerbated by tobacco smoke exposure in the rats. Cessation of cigarette smoke exposure did not result in reversal of the silica-induced lung toxicity despite exacerbation of the toxicity by tobacco smoke.

2024-12-31 | GSE155924 | GEO

Threshold of Biologic Response of the Small Airway Epithelium to Low Levels of Tobacco Smoke

Project description: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. Results: There was no threshold of urine nicotine without an abnormal small airway epithelial response, and only a slightly above detectable threshold abnormal response for cotinine. The nicotine ID50 for nicotine was 25 ng/ml and cotinine 104 ng/ml. Conclusions: The small airway epithelium detects and responds to low levels of tobacco smoke with transcriptome modifications. This provides biologic correlates of epidemiologic studies linking low level tobacco smoke exposure to lung health risk, health, identifies genes in the lung cells most sensitive to tobacco smoke and defines thresholds at the lung epithelium responds to inhaled tobacco smoke.

2011-02-02 | GSE19667 | GEO

Comparison of the Biological Effects of Long-Term Treatment of Human Bronchial Epithelial Cells with 3R4F Cigarette Smoke or THS2.2 Aerosol Total Particulate Matter (mRNA data)

Project description:Cigarette smoking is the leading cause of lung cancer worldwide. Carcinogens in smoke produced during the combustion of cigarette tobacco are responsible for airway epithelial changes underlying lung carcinogenesis. Reduction of harmful constituents by heating rather than combusting tobacco would be a sound strategy to reduce the risk for lung cancer. In this study we characterized the functional and molecular changes during long-term treatment of human bronchial epithelial cells with total particulate matter (TPM) from a new candidate modified risk tobacco product (cMRTP), the tobacco heated system 2.2 (THS2.2) in comparison with TPM from combustible 3R4F reference cigarettes.

2018-03-08 | E-MTAB-5697 | biostudies-arrayexpress

Comparison of the Biological Effects of Long-Term Treatment of Human Bronchial Epithelial Cells with 3R4F Cigarette Smoke or THS2.2 Aerosol Total Particulate Matter (microRNA data)

2018-03-08 | E-MTAB-6119 | biostudies-arrayexpress

E-MTAB-8155

Project description:Repeated exposure and switching study of cigarette smoke and next generation tobacco product using 3D human bronchial epithelial cells

2025-01-16 | E-MTAB-8155 | ExpressionAtlas

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