E-MTAB-6558
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6558 | ExpressionAtlas | 2025-01-23
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-6558-analysis-methods.tsv | Tabular | |||
| E-MTAB-6558-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-6558-configuration.xml | Xml | |||
| E-MTAB-6558-percentile-ranks.tsv | Tabular | |||
| E-MTAB-6558.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 189 |
Similar Datasets
Project description:Transcriptional profiling of blood exposure response gene signature across clinical studies on The Tobacco Heating System 2.2 (THS 2.2) dataset 2
2025-01-23 | E-MTAB-6559 | ExpressionAtlas
Project description:As part of current harm reduction strategies, candidate modified risk tobacco products (MRTP)s are developed to offer adult smokers who want to continue using tobacco products as an alternative to cigarettes while potentially reducing individual risk and population harm compared to smoking cigarettes. One of these candidate MRTPs is the Tobacco Heating System (THS) 2.2 which does not burn tobacco, but instead heats it, thus producing significantly reduced levels of harmful and potentially harmful constituents (HPHC)s compared with combustible cigarettes (CC). The assessment of MRTPs against combustible cigarettes requires the establishment of exposure-response markers. Biomarkers derived from blood offer for the general population a less invasive alternative than sampling the primary site, such as the airways. Various diseases and exposures, including cigarette smoke, have been shown to alter the molecular profile of the blood. Leveraging this fact, a whole blood derived gene signature that can distinguish current smokers from either non-smokers or former smokers with high specificity and sensitivity was previously reported. Four controlled, parallel randomized groups, open-label clinical studies were conducted with subjects randomized to three groups: (1) switching from CCs to THS2.2 (or its mentholated version, respectively); (2) continuous use of CC; or (3) smoking abstinence. These studies had an investigational period of five days in confinement which was followed by an 85 day ambulatory period for two of them. By measuring biomarkers of exposure to selected HPHCs, these studies showed a consistent reduced exposure in subjects that either stopped smoking or switched to THS2.2 (including mentholated version), compared with subjects who continued smoking their own cigarettes at both day 5 and at day 90. To complement the classical exposure measurements, we tested the small signature consisting of only 11 genes on the blood transcriptome of subjects enrolled in the clinical studies. We show that in all four clinical studies tested, the signature scores were consistently reduced in subjects that either stopped smoking or switched to THS2.2 compared with subjects who continued smoking their conventional tobacco products at both day 6 and at day 91.
2019-06-30 | E-MTAB-6558 | biostudies-arrayexpress
Project description:As part of current harm reduction strategies, candidate modified risk tobacco products (MRTP)s are developed to offer adult smokers who want to continue using tobacco products as an alternative to cigarettes while potentially reducing individual risk and population harm compared to smoking cigarettes. One of these candidate MRTPs is the Tobacco Heating System (THS) 2.2 which does not burn tobacco, but instead heats it, thus producing significantly reduced levels of harmful and potentially harmful constituents (HPHC)s compared with combustible cigarettes (CC). The assessment of MRTPs against combustible cigarettes requires the establishment of exposure-response markers. Biomarkers derived from blood offer for the general population a less invasive alternative than sampling the primary site, such as the airways. Various diseases and exposures, including cigarette smoke, have been shown to alter the molecular profile of the blood. Leveraging this fact, a whole blood derived gene signature that can distinguish current smokers from either non-smokers or former smokers with high specificity and sensitivity was previously reported. Four controlled, parallel randomized groups, open-label clinical studies were conducted with subjects randomized to three groups: (1) switching from CCs to THS2.2 (or its mentholated version, respectively); (2) continuous use of CC; or (3) smoking abstinence. These studies had an investigational period of five days in confinement which was followed by an 85 day ambulatory period for two of them. By measuring biomarkers of exposure to selected HPHCs, these studies showed a consistent reduced exposure in subjects that either stopped smoking or switched to THS2.2 (including mentholated version), compared with subjects who continued smoking their own cigarettes at both day 5 and at day 90. To complement the classical exposure measurements, we tested the small signature consisting of only 11 genes on the blood transcriptome of subjects enrolled in the clinical studies. We show that in all four clinical studies tested, the signature scores were consistently reduced in subjects that either stopped smoking or switched to THS2.2 compared with subjects who continued smoking their conventional tobacco products at both day 6 and at day 91.
2019-06-30 | E-MTAB-6559 | biostudies-arrayexpress
Project description:As part of current harm reduction strategies, candidate modified risk tobacco products (MRTP) are developed to offer adult smokers who want to continue using tobacco product an alternative to cigarettes while potentially reducing individual risk and population harm compared to smoking cigarettes. One of these candidate MRTPs is the Tobacco Heating System (THS) 2.2 which does not burn tobacco, but instead heats it, thus producing significantly reduced levels of harmful and potentially harmful constituents (HPHC) compared with combustible cigarettes (CC). A controlled, parallel group, open-label clinical study was conducted with subjects randomized to three monitored groups: (1) switching from CCs to THS2.2; (2) continuous use of non-menthol CC brand (CC arm); or (3) smoking abstinence (SA arm) for five days. Exposure response was assessed by measuring biomarkers of exposure to selected HPHCs. To complement the classical exposure response measurements, we have used the previously reported whole blood derived gene signature that can distinguish current smokers from either non-smokers or former smokers with high specificity and sensitivity. We tested the small signature consisting of only 11 genes on the blood transcriptome of subjects enrolled in the clinical study and showed a reduced exposure response in subjects that either stopped smoking or switched to a candidate MRTP, the THS2.2, compared with subjects who continued smoking their regular tobacco product.
2017-08-05 | E-MTAB-5332 | biostudies-arrayexpress
Project description:Transcription profiling of blood from smokers, non-smokers and former smokers to identify gene expression signature for cigarette smoke exposure response
2025-01-23 | E-MTAB-5279 | ExpressionAtlas
Project description:Gene expression signatures help to provide a global and robust view of biological processes in normal and pathological situations. Additionally, such signatures can be used in toxicology to assess both the level and impact of toxicant exposure, which is in line with the 21st century vision of toxicology. An 11 gene signature extracter by Martin et al. assist us in the evaluation of the reduction in exposure response in subjects enrolled in PMI clinical trials for THS 2.2 and THS 2.2 menthol assessment. The signature was applied to gene expression profiles from blood after 5-day cessation confinement studies, which showed a consistent decrease of the signature scores. Similarly, upon switching to THS2.2 for 5 days, a significant decrease in the signature score was consistently observed. Finally, in a study where a 5-day confinement period was followed by an 85-day ambulatory period, a similar decrease was observed for both cessation and switching to mentholated THS2.2.
2017-08-05 | E-MTAB-5333 | biostudies-arrayexpress
Project description:AIM: To investigate the molecular, structural, and functional impact of aerosols from two heat-not-burn-based MRTPs, the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of cigarette mainstream smoke (CS) on the cardiovascular system of ApoE-/- mice. METHOD: Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from 3R4F for up to 6 months at matching nicotine concentrations. A cessation and a switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated using echocardiography, histopathology, immunohistochemistry, and transcriptomics. RESULTS: Continuous exposure to aerosols from CHTP 1.2 and THS 2.2 did not affect the atherosclerosis progression, heart function, left ventricular structure and cardiovascular transcriptome. Exposure to CS from 3R4F triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart left ventricle hypertrophy and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, smoking cessation and switching to CHTP 1.2 aerosol similarly improved the structural, functional, and molecular changes caused by 3R4F CS. CONCLUSION: Exposure to aerosols from CHTP 1.2 and THS 2.2 lacked most of the CS exposure-related functional, structural and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused a similar recovery from the 3R4F CS effect in the ApoE-/- model with no further acceleration of plaque progression beyond the aging-related rate.
2021-08-16 | E-MTAB-7981 | biostudies-arrayexpress
Project description:AIM: To investigate the molecular, structural, and functional impact of aerosols from two heat-not-burn-based MRTPs, the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of cigarette mainstream smoke (CS) on the cardiovascular system of ApoE-/- mice. METHOD: Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from 3R4F for up to 6 months at matching nicotine concentrations. A cessation and a switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated using echocardiography, histopathology, immunohistochemistry, and transcriptomics. RESULTS: Continuous exposure to aerosols from CHTP 1.2 and THS 2.2 did not affect the atherosclerosis progression, heart function, left ventricular structure and cardiovascular transcriptome. Exposure to CS from 3R4F triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart left ventricle hypertrophy and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, smoking cessation and switching to CHTP 1.2 aerosol similarly improved the structural, functional, and molecular changes caused by 3R4F CS. CONCLUSION: Exposure to aerosols from CHTP 1.2 and THS 2.2 lacked most of the CS exposure-related functional, structural and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused a similar recovery from the 3R4F CS effect in the ApoE-/- model with no further acceleration of plaque progression beyond the aging-related rate.
2021-08-16 | E-MTAB-7980 | biostudies-arrayexpress
Project description:Smoking is one of the major modifiable risk factors in the development and progression of chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD). Modified-risk tobacco products (MRTP) are being developed to provide substitute products for smokers who are unable or unwilling to quit, to lessen the smoking-related health risks. In this study, the ApoE-/- mouse model was used to investigate the impact of cigarette smoke (CS) from the reference cigarette 3R4F, or aerosol from two potential MRTPs based on the heat-not-burn principle, carbon-heated tobacco product 1.2 (CHTP 1.2) and tobacco heating system 2.2 (THS 2.2), on the cardiovascular and respiratory system over a 6-month period. In addition to chronic exposure, cessation or switching to CHTP1.2 after 3 months of CS exposure was assessed. A systems toxicology approach combining physiology, histology and molecular measurements (transcriptomics and proteomics) was used to evaluate the impact of MRTP aerosols in comparison to CS. The current data represent the lung transcriptomics analysis. Note that the animal identifier (CAN) can be used for sample matching across different sample types and data modalities.
2019-04-18 | E-MTAB-7444 | biostudies-arrayexpress
Project description:Smoking is one of the major modifiable risk factors in the development and progression of chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD). Modified-risk tobacco products (MRTP) are being developed to provide substitute products for smokers who are unable or unwilling to quit, to lessen the smoking-related health risks. In this study, the ApoE-/- mouse model was used to investigate the impact of cigarette smoke (CS) from the reference cigarette 3R4F, or aerosol from two potential MRTPs based on the heat-not-burn principle, carbon-heated tobacco product 1.2 (CHTP 1.2) and tobacco heating system 2.2 (THS 2.2), on the cardiovascular and respiratory system over a 6-month period. In addition to chronic exposure, cessation or switching to CHTP1.2 after 3 months of CS exposure was assessed. A systems toxicology approach combining physiology, histology and molecular measurements (transcriptomics and proteomics) was used to evaluate the impact of MRTP aerosols in comparison to CS. The current data represent the lung transcriptomics analysis. Note that the animal identifier (CAN) can be used for sample matching across different sample types and data modalities.
2019-04-18 | E-MTAB-7892 | biostudies-arrayexpress