Epigenome-wide profiling of buccal DNAm in samples obtained from children of pregnant smokers enrolled in the VCSIP RCT: NCT03203603
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PROVIDER: PRJNA1058457 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:DNA methylation analysis was performed for buccal samples from children exposed in utero to maternal smoking during pregnancy (with or without vitamin C supplementation) and in a smaller number of non-smoker controls
2024-03-19 | GSE252169 | GEO
Project description:Epigenome-wide profiling of placental DNAm in samples obtained from 72 smokers enrolled in the VCSIP RCT: NCT03203603 (35 supplemented with placebo, 37 supplemented with vitamin C) and 24 never-smokers for reference.
2021-09-20 | GSE169598 | GEO
Project description:Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. Experiment Overall Design: Buccal and nasal epithelial cell samples were collected from healthy current and never smokers. RNA was isolated from these samples and hybridized to Affymetrix microarrays. Gene expression from never smokers was compared to never smoker gene expression from bronchial epithelium as well as expression data from other tissues to determine commonalities in expression patterns in normal extra- and intra-thoracic samples. In addition, gene expression from smokers and nonsmokers was compared in bronchial, nasal, and buccal epithelium to determine similarities in gene expression in these tissues in response to cigarette smoker exposure.
2008-10-20 | E-GEOD-8987 | biostudies-arrayexpress
Project description:RNAseq analysis of placental gene expression in samples obtained from 59 smokers (enrolled in the VCSIP RCT: NCT03203603) and 20 never-smokers for reference.
2024-03-07 | GSE253158 | GEO
Project description:Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. Keywords: cross sectional
2008-07-03 | GSE8987 | GEO
Project description:A tissue like buccal mucosa (from cheek swabs) would be an ideal sample material for rapid, easy collection for testing of biomarkers as an alternative to blood. A limited number of studies, primarily in the smoker/oral cancer literature, address this tissue's efficacy for quantitative PCR or microarray gene expression analysis. In this study both qPCR and microarray analyses were used to evaluate gene expression in buccal cells. An initial study comparing blood and buccal cells from the same individuals looked at relative amounts of four genes. The RNA isolated from buccal cells was degraded but was of sufficient quality to be used with RT-qPCR to detect expression of specific genes. Second, buccal cell RNA was used for microarray-based differential gene expression studies by comparing gene expression between smokers and nonsmokers. The isolation and amplification protocol allowed use of 150-fold less buccal cell RNA than had been reported previously with human microarrays. We report here the finding of a small number of significant gene expression differences between smokers and nonsmokers, using buccal cells as target material. Additionally, Gene Set Enrichment Analysis confirmed that these genes were changing expression in the same pattern as seen in an earlier buccal cell study performed by another group. Our results suggest that in spite of a high degree of RNA degradation, buccal cells from cheek mucosa could be used to detect differential gene expression between smokers and nonsmokers. However the RNA degradation, increase in sample variability and microarray failure rate show that buccal samples should be used with caution as source material in expression studies.
2010-03-01 | GSE16149 | GEO
Project description:A tissue like buccal mucosa (from cheek swabs) would be an ideal sample material for rapid, easy collection for testing of biomarkers as an alternative to blood. A limited number of studies, primarily in the smoker/oral cancer literature, address this tissue's efficacy for quantitative PCR or microarray gene expression analysis. In this study both qPCR and microarray analyses were used to evaluate gene expression in buccal cells. An initial study comparing blood and buccal cells from the same individuals looked at relative amounts of four genes. The RNA isolated from buccal cells was degraded but was of sufficient quality to be used with RT-qPCR to detect expression of specific genes. Second, buccal cell RNA was used for microarray-based differential gene expression studies by comparing gene expression between smokers and nonsmokers. The isolation and amplification protocol allowed use of 150-fold less buccal cell RNA than had been reported previously with human microarrays. We report here the finding of a small number of significant gene expression differences between smokers and nonsmokers, using buccal cells as target material. Additionally, Gene Set Enrichment Analysis confirmed that these genes were changing expression in the same pattern as seen in an earlier buccal cell study performed by another group. Our results suggest that in spite of a high degree of RNA degradation, buccal cells from cheek mucosa could be used to detect differential gene expression between smokers and nonsmokers. However the RNA degradation, increase in sample variability and microarray failure rate show that buccal samples should be used with caution as source material in expression studies. Samples were collected from eight subjects, four smokers (Sm)and four nonsmokers (NS). Each cheek was sampled creating an a and b sample for each subject which is reflected in the array name. All samples were isolated separately for total RNA. Each was hybridzed to microarrays to examine for differential gene expression between smokers and nonsmokers. There are 14 total samples in the main dataset (Set 2). One cheek sample failed in microarray analysis for two individuals, 08BCNS23 a and 08BCSm27 a, and so are not included here. A sample set (Set 1) was created which contains the four samples shown in this file. They represent repeated sampling of both cheeks for two individuals to test for reproducibility. There is a separate RMA file and metadata file (this file) for these data. These included samples 08BC11Sm a and b, a smoker, and 08BC12NSa and b a nonsmoker.
2010-03-07 | E-GEOD-16149 | biostudies-arrayexpress
Project description:Alternations in gene methylation and other epigenetic changes regulate normal development as well as drive disease progression. Chronic cigarette smoking causes hyper- and hypo-methylation of genes that could contribute to smoking-related diseases. It is unclear whether consumers of non-combustible tobacco, such as moist snuff, also exhibit such perturbations in their methylome. Here, we present global methylation changes relative to non-tobacco consumers in buccal cells collected from smokers (SMK) and moist snuff consumers (MSC). Generally healthy adult male study subjects were recruited into SMK, MSC and Non-Tobacco Consumer (NTC) cohorts (40 subjects/cohort). Global methylation profiling was performed on the Illumina 450K methylation array using buccal cell DNA. A total of 1,252 loci were found to be significantly differentially methylated in tobacco consumers relative to non-tobacco consumers. Overall, the SMK cohort exhibited larger qualitative and quantitative changes relative to MSC. Approximately half of the total number of gene loci, classified as Combustible Tobacco-Related signatures, and a third of the changes, termed Tobacco-Related signatures, were commonly detected in the tobacco consumers. Very few differences were detected between MSC and NTC, and hierarchical clustering of the top 50 significant gene loci suggested that MSC and NTC co-cluster. Consistent with physiological functions of AhR, combustible tobacco drives profound changes in buccal cell methylation status, principally impacting cell development and immune response pathways. These results aid in placing combustible and non-combustible tobacco products along a risk continuum and provide additional insights into the effects of tobacco consumption.
2017-12-01 | GSE94876 | GEO
Project description:We determined the global expression profile of DNAM-1+ and DNAM-1- NK cell purified by flow cytometry from 6 different groups of C57BL/6 WT mice. Natural killer (NK) cells comprise a heterogeneous population of cells important for pathogen defense and cancer surveillance. However, the functional significance of this diversity is not fully understood. Here, we demonstrate through transcriptional profiling and functional studies that the activating receptor DNAM-1 (CD226) identifies two distinct NK cell functional subsets: DNAM-1+ and DNAM-1- NK cells. DNAM-1+ NK cells have enhanced Interleukin 15 signaling, proliferate vigorously and produce high levels of inflammatory cytokines. By contrast, DNAM-1- NK cells that differentiate from DNAM-1+ NK cells, have greater expression of NK cell receptor related genes and are higher producers of chemokines. Together our findings highlight the existence of two distinct effector programs in innate lymphocytes controlled through DNAM-1 expression. NK1.1+NKp46+CD3- DNAM-1+ and DNAM-1- NK cell were purified by flow cytometry from 6 different groups of C57BL/6 WT mice and total RNA were extracted
2015-02-26 | E-GEOD-66281 | biostudies-arrayexpress
Project description:The development of current biological markers of aging has primarily focused on adult samples. The epigenetic clock is one promising tool for measuring biological age that shows impressive accuracy across most tissues and age ranges. In adults, deviations from the DNA methylation (DNAm) age prediction are correlated with several agerelated phenotypes, such as mortality and frailty. In children, however, fewer such associations have been made, possibly because DNAm changes are more dynamic in pediatric populations as compared to adults. To address this crucial gap, we aimed to develop a highly accurate, noninvasive biological measure age specific to pediatric samples by using buccal epithelial cell DNAm. We gathered 1,721 genome-wide DNAm profiles from 11 different cohorts of typically developing individuals aged 0 to 20 y old. Elastic net penalized regression was used to select 94 CpG sites from a training dataset (n = 1,032) and the performance was assessed in a separate dataset (n = 689). The DNAm at 94 CpG sites was highly predictive of age in the test cohorts (median absolute error = 0.35 y). The Pediatric-Buccal-Epigenetic (PedBE) clock was characterized in additional cohorts, showcasing the accuracy in longitudinal data, the performance in nonbuccal tissues and adult age ranges, and the association with obstetric outcomes. The PedBE tool for measuring biological age in children might help in understanding the environmental and contextual factors that shape the DNA methylome during child development, and how it, in turn, might relate to child health and disease.
2019-09-17 | GSE137495 | GEO