Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA191639 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Epigenomics is developing a colon cancer screening assay based on differential methylation of specific CpG sites for the detection of early stage disease. A genome-wide methylation analysis and oligonucleotide array study using DNA from various stages of colon cancer and normal tissue have been completed to obtain candidate CpG markers. Based on results obtained in the above studies, Epigenomics has moved to the final stages of feasibility with a specific, highly sensitive real-time marker assay that is able to detect colon cancer DNA in blood plasma.
| 2056787 | ecrin-mdr-crc
Project description:Background: The obesity epidemic and the aging population of many western countries together with their associated diseases are major challenges for the healthcare. As obesity is a risk factor for many age related diseases, such as cancer, it is of importance to understand their interaction and the underlying molecular mechanisms. Lately, epigenetic programming in the form of DNA methylation and have been recognized for its importance in aging, obesity and several diseases. Method: Herein, the methylation level was determined for around 27000 CpG-islands in 46 DNA samples from adult peripheral blood with microarrays. The dependence for each CpG island with age, obesity and their interaction was ascertained with a general linear model. Results: The methylation level of more than 100 genomic sites were significantly altered with increasing age together with 10 additional sites that were differentially methylated with age in obese and lean individuals. The majority of the genomic sites were hypermethylated during aging, including the telomerase catalytic subunit (TERT). However, age dependent hypermethylation was prohibited or reverted in 8 of 10 regions in obese where an interaction between age and obesity was observed. Moreover, one region (LINC00304) was differentially methylated in obese and lean. Conclusion: This study provides evidence for an obesity influence on age driven epigenetic changes, which provide a molecular link between aging and obesity. This link and the identified markers may prove to be valuable biomarkers for the understanding of the molecular basis of aging, obesity and associated diseases. Bisulphite converted DNA from the 24 obese and 22 lean women were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2
2014-07-09 | E-GEOD-44763 | biostudies-arrayexpress
Project description:Background: The obesity epidemic and the aging population of many western countries together with their associated diseases are major challenges for the healthcare. As obesity is a risk factor for many age related diseases, such as cancer, it is of importance to understand their interaction and the underlying molecular mechanisms. Lately, epigenetic programming in the form of DNA methylation and have been recognized for its importance in aging, obesity and several diseases. Method: Herein, the methylation level was determined for around 27000 CpG-islands in 46 DNA samples from adult peripheral blood with microarrays. The dependence for each CpG island with age, obesity and their interaction was ascertained with a general linear model. Results: The methylation level of more than 100 genomic sites were significantly altered with increasing age together with 10 additional sites that were differentially methylated with age in obese and lean individuals. The majority of the genomic sites were hypermethylated during aging, including the telomerase catalytic subunit (TERT). However, age dependent hypermethylation was prohibited or reverted in 8 of 10 regions in obese where an interaction between age and obesity was observed. Moreover, one region (LINC00304) was differentially methylated in obese and lean. Conclusion: This study provides evidence for an obesity influence on age driven epigenetic changes, which provide a molecular link between aging and obesity. This link and the identified markers may prove to be valuable biomarkers for the understanding of the molecular basis of aging, obesity and associated diseases.
2014-07-09 | GSE44763 | GEO
Project description:Epidemiological studies in humans suggest that acquired paternal traits, such as obesity, are associated with a higher risk of fathering small for gestational age offspring. Studies in non-human mammals suggest that such associations could be mediated by DNA methylation changes in spermatozoa that influence offspring development in utero. Human obesity is associated with differential DNA methylation in peripheral blood. It is unclear, however, whether this differential DNA methylation is reflected in less readily available tissues such as spermatozoa. In this study, we profiled genome-wide DNA methylation with the Infinium MethylationEPIC array in matched samples of human blood and sperm from lean (discovery n = 47; replication n = 21) and obese (n = 22) healthy males of proven fertility. To characterize sperm-specific DNA methylation signatures, we compared spermatozoal DNA methylation data to that of nearly 6,000 somatic tissue samples available on the Gene Expression Omnibus database. We studied covariation patterns between whole blood and sperm and investigated consistent obesity-associated DNA methylation differences.
2020-05-03 | GSE149318 | GEO
Project description:Obesity-associated asthma is recognized as a distinct entity with non-atopic T-helper 1 polarized systemic inflammation. DNA methylation is linked with T helper cell maturation and is associated with inflammatory patterns in asthma and obesity. However, it is unknown whether pathologic dysregulation of DNA methylation patterns occurs in obesity-associated asthma. Using HELP-tagging, we studied epigenome wide DNA methylation in peripheral blood mononuclear cells in 8 urban minority obese asthmatic pre-adolescent children and compared it to methylation in groups of 8 children with asthma alone, obesity alone and healthy controls. Ingenuity Pathway Analysis was used to identify biological pathways that were differentially targeted by methylation dysregulation. We found that obese asthmatics had distinct epigenome wide methylation patterns associated with decreased promoter methylation of a subset of genes, including RANTES, IL-12R and TBX21 and increased promoter methylation of CD23, a low affinity receptor for IgE and of TGFM-NM-2, inhibitor of Th cell activation. T cell signaling and macrophage activation were the two primary pathways that were selectively hypomethylated in obese asthmatics. These methylation patterns suggest that methylation is associated with non-atopic inflammation observed in obese asthmatic children compared to children with asthma alone and obesity alone. Our findings suggest a role of DNA methylation in the observed inflammatory patterns in pediatric obesity-associated asthma in minorities. 32 HpaII test
2014-04-14 | E-GEOD-43705 | biostudies-arrayexpress
Project description:The purpose of the current study was to use an epigenome-wide association approach (EWAS) to identify a potential DNA methylation alterations associated with obesity using twins discordant on obesity status. Buccal cells (from a cheek swab) were used as a purified marker cell for the epigenetic analysis. Analysis of differential DNA methylation regions (DMRs) was used to identify epigenetic associations with metabolic and dietary measures in obesity parameters discordant twins. An edgeR analysis provided a DMR signature with p<1e-04, but a false discovery rate analysis demonstrated a lack of significance due to low sample size and known multivariant origins of obesity.
2023-02-18 | GSE218363 | GEO
Project description:Obesity-associated asthma is recognized as a distinct entity with non-atopic T-helper 1 polarized systemic inflammation. DNA methylation is linked with T helper cell maturation and is associated with inflammatory patterns in asthma and obesity. However, it is unknown whether pathologic dysregulation of DNA methylation patterns occurs in obesity-associated asthma. Using HELP-tagging, we studied epigenome wide DNA methylation in peripheral blood mononuclear cells in 8 urban minority obese asthmatic pre-adolescent children and compared it to methylation in groups of 8 children with asthma alone, obesity alone and healthy controls. Ingenuity Pathway Analysis was used to identify biological pathways that were differentially targeted by methylation dysregulation. We found that obese asthmatics had distinct epigenome wide methylation patterns associated with decreased promoter methylation of a subset of genes, including RANTES, IL-12R and TBX21 and increased promoter methylation of CD23, a low affinity receptor for IgE and of TGFβ, inhibitor of Th cell activation. T cell signaling and macrophage activation were the two primary pathways that were selectively hypomethylated in obese asthmatics. These methylation patterns suggest that methylation is associated with non-atopic inflammation observed in obese asthmatic children compared to children with asthma alone and obesity alone. Our findings suggest a role of DNA methylation in the observed inflammatory patterns in pediatric obesity-associated asthma in minorities.
2014-04-14 | GSE43705 | GEO
Project description:Markers of biological ageing have potential utility in primary care and public health. We developed a model of age based on untargeted metabolic profiling across multiple platforms, including nuclear magnetic resonance spectroscopy and liquid chromatography-mass spectrometry in urine and serum, within a large sample (N=2,239) from the UK Airwave cohort. We validated a subset of model predictors in a Finnish cohort including repeat measurements from 2,144 individuals. DNA methylation age was assessed for 1,110 participants using the Infinium HumanMethylation EPIC BeadChip. We investigated the determinants of accelerated ageing, including lifestyle and psychological risk factors for premature mortality. The metabolomic age model was well correlated with chronological age (mean r=0.86 across independent test sets). Increased metabolomic age acceleration (mAA) was associated after false discovery rate (FDR) correction with overweight/obesity, diabetes, heavy alcohol use and depression. DNA methylation age acceleration measures were uncorrelated with mAA. Increased DNA methylation phenotypic age acceleration (N = 1,110) was associated after FDR correction with heavy alcohol use, hypertension and low income. In conclusion, metabolomics is a promising approach for the assessment of biological age and appears complementary to established epigenetic clocks.
2020-05-19 | GSE147740 | GEO
Project description:It is evident that epigenetic factors, especially DNA methylation, play essential roles in obesity development. To learn systematic association of DNA methylation to obesity, we used pig as a model, and sampled eight diverse adipose tissues and two distinct skeletal muscle tissues from three pig breeds with distinguished fat levels: the lean Landrace, the fatty Rongchang, and the feral Tibetan pig. We sequenced 180 methylated DNA immunoprecipitation (MeDIP) libraries, generated 1,381 Gbp sequence data, and provided a genome-wide DNA methylation map for pig adipose and muscle studies. The analysis showed global similarities and differences between breeds, genders and tissues, and identified the differentially methylated regions (DMRs) that are preferentially located in intermediate CpG promoters and CpG island shores. The DMRs in promoters are highly associated to obesity development. We also analyzed methylation and regulation of the known obesity-related genes and predicted novel candidate genes. The comprehensive map here provides a solid base for exploring epigenetic mechanisms of adipose deposition and muscle growth. We collected eight diverse adipose tissues and two phenotypically distinct skeletal muscle tissues from three well-defined pig models with distinct fat rates, and studied genome-wide DNA methylation differences among breeds, males and females, and tissues.
2012-05-16 | E-GEOD-30344 | biostudies-arrayexpress
Project description:DNA methylation variations are prevalent in human obesity but evidence of a causative role in disease pathogenesis is limited. Here, we combine epigenome-wide association and integrative genomics to investigate the impact of adipocyte DNA methylation variations in human obesity. We discover extensive DNA methylation changes that are robustly associated with obesity (N=190 samples, 691 loci in subcutaneous and 173 loci in visceral adipocytes, P<1x10-7). We connect obesity-associated methylation variations to transcriptomic changes at >500 target genes, and identify putative methylation-transcription factor interactions. Through Mendelian Randomisation, we infer causal effects of methylation on obesity and obesity-induced metabolic disturbances at 59 independent loci. Targeted methylation sequencing, CRISPR-activation and gene silencing in adipocytes, further identifies regional methylation variations, underlying regulatory elements and novel cellular metabolic effects. Our results indicate DNA methylation is an important determinant of human obesity and its metabolic complications, and reveal mechanisms through which altered methylation may impact adipocyte functions.
2023-04-14 | GSE222595 | GEO