Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

An epigenome-wide DNA methylation study conducted on 96 patients six months after COVID-19 infection reveals biological age acceleration and increased epigenetic drift.

ABSTRACT: An epigenome-wide DNA methylation study conducted on 96 patients six months after COVID-19 infection reveals biological age acceleration and increased epigenetic drift.

PROVIDER: PRJNA1040842 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

An epigenome-wide DNA methylation study conducted on 96 patients six months after COVID-19 infection reveals biological age acceleration and increased epigenetic drift.

Project description:We performed a whole-genome DNA methylation analysis using EPIC Illumina BeadArrays on blood samples of a cohort of 96 individuals collected six months after COVID-19 infection.

2024-09-10 | GSE247869 | GEO

Transcription profiling of rat mixed-tissue RNA samples over 8.5 months to monitor processing drift

Project description:Process drift at one site was monitored by assaying the rat Mixed Tissue RNA Reference Material (see E-TABM-16) multiple times a week for 8.5 months.

2008-04-16 | E-MEXP-1565 | biostudies-arrayexpress

Implications of epigenetic drift in colorectal neoplasia

Project description:Many normal tissues undergo age-related DNA methylation drift providing a quantitative measure of tissue age. However this drift has not been demonstrated in neoplastic tissues. Here we identify and validate 781 CpG-islands (CGIs) that undergo significant methylomic drift in normal colorectal tissues continue to drift in neoplasia and remain significantly correlated with one another across tissue samples. However compared with normal colon this drift advances (~3-4 fold) faster in neoplasia consistent with increased cell proliferation during neoplastic progression. Furthermore we show that the observed drift patterns are broadly consistent with modeled adenoma-carcinoma sojourn time distributions from colorectal cancer (CRC) incidence data. These results support the hypothesis that beginning with the founder premalignant cell cancer precursors frequently sojourn for decades before turning into cancer which implies that the founder cell typically arises early in life. We estimate that at least 77-89% of the observed drift variance in distal and rectal tumors is explained by stochastic variability associated with neoplastic progression while only 55% of the variance is explained for proximal tumors. However >50% of identified gene-CGI pairs in the proximal colon that undergo drift are significantly and mainly negatively correlated with cancer gene expression suggesting that methylomic drift participates in the clonal evolution of CRCs. Significance: Methylomic drift advances in colorectal neoplasia consistent with extended sojourn time distributions explaining a significant fraction of epigenetic heterogeneity in CRCs. Importantly the estimated long-duration premalignant sojourn times suggest that early dietary and lifestyle interventions may be more effective than later changes in reducing CRC incidence.

2019-04-19 | GSE113904 | GEO

Time makes histone H3 modifications drift

Project description:To disclose the epigenetic drift of time passing, we determined the genome-wide distributions of mono- and tri-methylated lysine 4 and acetylated and tri-methylated lysine 27 of histone H3 in the livers of healthy 3, 6 and 12 months old C57BL/6 mice. The comparison of different age profiles of histone H3 marks revealed global redistribution of histone H3 modifications with time, in particular in intergenic regions and near transcription start sites, as well as altered correlation between the profiles of different histone modifications. Moreover, feeding mice with caloric restriction diet, a treatment known to retard aging, preserved younger state of histone H3 in these genomic regions.

2022-07-13 | GSE179090 | GEO

Identification of a key role of widespread epigenetic drift in Barrett’s esophagus and esophageal adenocarcinoma

Project description:Our analysis reveals an extensive methylomic drift between normal squamous esophagus and BE tissues in nonprogressed BE patients, with differential drift affecting 4024 (24%) of 16,984 normally hypomethylated cytosine-guanine dinucleotides (CpGs) occurring in CpG islands. The majority (63%) of islands that include drift CpGs are associated with gene promoter regions. Island CpGs that drift have stronger pairwise correlations than static islands, reflecting collective drift consistent with processive DNA methylation maintenance. Individual BE tissues are extremely heterogeneous in their distribution of methylomic drift and encompass unimodal low-drift to bimodal high-drift patterns, reflective of differences in BE tissue age. Further analysis of longitudinally collected biopsy samples from 20 BE patients confirm the time-dependent evolution of these drift patterns. Drift patterns in EAC are similar to those in BE, but frequently exhibit enhanced bimodality and advanced mode drift. To better understand the observed drift patterns, we developed a multicellular stochastic model at the CpG island level. Importantly, we find that nonlinear feedback in the model between mean island methylation and CpG methylation rates is able to explain the widely heterogeneous collective drift patterns. Using matched gene expression and DNA methylation data in EAC from TCGA and other publically available data, we also find that advanced methylomic drift is correlated with significant transcriptional repression of ~ 200 genes in important regulatory and developmental pathways, including several checkpoint and tumor suppressor-like genes. Taken together, our findings suggest that epigenetic drift evolution acts to significantly reduce the expression of developmental genes that may alter tissue characteristics and improve functional adaptation during BE and EAC progression.

2017-10-31 | GSE104707 | GEO

Acinetobacter baumannii strain:96 | isolate:96

Project description:Acinetobacter baumannii strain:96 | isolate:96 Genome sequencing and assembly

| PRJNA939738 | ENA

Klebsiella pneumoniae strain:219-96 | isolate:219-96

Project description:Klebsiella pneumoniae strain:219-96 | isolate:219-96 Genome sequencing

| PRJNA1182961 | ENA

Time makes histone H3 modifications drift

Project description:Time makes histone H3 modifications drift

| PRJNA742128 | ENA

Bradyrhizobium japonicum strain:USDA 96 | isolate:USDA 96

Project description:Bradyrhizobium japonicum USDA 96 genome sequencing