Ontology highlight
ABSTRACT:
PROVIDER: PRJNA175630 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR575338.fastq.gz | Fastqsanger.gz | |||
| SRR575339.fastq.gz | Fastqsanger.gz | |||
| SRR575340.fastq.gz | Fastqsanger.gz | |||
| SRR575341.fastq.gz | Fastqsanger.gz | |||
| SRR575342.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE41048: Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues (ChIP-Seq and MeDIP-Seq) GSE41049: Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues (Gene Expression data) Refer to individual Series
2012-09-24 | E-GEOD-41050 | biostudies-arrayexpress
Project description:Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues (Gene Expression data)
| PRJNA175632 | ENA
Project description:Epigenetic polymorphism and the stochastic formation of differentially methylated regions in normal and cancerous tissues (ChIP-Seq and MeDIP-Seq)
| PRJNA175631 | ENA
Project description:DNA methylation has been comprehensively profiled in normal and cancer cells, but the dynamics that form, maintain and reprogram differentially methylated regions remain enigmatic. We show that methylation patterns within populations of cells from individual somatic tissues are heterogeneous and polymorphic. Using in vitro evolution of immortalized fibroblasts for over 300 generations, we track the dynamics of polymorphic methylation at regions developing significant differential methylation on average. The data indicate that changes in population-averaged methylation occur through a stochastic process that generates a stream of local and uncorrelated methylation aberrations. Despite the stochastic nature of the process, nearly deterministic epigenetic remodeling emerges on average at loci that lose or gain resistance to methylation accumulation. Changes in the susceptibility to methylation accumulation are correlated with changes in histone modifications and CTCF occupancy. Characterizing epigenomic polymorphism within cell populations is therefore critical for understanding methylation dynamics in normal and cancer cells. Gene expression profiled in duplicate throughout the microevolutionary timecourse using Affymetrix Gene 1.0 ST arrays.
2012-09-24 | E-GEOD-41049 | biostudies-arrayexpress
Project description:DNA methylation has been comprehensively profiled in normal and cancer cells, but the dynamics that form, maintain and reprogram differentially methylated regions remain enigmatic. We show that methylation patterns within populations of cells from individual somatic tissues are heterogeneous and polymorphic. Using in vitro evolution of immortalized fibroblasts for over 300 generations, we track the dynamics of polymorphic methylation at regions developing significant differential methylation on average. The data indicate that changes in population-averaged methylation occur through a stochastic process that generates a stream of local and uncorrelated methylation aberrations. Despite the stochastic nature of the process, nearly deterministic epigenetic remodeling emerges on average at loci that lose or gain resistance to methylation accumulation. Changes in the susceptibility to methylation accumulation are correlated with changes in histone modifications and CTCF occupancy. Characterizing epigenomic polymorphism within cell populations is therefore critical for understanding methylation dynamics in normal and cancer cells.
2012-09-24 | GSE41049 | GEO
Project description:DNA methylation has been comprehensively profiled in normal and cancer cells, but the dynamics that form, maintain and reprogram differentially methylated regions remain enigmatic. We show that methylation patterns within populations of cells from individual somatic tissues are heterogeneous and polymorphic. Using in vitro evolution of immortalized fibroblasts for over 300 generations, we track the dynamics of polymorphic methylation at regions developing significant differential methylation on average. The data indicate that changes in population-averaged methylation occur through a stochastic process that generates a stream of local and uncorrelated methylation aberrations. Despite the stochastic nature of the process, nearly deterministic epigenetic remodeling emerges on average at loci that lose or gain resistance to methylation accumulation. Changes in the susceptibility to methylation accumulation are correlated with changes in histone modifications and CTCF occupancy. Characterizing epigenomic polymorphism within cell populations is therefore critical for understanding methylation dynamics in normal and cancer cells.
2012-09-24 | GSE41048 | GEO
Project description:DNA methylation has been comprehensively profiled in normal and cancer cells, but the dynamics that form, maintain and reprogram differentially methylated regions remain enigmatic. We show that methylation patterns within populations of cells from individual somatic tissues are heterogeneous and polymorphic. Using in vitro evolution of immortalized fibroblasts for over 300 generations, we track the dynamics of polymorphic methylation at regions developing significant differential methylation on average. The data indicate that changes in population-averaged methylation occur through a stochastic process that generates a stream of local and uncorrelated methylation aberrations. Despite the stochastic nature of the process, nearly deterministic epigenetic remodeling emerges on average at loci that lose or gain resistance to methylation accumulation. Changes in the susceptibility to methylation accumulation are correlated with changes in histone modifications and CTCF occupancy. Characterizing epigenomic polymorphism within cell populations is therefore critical for understanding methylation dynamics in normal and cancer cells. Genomewide sequencing data is included herein: H3K27me3 profiled throughout the microevolutionary timecourse using ChIP-seq, DNA methylation profiled through the timecourse using MeDIP-seq, and H3K4me3 and CTCF profiled in late and early timepoints using ChIP-seq. Deep Bisulfite sequencing amplicon data and results can be obtained at: http://compgenomics.weizmann.ac.il/tanay/?page_id=99 .
2012-09-24 | E-GEOD-41048 | biostudies-arrayexpress
Project description:Compared with non-cancerous lung tissues, lung cancer in Xuanwei tissues expressed a total of 6,899 differentially methylated regions, including 5,788 hypermethylated regions and 1,111 hypomethylated regions. Many differentially methylated regions have been found in lung cancer in Xuanwei.
2018-04-21 | GSE113432 | GEO
Project description:DNA methylation (5-mC) and hydroxymethylation (5-hmC) are regarded as important epigenetic hallmarks in the carcinogenesis of colorectal cancer by transcriptional regulation. 5hmC is an intermediate during active demethylation and maintains the equilibrium of DNA methylation. Previous studies on DNA methylation don’t differentiate 5-hmC from 5-mC. Here, in order to elucidate the epigenetic mechanisms of carcinogenesis of colorectal cancer, we integrate genome wide levels of 5-mC, 5-hmC and Transcriptional expression. 12 samples, including six colorectal tumor tissues and corresponding normal colonic tissues were recruited after surgery. Genome-wide DNA methylation was determined by methylated DNA immune- precipitation sequencing (MeDIP-seq), and hydroxymethylation by hydroxyl- methylated DNA immune-precipitation sequencing (hMedip-seq). Transcriptional expression was determined by RNA-seq. Group-wise different methylation region (DMR), different hydroxyl methylation region (DhMR) and different expressed gene (DEG) were identified. Epigenetic biomarkers were screened by integrating DMR, DhMR and DEG. We found that a genome-scale distinct hydroxymethylation pattern could be used as epigenetic biomarker for clearly differentiating colorectal cancer from normal tissues. 59249 differentially methylated regions (DMR), 187172 differentially hydroxymethylated region (DhMR) and 948 differentially expressed genes (DEGs) were identified. After cross-matched genes containing DMRs or DhMRs with DEGs, seven genes were screened. Furthermore, hypermethylation of HADHB was persistently found to be correlated with its down-regulation of transcription in CRC, potentially suggesting its role as TSG. The differences of methylation, hydroxymethylation and transcriptional expression in HADHB between cancerous and normal tissues were validated among additional colorectal cancer patients. To further validate this assumption, we also performed functional analysis and found that the expression of HADHB obviously reduced cancer cells migration and invasiveness. This study provided valuable basic data for screening epigenetic biomarkers and elucidated the epigenetic mechanisms of carcinogenesis of colorectal cancer.
2018-12-31 | GSE87096 | GEO
Project description:A field for cancerization, or a field defect, is formed by the accumulation of genetic and epigenetic alterations in normal-appearing tissues, and is involved in various cancers, especially multiple cancers. Epigenetic alterations are frequently present in chronic inflammation-exposed tissues, but information on individual genes involved in the formation of a field defect is still fragmental. Here, using noncancerous gastric tissues of cancer patients, we isolated 16 aberrantly methylated genes, and identified chromatin remodelers ACTL6B and SMARCA1 as novel genes frequently methylated in non-cancerous tissues. SMARCA1 was expressed at high levels in normal gastric tissues, but was frequently silenced by aberrant methylation in gastric cancer cells. Moreover, somatic mutations of additional chromatin remodelers, such as ARID1A, SMARCA2, and SMARCA4, were found in 30% of gastric cancers. Mutant allele frequency suggested that the majority of cancer cells harbored a mutation when present. Depletion of a chromatin remodeler, SMARCA1 or SMARCA2, in cancer cell lines promoted their growth. These results showed that epigenetic and genetic alterations of chromatin remodelers are induced at an early stage of carcinogenesis and are frequently involved in the formation of a field defect.
2022-08-31 | GSE211580 | GEO