CpG island methylation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2653 | GEO | 2005/07/03
SECONDARY ACCESSION(S): PRJNA92117
REPOSITORIES: GEO
Similar Datasets
Project description:We compare the methylation status of CpG island clones by MeDIP in SW48 colon cancer cells relative to normal colon mucosa and WI38 primary fibroblasts.
2010-06-09 | E-GEOD-2653 | biostudies-arrayexpress
Project description:We used Illumina Infinium 27k Human DNA Methylation BeadChip v1.2 to assess genome-wide DNA methylation profiling of normal colon epithelial, adenomas and colorectal adenocarcinomas across approximately 27,000 CpGs in fresh frozen colorectal tissue samples. We found that cancer-associated methylation changes with impact on transcription occur nearly as frequent at non-CpG island as CpG island promoters in colorectal cancer (CRC).
2013-06-15 | GSE40055 | GEO
Project description:We used Illumina Infinium 27k Human DNA Methylation BeadChip v1.2 to assess genome-wide DNA methylation profiling of normal colon epithelial, adenomas and colorectal adenocarcinomas across approximately 27,000 CpGs in fresh frozen colorectal tissue samples. We found that cancer-associated methylation changes with impact on transcription occur nearly as frequent at non-CpG island as CpG island promoters in colorectal cancer (CRC). Samples included 6 normal colon epithelial tissue samples, 6 adenomas, and 30 colorectal adenocarcinomas. Bisulfite-converted DNA from the 42 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2.
2013-06-15 | E-GEOD-40055 | biostudies-arrayexpress
Project description:Methylation profiling of CpG Island Methylation of genomic DNA samples extracted from placentae of Intra-Uterine Growth Restricted newborns and gestational age matched controls. These data can be used for methylation comparisons between these two types of samples. The results of such comparisons can be used to generate hypotheses on the involvement of DNA methylation variation in placenta development and fetal growth. Two-condition Methyl DNA Immunoprecipitation (MeDIP) experiment, IUGR vs. Control placenta samples. Biological replicates: 8 control, 8 IUGR cases.
2011-04-11 | E-GEOD-22326 | biostudies-arrayexpress
Project description:The concept of the CpG island methylator phenotype (CIMP) in colorectal cancer (CRC) is widely accepted, though the timing of its occurrence and its interaction with other genetic defects are not fully understood. Our aim in this study was to unravel the molecular development of CIMP cancers by dissecting their genetic and epigenetic signatures in precancerous and malignant colorectal lesions. A total of 88 samples (16 normal colon tissues taken from adjacent tumor tissue, 70 colorectal tumor tissues and 2 cell lines) was analyzed using MCA microarray. Aberrant DNA methylation was compared with clinicopathological features and copy number.
2012-08-31 | E-GEOD-35508 | biostudies-arrayexpress
Project description:Integration of synthetic CpG Free DNA induces de novo DNAme in the flanking CpG island. Cellular differentiation requires global changes to DNA methylation (DNAme), where it functions to regulate transcription factor and chromatin remodeling activity, and genome interpretation. Here, we describe a simple DNAme engineering approach in pluripotent stem cells (PSCs), extending across large stretches of CpG dense “islands (CGIs).” Integration of synthetic CpG free single-stranded DNA (ssDNA) induces a target CpG Island Methylation Response (CIMR) in multiple PSC lines, Nt2d1 embryonal carcinoma cells, and mouse PSCs, but not in highly methylated CpG Island Methylator Phenotype (CIMP) positive cancer lines. CIMR DNAme at MLH1 spans the CGI, is robustly maintained throughout cellular differentiation, suppresses target gene activity, and sensitizes derived cardiomyocytes and thymic epithelial cells to the chemotherapy cisplatin. Additional CIMR DNAme is reported on at TP53 and ONECUT1 CGIs. Collectively, this new resource enables total CpG Island DNAme engineering in pluripotency and the genesis of novel epigenetic models of development and disease
2023-06-21 | GSE210680 | GEO
Project description:In order to elucidate the general rules for gene localization and regulation mediated by CpG islands, we reanalyzed diverse published data of DNaseI-seq, MeDIP-seq, LMNB1-DamID-seq, PolII ChIA-pet, and Hi-C analysis.
2018-02-15 | GSE80795 | GEO
Project description:Genome-wide methylation analysis was performed by methylated DNA immunoprecipitation (MeDIP)-CpG island (CGI) microarray analysis to identify candidate CGIs specifically methylated in mouse colon tumors associated with colitis. We sucessfully identified 23 candidate CGIs methylated in tumors.
2011-06-30 | GSE21333 | GEO
Project description:BACKGROUND & AIM: Sessile serrated adenoma/polyps (SSA/Ps) are the likely culprit of ~20% colon cancers but they are molecularly poorly understood. We investigated their epigenetic phenotype using high-throughput analysis of DNA methylation and gene expression. METHODS: 17 SSA/Ps and, as a comparative group, 15 conventional adenomas (all with matched samples of normal mucosa) were prospectively collected during colonoscopy. DNA from the 64 tissues was analyzed, via bisulfite next generation sequencing, for methylation at ~2.7 million CpG sites located prevalently in gene regulatory regions spanning 80.5Mb (~2.5% of the genome). The transcriptome of these samples was also investigated using RNA sequencing. An independent series of 61 archival lesions was used for targeted verification of DNA methylation. RESULTS: Both SSA/Ps and conventional adenomas showed a profound remodelling of their methylome. Cytosine hypermethylation was more pervasive in SSA/Ps than adenomas, in terms of number of hypermethylated regions (22,147 vs 15,965, respectively) and genes (4938 vs 3443, respectively). In addition, the extent of hypermethylation in a given region was higher in SSA/Ps than adenomas. This methylation pattern of SSA/Ps was reminiscent of the CpG island methylator phenotype (CIMP) of their descendant cancers. We have called this phenotype proto-CIMP since most of the hypermethylation occurred in CpG islands and shores. SSA/Ps were also protected from a wave of demethylation that instead occurred in adenomas outside of CpG islands/shores (4288 vs 18,417 hypomethylated regions in SSAPs vs adenomas). Verification studies of six hypermethylated regions demonstrated the high potential of DNA methylation markers for predicting the diagnosis of SSA/Ps and/or adenomas. Proto-CIMP of SSA/Ps was surprisingly associated with a higher number of up- (618) than downregulated (349) genes, while adenomas showed the opposite trend (516 up- vs 712 downregulated genes). CONCLUSIONS: The epigenetic landscape of SSA/Ps differs substantially from that of conventional adenomas. This huge amount of epigenetic variation represents a rich source of promising diagnostic tools, such as novel DNA markers or histologic stainings, for the tailored management of the two most frequent colon cancer precursors.
2018-11-22 | E-MTAB-6952 | biostudies-arrayexpress
Project description:BACKGROUND & AIM: Sessile serrated adenoma/polyps (SSA/Ps) are the likely culprit of ~20% colon cancers but they are molecularly poorly understood. We investigated their epigenetic phenotype using high-throughput analysis of DNA methylation and gene expression. METHODS: 17 SSA/Ps and, as a comparative group, 15 conventional adenomas (all with matched samples of normal mucosa) were prospectively collected during colonoscopy. DNA from the 64 tissues was analyzed, via bisulfite next generation sequencing, for methylation at ~2.7 million CpG sites located prevalently in gene regulatory regions spanning 80.5Mb (~2.5% of the genome). The transcriptome of these samples was also investigated using RNA sequencing. An independent series of 61 archival lesions was used for targeted verification of DNA methylation. RESULTS: Both SSA/Ps and conventional adenomas showed a profound remodelling of their methylome. Cytosine hypermethylation was more pervasive in SSA/Ps than adenomas, in terms of number of hypermethylated regions (22,147 vs 15,965, respectively) and genes (4938 vs 3443, respectively). In addition, the extent of hypermethylation in a given region was higher in SSA/Ps than adenomas. This methylation pattern of SSA/Ps was reminiscent of the CpG island methylator phenotype (CIMP) of their descendant cancers. We have called this phenotype proto-CIMP since most of the hypermethylation occurred in CpG islands and shores. SSA/Ps were also protected from a wave of demethylation that instead occurred in adenomas outside of CpG islands/shores (4288 vs 18,417 hypomethylated regions in SSAPs vs adenomas). Verification studies of six hypermethylated regions demonstrated the high potential of DNA methylation markers for predicting the diagnosis of SSA/Ps and/or adenomas. Proto-CIMP of SSA/Ps was surprisingly associated with a higher number of up- (618) than downregulated (349) genes, while adenomas showed the opposite trend (516 up- vs 712 downregulated genes). CONCLUSIONS: The epigenetic landscape of SSA/Ps differs substantially from that of conventional adenomas. This huge amount of epigenetic variation represents a rich source of promising diagnostic tools, such as novel DNA markers or histologic stainings, for the tailored management of the two most frequent colon cancer precursors.
2018-11-22 | E-MTAB-6951 | biostudies-arrayexpress