COHCAP: City of Hope CpG Island Analysis Pipeline
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PROVIDER: PRJNA181146 | ENA |
REPOSITORIES: ENA
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Project description:COHCAP (City of Hope CpG Island Analysis Pipeline) is an algorithm to analyze single-nucleotide resolution DNA methylation data. It provides QC metrics, differential methylation for CpG Sites, differential methylation for CpG Islands, integration with gene expression data, and visualization of methylation values. COHCAP is currently the only DNA methylation package that can handle integration with gene expression data, and the results of this study show that COHCAP can identify regions of differential methylation with ~50% concordance with gene expression. COHCAP is scalable for analysis of both cell line data and heterogeneous patient data, and it can identify known cancer biomarkers as well as intriguing new roles of epigenetic regulation in cancer (such as methylation of estrogen receptor in breast cancer patients). This study also uses cell line data to show that COHCAP is capable of analyzing Illumina methylation array and targeted bisulfite sequencing data, with either 1-group or 2-group study designs. The accuracy of COHCAP is accessed using qPCR, EpiTect, and comparison of COHCAP regions of differential methylation with MIRA peaks. This software is freely available at https://sourceforge.net/projects/cohcap/. The following third-party datasets were utilized in the paper: BS-Seq data: GSE26826 Additional Microarray Data: GSE29290 This SuperSeries is composed of the SubSeries listed below.
2013-06-08 | GSE42310 | GEO
Project description:COHCAP (City of Hope CpG Island Analysis Pipeline) is an algorithm to analyze single-nucleotide resolution DNA methylation data. It provides QC metrics, differential methylation for CpG Sites, differential methylation for CpG Islands, integration with gene expression data, and visualization of methylation values. COHCAP is currently the only DNA methylation package that can handle integration with gene expression data, and the results of this study show that COHCAP can identify regions of differential methylation with ~50% concordance with gene expression. COHCAP is scalable for analysis of both cell line data and heterogeneous patient data, and it can identify known cancer biomarkers as well as intriguing new roles of epigenetic regulation in cancer (such as methylation of estrogen receptor in breast cancer patients). This study also uses cell line data to show that COHCAP is capable of analyzing Illumina methylation array and targeted bisulfite sequencing data, with either 1-group or 2-group study designs. The accuracy of COHCAP is accessed using qPCR, EpiTect, and comparison of COHCAP regions of differential methylation with MIRA peaks. This software is freely available at https://sourceforge.net/projects/cohcap/. The following third-party datasets were utilized in the paper: BS-Seq data: GSE26826 Additional Microarray Data: GSE29290 This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.
2013-06-08 | E-GEOD-42310 | biostudies-arrayexpress
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. Keywords: ordered
2005-07-03 | GSE2653 | GEO
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: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:Astrocytomas are common and lethal human brain tumors. Here, we have analyzed the methylation status of over 28,000 CpG islands and 18,000 promoters in normal human brain and in astrocytomas of various grades using the methylated-CpG island recovery assay (MIRA). We identified six to seven thousand methylated CpG islands in normal human brain. ~5% of the promoter-associated CpG islands in normal brain are methylated. Promoter CpG island methylation is inversely and intragenic methylation is directly correlated with gene expression levels in brain tissue. In astrocytomas, several hundred CpG islands undergo specific hypermethylation relative to normal brain with 428 methylation peaks common to more than 25% of the tumors. Genes involved in brain development and neuronal differentiation, such as POU4F3, GDNF, OTX2, NEFM, CNTN4, OTP, SIM1, FYN, EN1, CHAT, GSX2, NKX6-1, RAX, PAX6, DLX2, were strongly enriched among genes frequently methylated in tumors. There was an overrepresentation of homeobox genes and 31% of the most commonly methylated genes represent targets of the Polycomb complex. We identified several chromosomal loci in which many (sometimes more than 20) consecutive CpG islands were hypermethylated in tumors. Seven of such loci were near homeobox genes, including the HOXC and HOXD clusters, and the BARHL2, DLX1, and PITX2 genes. Two other clusters of hypermethylated islands were at sequences of recent gene duplication events. Our analysis offers mechanistic insights into brain neoplasia suggesting that methylation of genes involved in neuronal differentiation, perhaps in cooperation with other oncogenic events, may shift the balance from regulated differentiation towards gliomagenesis.
2010-01-01 | GSE19391 | GEO
Project description:Astrocytomas are common and lethal human brain tumors. Here, we have analyzed the methylation status of over 28,000 CpG islands and 18,000 promoters in normal human brain and in astrocytomas of various grades using the methylated-CpG island recovery assay (MIRA). We identified six to seven thousand methylated CpG islands in normal human brain. ~5% of the promoter-associated CpG islands in normal brain are methylated. Promoter CpG island methylation is inversely and intragenic methylation is directly correlated with gene expression levels in brain tissue. In astrocytomas, several hundred CpG islands undergo specific hypermethylation relative to normal brain with 428 methylation peaks common to more than 25% of the tumors. Genes involved in brain development and neuronal differentiation, such as POU4F3, GDNF, OTX2, NEFM, CNTN4, OTP, SIM1, FYN, EN1, CHAT, GSX2, NKX6-1, RAX, PAX6, DLX2, were strongly enriched among genes frequently methylated in tumors. There was an overrepresentation of homeobox genes and 31% of the most commonly methylated genes represent targets of the Polycomb complex. We identified several chromosomal loci in which many (sometimes more than 20) consecutive CpG islands were hypermethylated in tumors. Seven of such loci were near homeobox genes, including the HOXC and HOXD clusters, and the BARHL2, DLX1, and PITX2 genes. Two other clusters of hypermethylated islands were at sequences of recent gene duplication events. Our analysis offers mechanistic insights into brain neoplasia suggesting that methylation of genes involved in neuronal differentiation, perhaps in cooperation with other oncogenic events, may shift the balance from regulated differentiation towards gliomagenesis. Comparison of methylation patterns of 30 astrocytomas and 6 controls
2010-05-16 | E-GEOD-19391 | biostudies-arrayexpress
Project description:Tissue-specific methylation patterns suggest a role for CpG island methylation in differentiation and cell-type-specific gene regulation. We have profiled CpG island methylation in different cells of the immune cell lineage to investigate this role. MBD-affinity purification combined with next generation sequencing was used to analyse CpG island methylation in dendritic cells, B cells, Th1, Th2 and naïve T cells. ChIP-seq was carried out to determine RNA polymerase II binding sites in these cell types and this was compared to the methylation profiles obtained. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ Abstract: We have profiled CpG island methylation in various immune system cell types and related this to gene expression in these cells.
2011-11-10 | E-ERAD-27 | biostudies-arrayexpress
Project description:In mammalian genomes, the vast majority of RNA polymerase II initiation events take place at CpG island promoters. Despite their relevance our understanding of their regulation remains limited. Here we identify Banp as the long sought-after TF that binds the orphan CGCG element in CpG islands by combining single-molecule footprinting with interaction proteomics. We show that Banp drives activity of CpG islands that control essential metabolic genes in the mouse and human genome. Banp binding is strongly repelled by DNA methylation of its motif in vitro and in vivo, which restricts most binding to CpG islands and accounts for its absence at aberrantly methylated CpG islands in cancer cells. Upon binding to an unmethylated motif, Banp opens chromatin and positions nucleosomes. These findings expand our understanding of CpG island gene regulation and put forth a model whereby CpG islands rely for their activity on methylation sensitive TFs capable of opening and organizing chromatin.
2021-05-17 | GSE155603 | GEO
Project description:In mammalian genomes, the vast majority of RNA polymerase II initiation events take place at CpG island promoters. Despite their relevance our understanding of their regulation remains limited. Here we identify Banp as the long sought-after TF that binds the orphan CGCG element in CpG islands by combining single-molecule footprinting with interaction proteomics. We show that Banp drives activity of CpG islands that control essential metabolic genes in the mouse and human genome. Banp binding is strongly repelled by DNA methylation of its motif in vitro and in vivo, which restricts most binding to CpG islands and accounts for its absence at aberrantly methylated CpG islands in cancer cells. Upon binding to an unmethylated motif, Banp opens chromatin and positions nucleosomes. These findings expand our understanding of CpG island gene regulation and put forth a model whereby CpG islands rely for their activity on methylation sensitive TFs capable of opening and organizing chromatin.
2021-05-17 | GSE155601 | GEO