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Omics score: 5

Screening for abnormal CGI methylation in primary colorectal tumours

ABSTRACT: A common hallmark of neoplastic cells is abnormal acquisition of CpG island (CGI) methylation and the silencing of associated gene promoters. To determine the extent and distribution of CGI methylation in colorectal cancer, we solexa sequenced MBD affinity purified DNA prepared from five colorectal tumours and matched colon mucosa from the same individuals.

PROVIDER: EGAS00001000076 | EGA |

REPOSITORIES: EGA

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MBD-Seq of human primary colorectal tumours to explore abnormal CGI methylation

Project description:A common hallmark of neoplastic cells is abnormal acquisition of CpG island (CGI) methylation and the silencing of associated gene promoters. To determine the extent and distribution of CGI methylation in colorectal cancer, we solexa sequenced MBD affinity purified DNA prepared from five colorectal tumours and matched colon mucosa from the same individuals.

2012-08-01 | E-ERAD-12 | biostudies-arrayexpress

Functional characterisation of CpG islands in human and mouse tissues

Project description:Tissue-specific methylation patterns suggest a role for CpG island (CGI) methylation in differentiation and cell-type-specific gene regulation. We have applied CXXC affinity purification (CAP), MBD affinity purification (MAP) and chromatin immunoprecipitation (ChIP) in combination with solexa sequencing to investigate the extent and functional significance of CGI methylation in sperm, blood, cerebellum and ES cells for both human and mouse.

| EGAS00001000075 | EGA

Screening for human epigenetic variation at CpG islands

Project description:Many human characteristics, including susceptibility to disease, are determined genetically. An unexplored alternative to such genetic determination concerns epigenetic mechanisms such as DNA methylation. CpG islands (CGIs) are generally constitutively hypomethylated, however there are circumstances in which they become heavily methylated and, when coincident with a gene promoter, this invariably causes transcriptional silencing. CGI methylation occurs in normal tissues during processes such as X-inactivation, but abnormal patterns of methylation have also been implicated in disease. The vast majority of evidence relates to cancer, where silencing of multiple genes in this way appears to be a causal contributor to the cancer state. To address the role and extent of CGI methylation in ‘normal’ and diseased cells we applied MBD-affinity purification in conjunction with next generation sequencing in a panel of human brain autopsy samples. These samples represent a panel of individuals as well as specific brain regions and neurological pathologies.

2012-03-20 | E-ERAD-10 | biostudies-arrayexpress

Functional characterisation of CpG islands in mouse tissues

2012-07-02 | E-ERAD-53 | biostudies-arrayexpress

Functional characterisation of CpG islands in human and mouse tissues

2014-01-21 | E-ERAD-11 | biostudies-arrayexpress

Screening for human epigenetic variation at CpG islands

| EGAS00001000074 | EGA

Comprehensive analysis of orphan CpG islands identifes novel promoters with conserved DNA methylation dynamics

Project description:We report the application of single molecule-based sequencing technology in combination with CXXC affinity purifcation (CAP-seq), MBD affinity purification (MAP-seq) and chromatin immunoprecipitation (ChIP-seq) to generate reciprocal methylation and chromatin modifcation maps in human and mouse. We find that contrary to sequence based prediction methods that humans and mice possess highly equivalent compliments of CpG islands (CGIs). The majority of these CGIs are positive for the active histone modification; H3K4me3 in embryonic stem cells (ES cells) the magnitude of which is correlated with the local density of non-methylated CpG. Approximately half of the human and mouse CGIs are distal to annotated gene promoters, yet more than 40% identify unanticipated transcription start sites as defined by RNA polymerase occupancy and published RNA mapping data. These orphans CGIs preferentially acquire DNA methylation in somatic cells, and this corresponds with a loss of H3K4me3 and RNA polymerase II at these sites. Conversely abnormal CGI methylation found in colorectal tumours showed a distinct distribution relative to that found in normal somatic tissues displaying preferential association with loci marked by H3K27me3 in human ES cells. This study provides a comprehensive functional assessment of CGIs in normal and diseased tissues. Examination of CGI methylation status in human and mouse primary tissues.

2010-10-04 | E-GEOD-21442 | biostudies-arrayexpress

Landscape of genome-wide DNA methylation profile of colorectal cancer metastasis

Project description:Genome-wide DNA methylation of colorectal cancer patients with lymph node metastases showed global loss of DNA methylation in CG-poor, non-CpG island (CGI) regions. Overall CGI methylation was increased in tumour samples. Differential methylation analysis of CGIs identified 60 putative biomarkers, with >20% increase in DNA methylation in both primary tumour and metastasis samples compared to normal adjacent tissue.

2020-11-02 | GSE151318 | GEO

EGAS00001000076-sc-20120802 - samples

Project description:Screening for abnormal CGI methylation in primary colorectal tumours

| EGAD00001000213 | EGA

Smchd1 dependent and independent pathways determine developmental dynamics of CpG island methylation on the inactive X chromosome.

Project description:X chromosome inactivation involves multiple levels of chromatin modification, established progressively and in a stepwise manner during early development. The chromosomal protein Smchd1 has recently been shown to play an important role in DNA methylation of CpG islands (CGIs), a late step in the X inactivation pathway required for long-term stability of gene silencing. Here we show that inactive X chromosome (Xi) CGI methylation can occur via either Smchd1 dependent or independent pathways. Smchd1 dependent CGI methylation, the primary pathway, is acquired gradually over an extended period, whereas Smchd1 independent CGI methylation occurs rapidly after the onset of X inactivation. The de novo methyltransferase Dnmt3b is required for methylation of both classes of CGI, whereas Dnmt3a and Dnmt3L are dispensable. Xi CGIs methylated by these distinct pathways differ in respect to their sequence characteristics and immediate chromosomal environment. We discuss the implications of these results for understanding CGI methylation during development.

2012-10-15 | GSE37333 | GEO

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