Colon
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00010002200 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Small Intestine Crypt - EPIC Methylation Array
| EGAD00010002201 | EGA
Project description:DNA of 124 normal mucosa biopsies from cecum (proximal) and sigmoid (distal) colon obtained at baseline (t1) and after 10years (t2) from 31 screening females was subjected to measure DNA methylation profiles by Illumina Infinium EPIC Human Methylation BeadChip across approximately 850,000 CpGs.
2020-11-09 | GSE142257 | GEO
Project description:The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation. 5 normal colon samples and 4 matching tumor samples were profiled for 5-hydroxymethylcytosine content genomewide using hmeDIP-seq. The colorectal cancer cell line HCT116 was profiled for binding of TET2 genomewide by chromatin immunoprecipitation sequencing (ChIP-seq).
2015-02-03 | E-GEOD-47590 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal colon samples. The Illumina Infinium HumanMethylation450 and EPIC Beadchip arrays were used to obtain DNA methylation profiles across approximately 450,000 and 850,000 CpGs. Samples were from nomal colons of 334 subjects with low, medium or high CRC risk according to their personal adenoma or cancer history.
2019-12-31 | GSE132804 | GEO
Project description:We aimed to investigate genome wide DNA methylation changes in human colon organoids in which the BRAF-V600E mutation was introduced by means of CRISPR genome editing and in BRAF-wildtype human colon cancer organoids. DNA methylation analysis was performed using the Infinium Methylation EPIC beadchip at the Pathology department of the UMC Utrecht (The Netherlands).
2023-12-20 | E-MTAB-13290 | biostudies-arrayexpress
Project description:We aimed to investigate genome wide DNA methylation changes in human colon cancer organoids with the BRAF-V600E mutation and in human colon cancer organoids in which the BRAF-V600E mutation was corrected by means of CRISPR genome editing. DNA methylation analysis was performed using the Infinium Methylation EPIC beadchip at the Pathology department of the UMC Utrecht (The Netherlands).
2023-12-20 | E-MTAB-13283 | biostudies-arrayexpress
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. Two samples were analyzed by MeDIP-CGI microarray. One is a pool of two AOM/DSS-induced colon tumors in BALB/c mice and another is a pool of two normal colonic epithelial cell samples obtained from untreated BALB/c mice by the crypt isolation technique. The pool of normal colonic epithelial cell samples was used as reference. Dye-swaps were not perfromed. The methylation statuses of CGIs identified by microarray were confirmed by another method, methylation-specific PCR.
2011-06-30 | E-GEOD-21333 | biostudies-arrayexpress
Project description:The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation. messenger RNA levels were measured in total RNA extracted from primary colon tissues. Normal away are at least 20cm from tumors.
2015-02-03 | E-GEOD-47063 | biostudies-arrayexpress
Project description:The discovery of cytosine hydroxymethylation (5-hmC) as a mechanism that potentially controls DNA methylation changes typical of neoplasia prompted us to investigate its behavior in colon cancer. 5-hmC is globally reduced in proliferating cells such as colon tumors and the gut crypt progenitors, from which tumors can arise. Here, we show that colorectal tumors and cancer cells express Ten-Eleven Translocation (TET) transcripts at levels similar to normal tissues. Genome-wide analyses show that promoters marked by 5-hmC in normal tissue, and those identified as TET2 targets in colorectal cancer cells, are resistant to methylation gain in cancer. In vitro studies of TET2 in cancer cells confirm that these promoters are resistant to methylation gain independently of sustained TET2 expression. We also find that a considerable number of the methylation gain-resistant promoters marked by 5-hmC in normal colon overlap with those that are marked with poised bivalent histone modifications in embryonic stem cells. Together our results indicate that promoters that acquire 5-hmC upon normal colon differentiation are innately resistant to neoplastic hypermethylation by mechanisms that do not require high levels of 5-hmC in tumors. Our study highlights the potential of cytosine modifications as biomarkers of cancerous cell proliferation. DNA methylation levels were measured in genomic DNA extracted from primary colon tissues.
2015-02-03 | E-GEOD-47071 | biostudies-arrayexpress