DNA methylation of colorectal cancer stem cells
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ABSTRACT:
PROVIDER: PRJNA508506 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Colorectal Cancer DNA Methylation
| PRJNA699596 | ENA
Project description:Colorectal cancer stem cells (CR-CSCs) are implicated in tumor development, metastasis, and therapy resistance, however little is known about their epigenetic features. Here we describe the DNA methylation profiles of eight CR-CSC lines and their distinctive patterns, which are maintained following in vivo passages in immune-compromised mice.
2020-01-15 | GSE123367 | GEO
Project description:DNA methylation in colorectal cancer diagnosis. The Illumina GoldenGate Methylation Cancer Panel I was used to select a set of candidates markers informative of colorectal cancer diagnosis from 807 cancer-related genes. In the discovery phase, tumor tissue and paired adjacent normal mucosa from 92 colorectal patients were analyzed.
2013-05-27 | GSE43369 | GEO
Project description:To characterize DNA methylation-based subgroups in colorectal cancer, we performed genome-scale DNA methylation profiling of 125 colorectal tumor samples and 29 histologically normal-adjacent colonic tissue samples using the Illumina Infinium DNA methylation assay, which assesses the DNA methylation status of 27,578 CpG sites located at the promoter regions of 14,495 protein-coding genes. We identified four DNA methylation-based subgroups of CRC using model-based cluster analyses. Each subtype shows characteristic genetic and clinical features, indicating that they represent biologically distinct subgroups. Bisulfite converted DNA from fresh frozen 125 colorectal tumors and 29 adjacent normal tissues were hybridized to the Illumina Infinium 27k Human Methylation Beadchip v1.2
2011-06-03 | E-GEOD-25062 | biostudies-arrayexpress
Project description:Genetic and epigenetic alterations are a fundamental aspect of colorectal cancer formation. There is considerable heterogeneity between colorectal cancers regarding the mutations and methylated genes they carry, and this heterogeneity may arise early in the polyp-cancer sequence. However, our understanding of the epigenetic alterations and gene mutations in colon adenomas and their relation to colorectal cancer is incomplete. Thus, we have assessed the methylome in normal colon mucosa, tubular adenomas, and colorectal adenocarcinomas and have determined the relationship of these findings between adenomas and cancer in the colon. Genome-wide alterations in DNA methylation were found in the normal colon mucosa adjacent to colorectal cancer, tubular adenomas, and colorectal cancer. Three subgroups of CRCs and two subgroups of adenomas were identified on the basis of their DNA methylation patterns. The adenomas separated into a high-frequency methylation class (Adenoma-H) and a low-frequency methylation class. The adenoma-H polyps have a methylated DNA signature similar to non-CIMP CRCs, whereas those of the Adenoma-L class have a similar methylation pattern to normal colon mucosa. The CpGs that account for these signatures are located in intragenic/intergenic regions, which suggests that these two groups of adenomas arise from different stem cell populations. We conducted genome-wide array-based studies and comprehensive data analyses of aberrantly methylated loci in 41 normal colon samples, 42 colon adenomas, and 64 colorectal cancers. Supplementary file 'GSE48684_Matrix_signal_intensities_1.txt.gz': includes the unmethylated and methylated signal intensities from Samples GSM1183439-GSM1183561. Supplementary file 'GSE48684_Matrix_signal_intensities_2.txt.gz': includes the unmethylated and methylated signal intensities from Samples GSM1235135-GSM1235158.
2014-09-08 | E-GEOD-48684 | biostudies-arrayexpress
Project description:DNA methylation in colorectal cancer diagnosis. The Illumina GoldenGate Methylation Cancer Panel I was used to select a set of candidates markers informative of colorectal cancer diagnosis from 807 cancer-related genes. In the discovery phase, tumor tissue and paired adjacent normal mucosa from 92 colorectal patients were analyzed. Bisulphite converted DNA from 92 colorectal tumor samples and paired adjacent normal mucosa were hybridised to the Illumina GoldenGate Methylation Cancer Panel I. Additionally, replicates were hybridised for five tumor tissue and their corresponding normal mucosa for reproducibility purposes, totalling 194 samples. Three samples (SAMPLEs 49, 51, and 162) and 50 loci did not reach the quality criteria required regarding the signal-to-noise ratio and were therefore excluded from further analysis. One additional non-tumoral sample (SAMPLE 15) was removed because it exhibited a methylation pattern quiet different from that shown by the rest of normal specimens, which could be indicative of hybridization errors. These Samples and loci are included in the raw data matrix to allow other investigators to use them if different criteria are applied. They have been also included in the Sample tables with missing values in order to preserve the structure of the data across records/files (See 'data processing' section for more details).
2013-05-27 | E-GEOD-43369 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal and tumor colorectal cancer samples, HCT116 DKO (DNMT1 (-/-) and DNMT3b (-/-)), M.sssI treated DKO cell lines, and human cervical cancer cell line HeLa. The Illumina Infinium Human DNA methylation EPIC Beadchip was used to obtain DNA methylation profiles across approximately 85,000 CpGs in the above samples.
2017-05-17 | GSE98990 | GEO
Project description:Genome wide DNA methylation profiling of colorectal cancer cell lines treated with acetyl-11-keto-β-boswellic acid (AKBA) or 5-aza-2’-deoxycytidine (DAC). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in the colorectal cancer cell line SW48. Samples included non-treated, AKBA-treated, and DAC-treated SW48 cells. Bisulphite converted DNA from the 3 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2
2012-12-01 | E-GEOD-32275 | biostudies-arrayexpress
Project description:To characterize DNA methylation-based subgroups in colorectal cancer, we performed genome-scale DNA methylation profiling of 125 colorectal tumor samples and 29 histologically normal-adjacent colonic tissue samples using the Illumina Infinium DNA methylation assay, which assesses the DNA methylation status of 27,578 CpG sites located at the promoter regions of 14,495 protein-coding genes. We identified four DNA methylation-based subgroups of CRC using model-based cluster analyses. Each subtype shows characteristic genetic and clinical features, indicating that they represent biologically distinct subgroups.
2011-06-03 | GSE25062 | GEO
Project description:Genetic and epigenetic alterations are a fundamental aspect of colorectal cancer formation. There is considerable heterogeneity between colorectal cancers regarding the mutations and methylated genes they carry, and this heterogeneity may arise early in the polyp-cancer sequence. However, our understanding of the epigenetic alterations and gene mutations in colon adenomas and their relation to colorectal cancer is incomplete. Thus, we have assessed the methylome in normal colon mucosa, tubular adenomas, and colorectal adenocarcinomas and have determined the relationship of these findings between adenomas and cancer in the colon. Genome-wide alterations in DNA methylation were found in the normal colon mucosa adjacent to colorectal cancer, tubular adenomas, and colorectal cancer. Three subgroups of CRCs and two subgroups of adenomas were identified on the basis of their DNA methylation patterns. The adenomas separated into a high-frequency methylation class (Adenoma-H) and a low-frequency methylation class. The adenoma-H polyps have a methylated DNA signature similar to non-CIMP CRCs, whereas those of the Adenoma-L class have a similar methylation pattern to normal colon mucosa. The CpGs that account for these signatures are located in intragenic/intergenic regions, which suggests that these two groups of adenomas arise from different stem cell populations.
2014-09-08 | GSE48684 | GEO