DNA methylation profiling in colon cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE39334 | GEO | 2013/01/22
SECONDARY ACCESSION(S): PRJNA170659
REPOSITORIES: GEO
Similar Datasets
Project description:Profiling of CpG island methylation in 19 primary colon cancer and paired normal samples Agilent 244k CpG island microarray
2013-01-22 | E-GEOD-39334 | biostudies-arrayexpress
Project description:Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. We found a strong association between BRAFV600E mutation and downregulation of the DNA demethylases TET1 and TET2. Expression of BRAFV600E in CIMP cancer cells suppressed TET1 transcription, which was sufficient to establish hypermethylation at CIMP genes promoters, including that of TET2. This phenotype was reverted by the BRAFV600E inhibitor vemurafenib. Thus, BRAFV600E, via impairment of cytosine de-methylation, is a genetic driver of CIMP in colon tumorigenesis.
2019-12-18 | GSE124915 | GEO
Project description:Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. We found a strong association between BRAFV600E mutation and downregulation of the DNA demethylases TET1 and TET2. Expression of BRAFV600E in CIMP cancer cells suppressed TET1 transcription, which was sufficient to establish hypermethylation at CIMP genes promoters, including that of TET2. This phenotype was reverted by the BRAFV600E inhibitor vemurafenib. Thus, BRAFV600E, via impairment of cytosine de-methylation, is a genetic driver of CIMP in colon tumorigenesis.
2019-12-18 | GSE108606 | GEO
Project description:Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. We found a strong association between BRAFV600E mutation and downregulation of the DNA demethylases TET1 and TET2. Expression of BRAFV600E in CIMP cancer cells suppressed TET1 transcription, which was sufficient to establish hypermethylation at CIMP genes promoters, including that of TET2. This phenotype was reverted by the BRAFV600E inhibitor vemurafenib. Thus, BRAFV600E, via impairment of cytosine de-methylation, is a genetic driver of CIMP in colon tumorigenesis.
2019-12-18 | GSE98533 | GEO
Project description:Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. We found a strong association between BRAFV600E mutation and downregulation of the DNA demethylases TET1 and TET2. Expression of BRAFV600E in CIMP cancer cells suppressed TET1 transcription, which was sufficient to establish hypermethylation at CIMP genes promoters, including that of TET2. This phenotype was reverted by the BRAFV600E inhibitor vemurafenib. Thus, BRAFV600E, via impairment of cytosine de-methylation, is a genetic driver of CIMP in colon tumorigenesis.
2019-12-18 | GSE98532 | 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:Promoter hypermethylation divides colon cancers into subtypes with and without a CpG island methylator phenotype (CIMP). Here, we performed genome-wide DNA methylation profiling of colonic normal and tumor tissues to dissect development of CpG hypermethylation in colon carcinogenesis. This identified age-environment related versus genetically driven CpG hypermethylation, the latter being associated with CIMP cancers. We found a strong association between BRAFV600E mutation and downregulation of the DNA demethylases TET1 and TET2. Expression of BRAFV600E in CIMP cancer cells suppressed TET1 transcription, which was sufficient to establish hypermethylation at CIMP genes promoters, including that of TET2. This phenotype was reverted by the BRAFV600E inhibitor vemurafenib. Thus, BRAFV600E, via impairment of cytosine de-methylation, is a genetic driver of CIMP in colon tumorigenesis. Genome-wide DNA methylation profiling of adjacent non-tumor colon tissue and colon adenocarcinoma samples. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs. Samples included 8 colon cancer tissues and their associated healthy mucosa (CAM).
2019-12-18 | GSE98531 | 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. Keywords: ordered
2005-07-03 | GSE2653 | GEO
Project description:Introduction: The dynamics of colorectal epigenetics during early carcinogenesis remain undocumented. In this study, we explore the DNA methylation dynamics in colorectal cancer oncogenesis from non-tumor colon tissues to low-grade, high-grade adenoma and adenocarcinoma. Methods: The methylome of 13 low-grade and 19 high-grade colorectal adenomas was determined using the EPIC v1 Human Methylation Beadchip. These methylation profiles were complemented with the methylomes of 206 non-tumor colon and 24 colon adenocarcinomas from GSE149282, GSE132804 series and the HCMI study. Differentially methylated CpG were identified by Student's t-test and used to monitor the evolution of the colon methylome during carcinogenesis. The differentially methylated promoters were used to infer the associated biological process using gene ontology. Results: 4.9% of the colon methylome is significantly altered (p < 10-4) during carcinogenesis with two thirds corresponding to DNA demethylation. 56.6% of the methylation changes occurs at the transition from non-tumor colon tissues to low-grades adenomas. 18.2% of the DNA methylation changes are transitory during low-grade and/or high-grade adenomas. The biological pathways sensory perception of odor and stimulus were early unmethylated, nervous system development and homophilic cell adhesion were early methylated, and chemical synaptic transmission and cell adhesion were transiently methylated. Conclusion: This study provides insight into the dynamics of colonic epigenetics during carcinogenesis, with early DNA methylation changes in the low-grade adenomas associated with transient DNA methylation changes. However, the causality of these changes remains to be elucidated.
2025-12-18 | GSE288652 | GEO
Project description:The methylation status of colon epithelial cells was profiled in wild type mice and mice expressing a Dnmt3b transgene. Genome-scale methylation profiles were generated using reduced representation bisulfite sequencing (RRBS), with CpG methylation scored by promoter and also summarized by gene. Dnmt3b expression is associated with a strong increase in de novo methylation of a discrete subset of "methylation sensitive" genes which show a strong concordance with genes methylated in human colon cancer. These results, together with further analysis, indicate that colon epithelial cell methylation in the Dnmt3b mouse model predicts DNA methylation of human colon cancer with high confidence.
2011-10-26 | GSE26758 | GEO