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Methylated CpG island amplification (MCA) microarray analysis of human colorectal tumors

ABSTRACT: The concept of the CpG island methylator phenotype (CIMP) in colorectal cancer (CRC) is widely accepted, though the timing of its occurrence and its interaction with other genetic defects are not fully understood. Our aim in this study was to unravel the molecular development of CIMP cancers by dissecting their genetic and epigenetic signatures in precancerous and malignant colorectal lesions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35508 | GEO | 2012/08/31

SECONDARY ACCESSION(S): PRJNA156105

REPOSITORIES: GEO

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Methylated CpG island amplification (MCA) microarray analysis of human colorectal tumors

Project description:The concept of the CpG island methylator phenotype (CIMP) in colorectal cancer (CRC) is widely accepted, though the timing of its occurrence and its interaction with other genetic defects are not fully understood. Our aim in this study was to unravel the molecular development of CIMP cancers by dissecting their genetic and epigenetic signatures in precancerous and malignant colorectal lesions. A total of 88 samples (16 normal colon tissues taken from adjacent tumor tissue, 70 colorectal tumor tissues and 2 cell lines) was analyzed using MCA microarray. Aberrant DNA methylation was compared with clinicopathological features and copy number.

2012-08-31 | E-GEOD-35508 | biostudies-arrayexpress

Array CGH analysis of human colorectal tumors

2012-08-31 | GSE35476 | GEO

Array CGH analysis of human colorectal tumors

Project description:The concept of the CpG island methylator phenotype (CIMP) in colorectal cancers (CRCs) is widely accepted, though the timing of its occurrence and its interaction with other genetic defects early during carcinogenesis remains largely unknown. Our aim was to uncover the molecular evolution of CIMP CRCs through integrative analysis of endoscopic, histological and molecular signatures in precancerous and malignant colorectal lesions. A total of 84 endoscopically obtained human colorectal tumor was analyzed using Agilent CGH microarray. Copy number aberration was compared with clinicopathological features and DNA methylation status.

2012-08-31 | E-GEOD-35476 | biostudies-arrayexpress

Transcription profiling of human colorectal cancer samples with CpG island methylator phenotype (CIMP)

Project description:The CpG island methylator phenotype (CIMP) in colorectal tumors can be recognized by an increased frequency of aberrant methylation in a specific set of genomic loci. Because of the strong association of CIMP with high microsatellite instability (MSI-H), the identification of CIMP+ tumors within microsatellite stable (MSS) colorectal cancers may not be straightforward. To overcome this potential limitation, we have built an improved 7-loci set of methylation markers that includes CACNA1G, IGF2, RUNX3, HTR6, RIZ1, MINT31 and MAP1B. This new set of CIMP markers revealed a bimodal distribution of methylation frequencies in a group of 95 MSS colorectal cancers, which allowed a clearer separation between CIMP classes. Correlation of CIMP+ tumors with bio-pathological traits revealed significant associations with location to the proximal colon, mucinous histology and chromosomal stability. Although not statistically significant, a trend toward an adverse prognosis for CIMP+ cases was observed. Microarray analysis revealed that CIMP+ tumors are characterized by a unique expression profile, a result that confirms that CIMP+ tumors represent a distinct molecular class within MSS colorectal cancers. Moreover, our results suggest that this expression pattern may represent the molecular background for the development of CIMP+ tumors that, in turn, develop MSI when aberrant methylation occurs at the MLH1 gene promoter.

2008-01-01 | E-TABM-328 | biostudies-arrayexpress

Methylated CpG island amplification (MCA) microarray analysis of human gastric mucosa and cancer

2012-09-01 | GSE39175 | GEO

Methylated CpG island amplification (MCA) microarray analysis of human gastric mucosa and cancer

Project description:Aberrant DNA methylation is implicated in the epigenetic field defect seen in gastric cancer (GC). Our aim in this study was to identify predictive biomarkers by screening for DNA methylation in noncancerous background gastric mucosa from GC patients. A total of 46 endoscopically obtained human gastric mucosa, 10 gastric cancer and 5 cell lines were analyzed using MCA microarray. Aberrant DNA methylation was compared with clinicopathological features. Healthy individuals were divided into two groups based on the types of chronic gastritis; A: antrum-predominant gastritis P or C: pangastritis or corpus-predominant gastritis

2012-09-01 | E-GEOD-39175 | biostudies-arrayexpress

Highly recurrent CBS epimutations in gastric cancer CpG island methylator phenotypes and inflammation

Project description:CIMP (CpG island methylator phenotype) is an epigenetic molecular subtype, observed in multiple malignancies and associated with the epigenetic silencing of tumour suppressors. Currently, for most cancers including gastric cancer [GC], mechanisms underlying CIMP remain poorly understood. We sought to discover molecular contributors to CIMP in GC, by performing global DNA methylation, gene expression, and proteomics profiling across 14 gastric cell lines, followed by similar integrative analysis in 50 GC cell lines and 467 primary GCs. We identify the cystathionine beta-synthase enzyme (CBS) as a highly recurrent target of epigenetic silencing in CIMP GC. Likewise, we show that CBS epimutations are significantly associated with CIMP in various other cancers, occurring even in premalignant gastroesophageal conditions and longitudinally linked to clinical persistence. Of note, CRISPR deletion of CBS in normal gastric epithelial cells induces widespread DNA methylation changes that overlap with primary GC CIMP patterns. Reflecting its metabolic role as a gatekeeper interlinking the methionine and homocysteine cycles, CBS loss in vitro also causes reductions in the anti-inflammatory gasotransmitter hydrogen sulphide (H2S), with concomitant increase in NF-κB activity. In a murine genetic model of CBS-deficiency, preliminary data indicate upregulated immune-mediated transcriptional signatures in the stomach. Our results implicate CBS as a bi-faceted modifier of aberrant DNA methylation and inflammation in GC and highlights H2S donors as a potential new therapy for CBS-silenced lesions.

2021-04-19 | GSE149411 | GEO

Sporadic early-onset colorectal carcinoma is a distinct clinicopathological and molecular entity

Project description:Sporadic early onset colorectal carcinoma (EOCRC) is a growing problem that remains poorly understood. Clinical specificities and mechanisms of tumorigenesis might be relevant to both diagnosis and treatment. In this prospective study, clinicopathological features, genomic and gene expression profiles of sporadic EOCRC were compared to other well defined groups of CRC. Seventy selected patients were divided into 4 groups according to age (< 45 or > 60 years) and mismatch repair status. Mutations of key genes involved in colorectal carcinogenesis (P53, KRAS, BRAF, PIK3CA) were detected and the methylator phenotype (CIMP) established. Gene expression profiles (GEP) were obtained using pangenomic Affymetrix GeneChip.

2014-08-04 | E-GEOD-39084 | biostudies-arrayexpress

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [Caco2 cell line]

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

DNA methylation instability by BRAF-mediated TET silencing and lifestyle-exposure divides colon cancer pathways [3 cell lines]

2019-12-18 | GSE98532 | GEO

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