Project description:Methylation profiles of paired normal adjacent mucosa and tumor samples from 96 individuals and 48 healthy colon mucosae, were obtained through Illumina Infinium Human Methylation 450K BeadChip. This dataset is in the context of the COLONOMICS project and to query additional information you can visit the project website www.colonomics.org.
Project description:Gene expression profiles of paired normal adjacent mucosa and tumor samples from 98 individuals and 50 healthy colon mucosae, were obtained through Affymetrix Human Genome U219 Arrays. This dataset is in the context of the COLONOMICS project and to query additional information you can visit the project website www.colonomics.org. Colon tumor and adjacent paired normal mucosa tissues samples used in this study were selected from a series of cases with a new diagnosis of colorectal adenocarcinoma histologically confirmed. Included cases were from a homogenous series of patients with more than three years of follow up, early stage (II), without neoadjuvant chemotherapy and microsatellite stable colon cancer. Additionally, samples of colon mucosa from 50 healthy donors without colonic lesions were obtained during colonoscopy.
Project description:Gene expression profiles of paired normal adjacent mucosa and tumor samples from 98 individuals and 50 healthy colon mucosae, were obtained through Affymetrix Human Genome U219 Arrays. This dataset is in the context of the COLONOMICS project and to query additional information you can visit the project website www.colonomics.org.
Project description:To develop a better understanding of the biology underlying risk for CRC posed by germ line APC mutations we performed DNA methylation analysis of colon organoids derived from normal-appearing colons of FAP subjects (n=7) and matched healthy individuals (n=16). We identified a large number (n=358) of differentially methylated regions (DMRs) between colon organoids of FAP and healthy subjects, many of which were also identified in a comparison of tumor and normal adjacent tissue (NAT) in two independent, sporadic CRC tumor cohorts.
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).