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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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TGFÎ² signaling directs serrated adenomas to the mesenchymal colorectal cancer subtype [organoids]

ABSTRACT: The aim of this study was to determine the effects of TGFÎ² at the premalignant stage of CRC development. Organoid cultures were isolated from normal colon and from tubular adenomas. One normal colon culture was genetically engineered using the CRISPR-Cas9 system to carry the BRAFV600E mutation. Organoid cultures of three different tubular adenomas and two normal colon samples, and one BRAFV600E-mutant organoid culture received TGFÎ² or control treatment after which gene expression was analyzed by microarray (Affymetrix U133+ PM Genechip Array).

ORGANISM(S): Homo sapiens

SUBMITTER: Sander Hooff

PROVIDER: E-GEOD-79461 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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TGFÎ² signaling directs serrated adenomas to the mesenchymal colorectal cancer subtype [adenomas]

Project description:Colorectal cancer can be divided into four consensus molecular subtypes, which might associate with distinct precursor lesions. The aim of this study was to determine the subtype affiliation of two types of colorectal adenomas: tubular adenomas (TAs) and sessile serrated adenomas (SSAs) and to determine the activity of TGFÎ² signaling and the role of this cytokine in subtype affiliation. Adenoma samples were collected in the Academic Medical Center (AMC), Amsterdam, The Netherlands. Tubular adenomas (TAs) were obtained from familial adenomatous polyposis (FAP) patients and sessile serrated adenomas (SSAs) were collected from serrated polyposis syndrome (SPS) patients. Gene expression was analyzed for 7 sessile serrated adenomas (SSA) and 9 tubular adenomas (TA).

2016-06-01 | E-GEOD-79460 | biostudies-arrayexpress

TGFÎ² signaling directs serrated adenomas to the mesenchymal colorectal cancer subtype

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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TGFβ signaling directs serrated adenomas to the mesenchymal colorectal cancer subtype [organoids]

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Project description:The majority of colon carcinomas are known to develop in tubular adenomas through multi-stage carcinogenesis. Recently, we have reported a simple and reproducible method for the expression profiling using microdissected cells from formalin-fixed tissue samples (Lee et al, World J Gastroenterol, 11:1937-1945, 2005). Using the method, we analyzed the expression profiling in colon tubular adenoma/carcinoma sequence. Epithelial cells of carcinoma, tubular adenoma, and normal colon mucosa were microdissected from colon tubular adenomas containing focal adenocarcinomas. Keywords: disease (colon cancer) state analysis

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Project description:Profiling project of a panel of tubular adenoma and serrated adenoma patient material collected in the Academic Medical Center (AMC) in Amsterdam, The Netherlands. The aim of the study was to compare the expression profiles of different types of colon cancer precursor lesions (tubular versus serrated adenomas) and determine their correspondence with a set of colon cancer patient-derived profiles that have distinct clinical outcomes. 6 serrated adenomas and 7 tubular adenomas are profiled in this study.

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Global DNA methylation alterations reveal multiple pathways in the initiation and progression of colorectal cancer

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