Project description:Gene expression profiles of 135 patients presenting with colorectal adenomas during surgery or colonoscopy were obtained using Affymetrix U133+ arrays.
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids.
Project description:Gene expression profiles of 70 patients presenting with concurrent colorectal adenomas and colorectal tumors were obtained using Affymetrix U133+ arrays.
Project description:We established human colorectal tumor organoids from benign adenoma, primary colorectal cancer or metastasized colorectal cancer. The gene signature of tumor organoids associated with their tumor progression status. We also generated genome-edited organoids from human intestinal organoids recapitulating adenoma-carcinoma sequence. Gene expression signature of the genome engineered organoids were similar to that of adenoma organoids. This result indicated multiple (up to five) genetic mutations were insufficient for gene expression reprogramming of colorectal cancer. We used microarrays to detail the global program of gene expression in human colorectal tumor organoids and artificially mutation introduced organoids. To assess the expression profiling of genome-engineered organoids, we prepared total-RNA from cultured adenoma, carcinoma and genome-engineered organoids. We produced two types of genome-engineered organoids using the CRISPR/Cas9 or lentivirus vector system. Each engineered gene and engineered methods are described as a single alphabet and method name, respectively, in the sample characteristics field. The abbreviations for the engineered genes are as follows. 1) Genome-engineered organoids with CRISPR/Cas9 A = APC deletion; K = KRAS G12V knock in; S = Smad4 deletion; T = TP53 deletion; P = PIK3CA E545K knock in. 2) Genome-engineered organoids with Lent virus vector B = CTNNB1 S33Y overexpression; K = KRAS G12V overexpression; S = Smad4 shRNA overexpression; T = TP53 shRNA overexpression; P = PIK3CA E545K overexpression.
Project description:Whole transcriptome expression levels of healthy colonic, colorectal adenoma and colorectal cancer biopsy samples were analyzed by HTA 2.0 microarrays
Project description:We evaluated the profile of lncRNA and mRNA expression in 6 colorectal adenoma (CRA), 6 colorectal adenoma (CRC) and 6 matched normal mucosa (NOR) using the Exiqon miRCURY lncRNA and mRNA array,7th generation. We found that global dysregulated lncRNA and mRNAs between colorectal lesions and normal mucosa. Our findings implicates that dysregulation of lncRNA and mRNAs may play important role in the carcinogenesis and present therapeutic targets for CRC.
Project description:We showed that a lot of genes were deregulated in colorectal adenocarcinomas in comparison with colorectal adenomas. 37 colorectal adenoma and 9 colorectal adenocarcinoma samples were analyzed. We generated a comparison between adenocarcinomas and adenomas.
Project description:We tried to examine whether the de novo colorectal carcinomas (CRCs) without an adenoma component can be discriminated from those deriving from adenoma by DNA copy-number alteration profile. The unsupervised clustering of DNA copy-number profiles of 112 colorectal cancer samples, using large-sized (≥ 9 probes) genes, disclosed 4 clusters: Clusters 1, 3, and 4 correspond to carcinoma with an adenoma component. Cluster 2 and some samples in cluster 3 correspond to carcinoma without adenoma component. Our approach suggested that Cluster 2 may represent de novo CRCs since penetrance plots were very different between cluster 2 and the other clusters. Adenocarcinoma in cluster 3 have higher potential for lymph node metastasis than those in cluster 1 and 4 and can derive from clusters 1/4 tumors.
Project description:We evaluated the profile of miRNA expression in 6 colorectal adenoma (CRA), 6 colorectal adenocarcinoma (CRC) and 6 matched normal mucosa (NOR) using the Exiqon miRCURY LNA microRNA array,7th generation. We found that global dysregulated miRNAs between colorectal lesions and normal mucosa. Our findings implicates that dysregulation of miRNAs may play important role in the carcinogenesis and present therapeutic targets for CRC.