Genome-wide DNA methylation study in bladder cancer
Ontology highlight
ABSTRACT: Genome-wide DNA methylation profiles were determined on a set of fresh 44 bladder cancer tissues using normal blood as control. DNA amplicons were prepared using Differential Methylation Hybridization (DMH) method, subsequently hybridized on to the Agilent Human CpG island Microarray. The goal was to unravel the DNA methylation patterns in different subgropus of bladder cancer along with finding markers for progresssion and early diagnosis. 44 bladder cancer tissues were profiled against commercially available normal human genomic blood DNA (Promega, Madison, WI, USA) as a reference
Project description:Genome-wide DNA methylation profiles were determined on a set of fresh 44 bladder cancer tissues using normal blood as control. DNA amplicons were prepared using Differential Methylation Hybridization (DMH) method, subsequently hybridized on to the Agilent Human CpG island Microarray. The goal was to unravel the DNA methylation patterns in different subgropus of bladder cancer along with finding markers for progresssion and early diagnosis.
Project description:To further elucidate the mechanism of calcium mediated chemoprevention of colorectal cancer,we have employed whole genome microarray expression profiling as a discovery platform to identify genes that differentially expressed in mice from high calcium group compared those from DMH group.The mice of DMH group were received normal diet (calcium concentration,1.24%) and subcutaneous injection of 1,2-Dimethylhydrazine at a dose of 20 mg/kg once weekly for 20 weeks,the mice of high calcium group were received high calcium diet(calcium concentration,3%) and subcutaneous injection of 1,2-Dimethylhydrazine at a dose of 20 mg/kg once weekly for 20 weeks.The mice were sarcrificed at 24 week.Nine normal colonic mucosa (3 from DMH group, 3 from high calcium group mice with tumors, and 3 from high calcium group mice without tumors) were used for the microarray analysis. The differentially expressed genes were indentified between high calcium group and DMH group,as long as differentially expressed pathways and gene ontology terms.
Project description:To further elucidate the mechanism of butyrate mediated chemoprevention of colorectal cancer,we have employed whole genome microarray expression profiling as a discovery platform to identify genes that differentially expressed in mice from Butyrate group compared those from DMH group. The mice of DMH group were received normal diet (calcium concentration,1.24%) and subcutaneous injection of 1,2-Dimethylhydrazine at a dose of 20 mg/kg once weekly for 20 weeks; the mice of Butyrate group were received high calcium diet (calcium concentration,3%) with 1.5% Butyrate and subcutaneous injection of 1,2-Dimethylhydrazine at a dose of 20 mg/kg once weekly for 20 weeks. The mice were sarcrificed at 24 week. Nine normal colonic mucosa (3 from DMH group, 3 from Butyrate group mice with tumors, and 3 from Butyrate group mice without tumors) were used for the microarray analysis. The differentially expressed genes were identified between butyrate group and DMH group,as long as differentially expressed pathways and gene ontology terms.
Project description:Gene expression analysis of 1,2-dimethylhydrazine (DMH)-induced colon cancer in F344 rats. 9 tumours and their paired normal mucosa were hybridized on 4x44K Agilent Whole rat arrays.
Project description:To investigate the impact of ablating Bcl9/Bcl9l on tumorigenesis, 6-8- week-old mice were exposed first to a single dose dimethylhydrazine (DMH, 44 mg/kg body weight), which is metabolized in the liver to carcinogenic azoxymethane (AOM), followed by 7 days oral administration of 2 % dextrane sulfate sodium (DSS) in the drinking water. This regimen results in the emergence of dysplastic adenomas, which progress to differentiated adenocarcinomas that are morphologically similar to human colorectal adenocarcinomas and typically harbor β-catenin stabilizing mutations of GSK3ß phosphorylation sites. Accordingly, these tumors present hallmarks of active Wnt signaling such as accumulation of nuclear β-catenin and expression of Wnt target genes. Total RNA of laser dissected samples from five different tumors each of two wild-type mice and three vil-Cre-Bcl9-/-/Bcl9l-/- mice was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_TumorID_MouseID_UniqueID.
Project description:344 rats were treated twice, one week apart, with subcutaneous injections of 1,2-dimethylhydrazine (150 mg/kg x 2). Thirty-two weeks after the first DMH injection, rats were sacrificed and colonic tumours (T) and normal colon mucosa (NM) harvested and stored in RNAlater. Genomic DNA was extracted from ten samples of paired T and NM and hybridized on Agilent Rat Genome CGH Microarray 2x105K.
Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after toxicant-induced malignant transformation. This study also puts the DNA methylation changes into context with respect to the aberrant DNA methylation events that occur in bladder and prostate carcinogenesis not associated with toxicant exposure. Immortalized UROtsa (n=3) and RWPE-1 (n=2) are compared to normal HUC (n=2) and PrEC (n=2), respectively. Arsenite (n=1), monomethylarsonous acid (n=2) or cadmium (n=1) transformed UROtsa are compared to parental UROtsa (n=3). Arsenite (n=2), cadmium (n=1) or MNU (n=1) transformed RWPE-1 cells are compared to parental RWPE-1 cells (n=2). Clinical bladder tumor biopsies (n=6), urothelial carcinoma cell lines (n=2) and prostate cancer cell lines (n=3) are compared to thier normal tissue counterparts HUC (n=2) and PrEC (n=2). Immunoprecipitation using anti-methylcytosine (5MeC) antibody.
Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after toxicant-induced malignant transformation. This study also puts the DNA methylation changes into context with respect to the aberrant DNA methylation events that occur in bladder and prostate carcinogenesis not associated with toxicant exposure. Immortalized UROtsa (n=3) and RWPE-1 (n=2) are compared to normal HUC (n=2) and PrEC (n=2), respectively. Arsenite (n=1), monomethylarsonous acid (n=2) or cadmium (n=1) transformed UROtsa are compared to parental UROtsa (n=3). Arsenite (n=2), cadmium (n=1) or MNU (n=1) transformed RWPE-1 cells are compared to parental RWPE-1 cells (n=2). Clinical bladder tumor biopsies (n=6), urothelial carcinoma cell lines (n=2) and prostate cancer cell lines (n=3) are compared to thier normal tissue counterparts HUC (n=2) and PrEC (n=2). Immunoprecipitation using anti-methylcytosine (5MeC) antibody.