Epigenome-Wide DNA Methylation Profiling Identifies Differential Methylation Biomarkers in High-Grade Bladder Cancer.

Epigenetic changes, including CpG island hypermethylation, occur frequently in bladder cancer (BC) and may be exploited for BC detection and distinction between high-grade (HG) and low-grade (LG) disease. Genome-wide methylation analysis was performed using Agilent Human CpG Island Microarrays to determine epigenetic differences between LG and HG cases. Pathway enrichment analysis and functional annotation determined that the most frequently methylated pathways in HG BC were enriched for anterior/posterior pattern specification, embryonic skeletal system development, neuron fate commitment, DNA binding, and transcription factor activity.

Integrated analysis of epigenomic and genomic changes by DNA methylation dependent mechanisms provides potential novel biomarkers for prostate cancer.

Epigenetic silencing mediated by CpG methylation is a common feature of many cancers. Characterizing aberrant DNA methylation changes associated with tumor progression may identify potential prognostic markers for prostate cancer (PCa). We treated two PCa cell lines, 22Rv1 and DU-145 with the demethylating agent 5-Aza 2'-deoxycitidine (DAC) and global methylation status was analyzed by performing methylation-sensitive restriction enzyme based differential methylation hybridization strategy followed by genome-wide CpG methylation array profiling.

Altered DNA methylation landscapes of polycomb-repressed loci are associated with prostate cancer progression and ERG oncogene expression in prostate cancer.

Purpose: To assess differentially methylated "landscapes" according to prostate cancer Gleason score (GS) and ERG oncogene expression status, and to determine the extent of polycomb group (PcG) target gene involvement, we sought to assess the genome-wide DNA methylation profile of prostate cancer according to Gleason score and ERG expression.

Experimental Design: Genomic DNA from 39 prostate cancer specimens was hybridized to CpG island microarrays through differential methylation hybridization. We compared methylation profiles between Gleason score and ERG expression status as well as Gleason score stratified by ERG expression status.

Correlation of ERG expression and DNA methylation biomarkers with adverse clinicopathologic features of prostate cancer.

Purpose: Fusion of the TMPRSS2 gene with the ERG oncogene and aberrant DNA methylation patterns are commonly found in prostate cancer. The aim of this study was to analyze the relationship between ERG expression, DNA methylation of three biomarkers, and clinicopathologic features of prostate cancer.

Experimental Design: Immunohistochemistry for ERG protein was conducted as a surrogate for TMPRSS2-ERG fusions.

Rac1b recruits Dishevelled and β-catenin to Wnt target gene promoters independent of Wnt3A stimulation.

We previously reported a functional interaction between aberrant Wnt signaling and Rac1/Rac1b GTPases in tumorigenesis. In this study, we further investigated the mechanistic role of nuclear Rac1b. Using chromatin immunoprecipitation (ChIP) studies, we show that Rac1b resides at the promoters of Wnt target genes, c-Myc and Cyclin D1, in HCT116 cells with aberrant Wnt pathway.