Genome-wide DNA methylation events in TMPRSS2:ERG fusion negative prostate cancers implicate an EZH2 dependent mechanism with miRNA-26a hypermethylation.

ABSTRACT: Prostate cancer is the second most common cancer among men worldwide. Alterations in the DNA methylation pattern can be one of the leading causes for prostate cancer formation. This study is the first high throughput sequencing study investigating genome-wide DNA methylation patterns in a large cohort of 51 tumor and 53 benign prostate samples using MeDIP-Seq. Comparative analyses identified more than 147,000 cancer-associated epigenetic alterations. Additionally, global methylation patterns demonstrate significant differences based on the TMPRSS2:ERG rearrangement status. We propose the hypermethylation of miRNA-26a as an alternative pathway of ERG rearrangement independent EZH2 activation. The observed increase in differential methylation events in fusion negative tumors can explain the tumorigenic process in the absence of genomic rearrangements. Genomewide examination of methylation profiles in 51 prostate cancer samples

ORGANISM(S): Homo sapiens

SUBMITTER: Michal-Ruth Schweiger 

PROVIDER: E-GEOD-35342 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress