Genome-wide DNA Methylation Events in <i>TMPRSS2–ERG</i> Fusion-Negative Prostate Cancers Implicate an EZH2-Dependent Mechanism with <i>miR-26a</i> Hypermethylation

Abstract

In contrast to TMPRSS2-ERG -rearranged tumors, the pathomechanism for gene fusion-negative tumors is completely unclear. Using a sequencing-based approach, our work uncovers significant global epigenetic alterations in TMPRSS2-ERG gene fusion-negative tumors and provides a mechanistic explanation for the tumor formation process.