In October 2005, a landmark report identified a recurring genetic rearrangement called a “translocation” that connected the testosterone responsive sequence of the gene TMPRSS2 onto two Ets family genes associated with sarcomas and breast cancers, ERG and ETV1. We have now demonstrated that ERG expression is sufficient to transform non-tumorigenic prostate cells into tumorigenic cells, and hypothesize that this is due to the ability of ERG to reprogram prostatic cells, causing them to grow faster thus making them more capable of migration and metastasis. We aim to: 1) determine if ERG can transform primary human and rodent prostate epithelial cells, and assess the ability of these and our previously developed models to migrate and metastasize in tissue culture and in animal models, and 2) use microarray expression profiling to identify genes whose expression is controlled by ERG. These studies will help explain how ERG causes prostate cancer and identify diagnostic and therapeutic targets for treating patients with these translocations.