p53-loss induced prostatic epithelial cell plasticity and invasion is driven by a crosstalk with the tumor microenvironment.

Prostate cancer is a heterogeneous disease with a slow progression and a highly variable clinical outcome. The tumor suppressor genes PTEN and TP53 are frequently mutated in prostate cancer and are predictive of early metastatic dissemination and unfavorable patient outcomes. The progression of solid tumors to metastasis is often associated with increased cell plasticity, but the complex events underlying TP53-loss-induced disease aggressiveness remain incompletely understood.

The Center for Prostate Disease Research (CPDR): a multidisciplinary approach to translational research.

This article describes the history, structure, and contributions of the Center for Prostate Disease Research. It divides the organization into the clinical program at Walter Reed Army Medical Center, the basic science program in Rockville, MD, and the multi-center national database. The emphasis of this article is not the achievements of the individual programs but their synergy, establishing a comprehensive multidisciplinary prostate center.