1. ¹Department of Medical Oncology, Dana Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA
2. ²Department of Internal Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA
3. ³Broad Institute of Harvard and MIT, 320 Charles Street, Cambridge, MA 02141, USA

Correspondence: WR Sellers, E-mail: William_Sellers@dfci.harvard.edu

Abstract

Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.