Prostate power play: Does pik3ca accelerate pten-deficient cancer progression?

Abstract

PI3K pathway alterations are frequently recurrent in metastatic prostate cancer and are associated with the development of currently incurable castration-resistant disease. Candidate inhibitors that target single PI3K pathway members lack efficacy as demonstrated in multiple clinical trials. In this issue, Pearson and colleagues examine the functional importance of co-occurring PIK3CA and PTEN aberrations using a novel mouse model and demonstrate a synergistic acceleration of tumorigenesis that may be responsible for de novo metastatic prostate cancer.