Abstract
The PI3K pathway is frequently activated in tumors, most commonly through p110α mutation or PTEN deletion. In contrast to p110α, p110β is oncogenic when over-expressed in the wild-type state, suggesting that its regulation by p85 is different than that of p110α. In this perspective, we summarize recent data concerning the regulation of p110β, which shows that wild-type p110β acts like an oncogenic mutant of p110α. We also discuss the significance of this altered regulation in tumor models of PTEN deletion, as well as the potential implications of the unique p110β regulation on GPCR-driven tumorigenesis.