Abstract
The phosphoinositide 3‐kinase (PI3K) pathway plays a critical role in cell growth regulation. PI3K generates the lipid, phosphatidylinositol‐3,4,5‐trisphosphate (PIP3), that acts as a membrane bound second messenger to activate AKT/PKB family protein Ser/Thr kinases as well Tec family protein‐Tyr kinases. PIP3 also regulates proteins that control Arf, Rac and Ras family GTP‐binding proteins. This lipid is elevated in cancers, either due to loss of PTEN, the phosphatases that degrades it, or due to constitutive PI3K activity because of activating mutations in PIK3CA or an upstream activator of PI3K. The ultimate consequence of activating PI3K is to generate changes in signaling networks and gene expression patterns that promote cell growth, cell survival and cell movement. In order to elucidate the role of the PI3K pathway in normal cell growth and in cancer, we have generated mice in which genes for PI3K are deleted or activated in specific tissues. In addition, we have investigated the biochemical mechanisms by which PI3K becomes activated in human cancers. Our progress in these areas will be summarized.
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