Noteworthy discoveries from the Cantley lab include the existence of lipid kinase, phosphoinositide 3-kinase (PI3K), and its critical function for oncogene-mediated cell transformation, as well as insulin-dependent stimulation of glucose uptake and metabolism. Further work revealed that lipid products of PI3K directly activate the AKT/PKB protein kinase to provide a cell survival signal via increasing uptake of glucose. Activating mutations in PI3K genes have been implicated in many cancers, along with inactivating mutations in the PTEN gene (encoding a phosphatase that degrades PI3K lipid products). These discoveries have stimulated pharmaceutical companies to develop PI3K pathway inhibitors for cancer therapy. We are currently testing the effects of combining PI3K inhibitors with emerging drugs as potential new ways to attack BRCA1 cancers, including the difficult-to-treat triple-negative breast cancer and ovarian cancer.
Recent studies from our lab have revealed that growth factors, through activation of PI3K and other signaling pathways, cause major changes in cellular metabolism that are critical for the growth of cancer cells. Ongoing studies are defining how oncogene transformation of cells alters the flux of metabolites such as glucose and glutamine.
The Cantley lab welcomes a diverse set of talents and fosters an interdisciplinary approach in its attempts to translate fundamental scientific discoveries into clinical innovations.