We have recently identified kinase-independent pro-survival functions of Akt, a critical component of the PI3K signalling network, and are currently working on 1) the molecular characterization of these novel functions, and 2) developing novel Akt inhibitors that can target the full repertoire of Akt activities.
We also have an interest in understanding the role of oncogenic signal transduction on metabolic addiction, and the development of new approaches to concurrently target metabolic and oncogene addictions in cancer.
Our initial studies on metabolic addiction suggest that the availability of specific nutrients (such as glucose and glutamine) to which cancer cells have developed addictions, tightly regulates the activity of driver oncogenes.
In fact, limiting the availability of these metabolites will cause cancer cell death through oncogene overdose. We plan to flesh out this phenomenon at a molecular level, and assess whether this type of functional interaction can uncover novel therapeutic targets or strategies.