Breast cancer is the leading cause of cancer-related mortality among women worldwide. Metastatic spread of disease is basis for lethality of this disease. The PI3K signaling pathway is mutationally activated in most breast tumors and has been shown to play key roles in cellular motility and invasiveness. However, we have found that the therapeutic potential for drugging the PI3K pathway in this disease is limited in part by physiologic feedback pathways that regulate PI3K signaling. We hypothesize that pharmacologic strategies that account for this feedback will be far more effective in blocking metastatic spread.
In this project, the student will analyze the effects of inhibitors of different components of the PI3K pathway alone and in combination with inhibitors of feedback pathways that we have identified. Studies on cellular motility and invasion will be done in various models of breast cancer that feature mutational activation of the PI3K pathway.
Preferred Project Dates
Students are expected to be in attendance all eight weeks, start and end dates inclusive.