Glioblastoma multiforme (GBM) is the most common, aggressive, and lethal type of brain tumor. GBMs are grade IV malignant gliomas characterized by necrosis and vascular proliferation. Despite advances in surgical resection, radiation, and chemotherapy almost all GBM tumors eventually recur with an average survival of 9 to 12 months after diagnosis. One of the main reasons why GBMs are not cured by conventional therapies is due to the diffuse, invasive, and complex nature of the disease. In 2009, the FDA approved bevacizumab (Avastin) to treat recurrent GBM in conjunction with radiation/chemotherapy. Bevacizumab is a recombinant humanized monoclonal antibody that inhibits angiogenesis by selectively binding and sterically inhibiting the action of VEGF with high affinity thereby preventing binding to its receptors. Currently, standard MRI is used to determine response to treatment by assessing changes in tumor growth. Although ~40% of GBM patients are deriving benefits from bevacizumab therapy, ~60% of patients do not respond or progress in disease after therapy. Identifying proteins associated with these two response groups will help to identify the unique disease mechanisms that mediate differential responses to treatment between patients and eventually aid in predicting patient response to bevacizumab treatment. Throughout the course of my research I will be using spectral counting quantification, a mass spectrometry based proteomics approach to correlate blood plasma and tumor biopsy protein signatures of GBM patients before therapy and their standard MRI results after bevacizumab treatment to establish profiles associated with disease mechanisms that mediate the differential responses to bevacizumab therapy.