TP53 and neoplasm: Molecular studies have revealed major genetically based events in the development of GBM: (1) Retinoblastoma tumor suppressor and p53 deactivation pathways; (2) phosphatidylinositol-3-OH kinase (PI3K) pathway activation; (3) growth factor signaling defects depending on receptor tyrosine kinase (RTK) activation [12,13].