TP53 and glioblastoma: Genetic changes characteristically associated with primary glioblastoma include amplification and/or overexpression of Epidermal Growth Factor Receptor (EGFR) (~60%) [15, 16] and Mouse double minute 2 (Mdm2) (a key negative regulator of the tumor suppressor p53) [17, 18], deletion mutations of Cyclin-Dependent Kinase inhibitor 2A (CDKN2A, also known as p16INK4A, a cell cycle regulator) [19], and inactivating mutations of Phosphatase and Tensin Homolog Deleted on Chromosome 10 (PTEN) [20, 21].