TP53 and glioblastoma: From a molecular point of view, GBM is featured by genomic instability, resulting in several genetic and epigenetic aberrations such as amplification and mutation of the epidermal growth factor receptor (egfr), loss of function of the phosphatase and tensin homolog (pten), mutations in the isocitrate dehydrogenase 1 (idh1), and tumor protein p53 (tp53) genes.