To identify factors that are important in driving tumor progression, we utilized orthotopic xenograft models established from patient-derived BTICs that are highly tumorigenic41, have the capacity to self-renew, differentiate12,42,43, harbor the spectrum of molecular genetic alterations that occur in human GBM (e.g., mutations in p53, PTEN, IDH1, EGFR, and MSH6 (refs. 13,44–46)) and model the human disease in vivo43,45,47. The gene discussed is TP53; the disease is glioblastoma.