TP53 and glioblastoma: The T98G cells exhibited more colocalization of oligomeric structures and M237I-p53 in the nuclei and the perinuclear region (Figures 1M, S2O, and S2P) than U138 cells (Figures 1I–L, S2K, and S2L), revealing that the M237I-p53 mutant assumes an aggregation-prone conformation that triggers amyloid oligomerization in this chemoresistant glioblastoma cell type.