TP53 and neuroblastoma: We used the gene expression profiles of 262 untreated primary NB tumors (Agilent262), for the majority of which we had information on the TMM activation in addition to other patient clinical and molecular data, such as age at diagnosis, ALT activation, event overall, event-free, TERT rearrangement, INSS stage, MYCN status, p53/RAS gene mutations, and spontaneous regression, in order to evaluate the association between hypoxia and TMM in NB [13].