castration-resistant tumor PC3: etoposide promotes cell death or unstable senescence (p53 null); repair looks non-performant; few scattered surviving cells undergo epigenetic reprogramming, possibly escaping from senescence and resuming proliferation so as to repopulate the depleted culture; repopulating cells acquire EMT and resistance to a second etoposide treatment. This evidence concerns the gene TP53 and neoplasm.