To develop an experimental system in which either senescence or apoptosis is specifically induced, we first investigated the phenotypes of two human tumor lines expressing the wild-type p53, hepatocarcinoma HepG2 cells and osteosarcoma U2OS cells, as a function of the dosage of etoposide, an anticancer drug that causes DNA double-strand breaks. The gene discussed is TP53; the disease is osteosarcoma.