TP53 and colorectal carcinoma: In contrast, except at very high concentrations of the drugs, no reductions in cell growth were measured in p53 knockout (p53KO; HCT116 p53−/−; B16-F10 p53−/−) and p53 mutant (p53mut; human colorectal carcinoma HT-29) cell lines treated in normoxia or hypoxia (Fig. 1d–f), confirming the wildtype p53-dependent mechanism of action of the inhibitors.