The other side of p53

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Abstract
In vertebrates, p53 induces death or arrest in mutant cells with damaged or unstable genomes. But tumour cells can themselves induce a permissive environment yielding a highly proliferative mesenchyme that has undergone p53 loss [1,2]. Turning on p53 may be responsible for the inhibition of cancer outgrowth with minimal toxic effects on the organism, since the stress signals activating p53 are absent in normal tissue but present in tumour [3]. In fact, this strategy had no effect on the normal tissue of mice carrying a re-activatable p53 knockout allele [4]. In mice, tumours developed in the complete absence of p53, without any selective pressure to desensitize p53 activators or downstream effectors. However, in human cancers reactivation of p53 could occur in a p53-resistant cellular environment.