About half of all cancers in humans have mutations in the tumor suppressor p53 (p53), most of which are missense mutations. Not only do p53 mutations impair its ability to suppress drugs, but they also give the missense mutant p53 (mutp53) oncogenic properties that are distinct from those of the wild-type p53. Restoring or stabilizing wtp53 conformation from mutp53, rescuing p53 nonsense mutations, depleting mutp53 proteins, and inducing p53 synthetic lethality or targeting vulnerabilities imposed by p53 deficiencies (activated retrotransposons) or mutations (enhanced YAP/TAZ) are some of the approaches that have been taken to develop novel cancer therapies because p53 mutations are specific to cancer. The mechanisms of action and activities of FDA-approved and clinically available drugs that target p53 mutations to stop the progression of cancer are summarized here Cancer spread is aided by mutations in the tumor suppressor p53 (p53).
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