Cancer predisposition, onset and therapeutic response can be critically determined by the integrity of the tumor suppressor p53. The majority of human cancers appear to exhibit either abnormal p53 or disrupted p53 activation pathways. Intervention to restore wild-type p53 activities is an attractive approach for cancer therapy. The manipulation of p53 and its targets is a challenging field that is still in its infancy, but witnessing some notable developments in the areas of p53 gene therapy, mutant reactivation and suppression of the negative p53 regulator Mdm2 using small molecules. In addition, wild-type p53 manipulation in healthy tissues of cancer patients in the context of chemotherapy and radiation therapies is offering the potential of enhanced patient recovery.
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Haupt et al. (2006) studied this question.
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