Abstract
p53 is a transcription factor that activates many genes involved in essential maintenance of genetic stability. P53 is the most frequently mutated gene in human cancers. One-third of these p53 mutations are structural, resulting in mutants with disrupted protein conformations. Here, we review current progress in p53-targeted drug development. These are strategies to reactivate wild-type function of a misfolded mutant p53. Most p53-targeted drugs are still at early stages of development and many of them are progressing slowly toward clinical implementation. There are significant challenges to meet before clinical translation of new antimisfolding p53-targeted drugs.
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