TP53 and cancer: Not only does expression of mutantp53 lead to impaired signaling, but p53 mutants can also exert a dominant-negativeeffect on remaining copies of the wild-type (WT) protein by heterotetramerizationor co-aggregation, and also inactivate the paralogous tumor suppressorsp63 and p73 by co-aggregation.11−13 Many cancers acquire furtherproliferative advantages by retaining only the mutated p53 allele,exhibiting an oncogenic gain-of-function that is associated with increasedcell growth, drug resistance, and metastatic potential.13−16