p53 is one of the most intensively studied tumor suppressor proteins, with mutations that lead to loss of wild-type p53 activity frequently detected in many different tumor types. Perturbations in p53 signaling pathways are believed to be required for the development of most cancers, and there is evidence to suggest that restoration or reactivation of p53 function will have significant therapeutic benefit. For the first 10 years of investigation, p53 was considered to be the product of an oncogene, with many studies describing proliferative and transforming activities for p53. This mistake in the initial classification of p53 was the result of a simple error; the TP53 gene that had been cloned and used in the initial experiments encoded a mutant version of the wild-type gene. The tumor suppressor credentials of wild-type p53 are no longer in doubt, but the early studies provided a tantalizing hint of what has become an extremely active area of study—the suggestion that mutations in p53 can result in both loss of wild-type activity and gain of a novel transforming function. Moving in a circle in the past 30 years, we have come back around to considering that p53, albeit mutant versions of p53, can function as oncoproteins.
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