The transcription factor p53, described as the “guardian of the genome”, becomes activated in response to malignancy- associated stress signals resulting in cell cycle arrest, senes- cence, differentiation, or apoptosis leading to the inhibition of tumor cell growth [1]. Inactivation of the p53 tumor- suppressor pathway is among the most common escape mechanisms allowing survival of malignant cells subjected to cytotoxic stress [2]. Inactivating TP53 mutations have been detected in ≤50% of cancers [3].
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