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Mutations in the tumor-suppressor gene TP53 are found in about 50% of tumors, making it the most frequently mutated gene in human cancer (1). The unusual mutational spectrum of TP53, dominated by missense mutations within p53’s central DNA-binding domain, including some hotspot mutations such as TP53R248Q, has traditionally been linked to the selection for gain-of-function properties acquired by the resulting aberrant missense mutant p53 variants (2, 3).
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