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- W2078989706 abstract "Mutations in the TP53 (p53) gene are present in a large fraction of human tumours, which frequently express mutant p53 proteins at high but heterogeneous levels. The clinical significance of this protein accumulation remains clouded. Mouse models bearing knock-in mutations of p53 have established that the mutant p53 proteins can drive tumour formation, invasion and metastasis through dominant negative inhibition of wild-type p53 as well as through gain of function or 'neomorphic' activities that can inhibit or activate the function of other proteins. These models have also shown that mutation alone does not confer stability, so the variable staining of mutant proteins seen in human cancers reflects tumour-specific activation of p53-stabilizing pathways. Blocking the accumulation and activity of mutant p53 proteins may thus provide novel cancer therapeutic and diagnostic targets, but their induction by chemotherapy may paradoxically limit the effectiveness of these treatments." @default.
- W2078989706 created "2016-06-24" @default.
- W2078989706 creator A5019407635 @default.
- W2078989706 creator A5059954339 @default.
- W2078989706 creator A5071167803 @default.
- W2078989706 date "2010-10-25" @default.
- W2078989706 modified "2023-10-12" @default.
- W2078989706 title "The role of mutant p53 in human cancer" @default.
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- W2078989706 doi "https://doi.org/10.1002/path.2784" @default.
- W2078989706 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21125670" @default.
- W2078989706 hasPublicationYear "2010" @default.
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