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One protein--p53--plays nemesis to most cancers by condemning damaged cells to death or quarantining them for repair. But the activity of p53 relies on its intact native conformation, which can be lost following mutation of a single nucleotide. With thousands of such mutations identified in patients, how can a future cancer drug buttress this fragile protein structure and restore the cell's natural defence?

Original publication

DOI

10.1038/35094077

Type

Journal article

Journal

Nat Rev Cancer

Publication Date

10/2001

Volume

1

Pages

68 - 76

Keywords

Animals, Benzamides, DNA, Humans, Imatinib Mesylate, Mutation, Piperazines, Protein Folding, Pyrimidines, Tumor Suppressor Protein p53