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Large-scale cancer genome studies have defined TP53, which encodes the anti-cancer gene and transcription factor p53, as the most common mutation gene in human cancer, and the p53 mutation has not yet been targeted for treatment.
challenges of targeting p53 mutant regime drugs include heterogeneous inerceration mechanisms and lack of widely applicable ostructive dosing points.
Recently, Lu Min and other teams worked together at Cancer Cell to identify arsenic trioxide (ATO), a mature drug for acute primary myeloid leukemia that can act as a cysteine reactive compound to save structural p53 mutations.
structure of the p53 mutant, which binds to arsenic, reveals a secret omnipotent site involving three arsenic-coordinated cysteine in the DNA binding domain, with zinc binding site at the far end.
arsenic binding stabilizes the ring-chip-helix structure of p53 at the DNA binding, as well as the overall β-sandwich folding configuration, thus giving the p53 mutant thermal stability and transcriptional activity.
in cell and mouse heterogeneity transplant models, the ATO reactivates the mutant p53 to suppress tumors.
study of the 25 most common p53 mutations provided a reference for patient strated clinical exploration.
, the results provide a mechanism basis for re-using the ATO to target p53 mutations for widely applicable and personalized cancer treatment.
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