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Recent elegant work has definitively identified that TP53 missense mutations in myeloid malignancies result in a dominant-negative effect without evidence of neomorphic gain-of-function activities, ultimately leading to a selection advantage when exposed to DNA damage.12 Thus, restoring wild-type function in TP53 mutant clones would be of profound beneficial impact

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doi: 10.1007/s40262-018-0649-2

Symposium article: molecular and physical mechanisms of first-pass extraction