BIO

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Solid tumors harboring mutations in the TP53 gene confer resistance to ionizing radiation due to the lack of DNA damage response governed by the wild-type (WT) form of p53. Here, we used a novel high-LET radiotherapy based on alpha-emitting atoms to investigate the response based on p53 status. We also combined the radiation treatment with APR-246, a systemic drug that converts specific mutant p53 proteins to their WT form, with the attempt to sensitize the tumors to the radiation treatment.

Email: oratsmon@gmail.com