Jill Bargonetti

This study shows mutant p53 uses its C-terminal domain to reprogram PARP activity, enabling replication stress adaptation and metastasis in TNBC, and identifies mtp53 as a biomarker for PARP inhibitor and DNA-damaging therapy.

This study identifies a cancer persistent DNA repair circuit involving mtp53, MDM2, and MDMX that recruits 53BP1 and MDC1 to chromatin, enhancing cell survival.

This study shows that tumor organoids with mutant p53 are more sensitive to the combination of PARP inhibitor and temozolomide than those with wild-type p53.