Mutant p53 Directs PARP to Regulate Replication Stress and Drive Breast Cancer Metastasis
This study reveals that mutant p53 (specifically the R273H variant) hijacks PARP via its C-terminal domain to facilitate replication stress adaptation and drive breast cancer metastasis, a mechanism that can be selectively targeted by the synergistic combination of the PARP inhibitor talazoparib and the alkylating agent temozolomide to suppress tumor growth and metastasis in triple-negative breast cancer models.