Matthew R. Jordan

This study identifies PARP1 catalytic domain mutations as a mechanism of high-level resistance to saruparib in BRCA1-deficient breast cancer cells, while retaining DDR vulnerabilities.

This study shows that p300-mediated acetylation of RPA enhances its ssDNA binding affinity, particularly during G1/S phase and UV damage, influencing DNA metabolic pathway choice.

This study shows that inhibiting RPA gap protection enhances PARP inhibitor efficacy in BRCA1-deficient cancers by increasing genomic instability and reducing tumor growth.