J. V. Forment

This study identifies H2AX's role in promoting replication fork degradation and chemosensitivity in BRCA-deficient tumours, independent of its classical DNA damage signalling function.

This study shows that PSMC3IP and MND1 depletion increases PARP inhibitor sensitivity in mitotic cells through impaired D-loop formation and homology-directed repair.

The paper identifies 110 genes linked to PARP inhibitor sensitivity through CRISPR screens and tumor data analysis, highlighting XRCC3 as a potential biomarker for prostate cancer.

This study analyzes reversion mutations in BRCA genes from clinical cases to identify DNA end-joining repair mechanisms linked to therapy resistance and suggests targeting these pathways to improve treatment outcomes.

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.