Arvind Panday

This study identifies FANCM as a synthetic lethal target in BRCA1-deficient breast cancer, showing it restricts structural genome instability and links replication stress to transcriptional changes.

The paper analyzes DNA repair and replication stress networks in genomically unstable breast cancer, identifying adaptive mechanisms that contribute to tumor resilience and therapeutic vulnerabilities.

This study identifies FANCM's role in regulating repair pathway choice at stalled replication forks and highlights its ATPase function as a potential therapeutic target for BRCA1 mutant cancers.