Sameer Bikram Shah

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.

This study shows that microhomology-mediated end joining (MMEJ) repairs single-ended DSBs at replication forks, working with BIR and being regulated by ATR and Pol{theta}.

This study shows that BIR is activated to repair R-loop-associated double-strand breaks in SETX-deficient cells, leading to hyper-recombination and synthetic lethality with PIF1, RAD52, and XPF.

This study shows that 53BP1 deficiency increases BIR-mediated hyperrecombination, leading to genome instability and potential cancer treatment opportunities.