Dragomir B. Krastev

This study identifies RER deficiency as a new DNA repair defect in cancer, detectable through mutational signatures and linked to therapeutic vulnerabilities.

This study identifies FANCM-RMI1/2 as a driver of PARP inhibitor sensitivity in BRCA2-deficient cells, revealing distinct adaptation mechanisms between BRCA1 and BRCA2 loss.

The paper identifies DDIAS as a DNA-binding effector of the CIP2A-TOPBP1 complex that suppresses single-stranded DNA during mitosis, protecting genome integrity and interacting genetically with DNA polymerase.

This study identifies nucleophagy as the mechanism by which trapped PARP1 is cleared, showing that inhibiting this process re-sensitizes PARPi-resistant cells to PARPi.

The paper shows HRd is a continuum with functional and mutational heterogeneity, highlighting the need for refined molecular classification for precision interventions.

The paper identifies BRCA1/2 reversion mutations associated with drug resistance in cancer patients and highlights key domains critical for resistance.

This paper identifies PARP inhibitors as sensitizers for oncolytic reovirus by enhancing DISC-mediated apoptosis and NF-kappa B-driven immune responses.

The paper identifies p97 ATPase as a key player in removing trapped PARP1 from chromatin, enhancing PARPi-induced cytotoxicity in homologous recombination-defective cells.