Andrew N.J. Tutt

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.

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.

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