Stephen J. Pettitt

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 a breast cancer risk locus by analyzing functional variants and target genes in mammary fibroblasts, showing their non-autonomous impact on breast cancer risk.

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

This study shows CDK12 loss drives prostate cancer development and identifies CDK13 as a therapeutic target through paralog-based synthetic lethality in CDK12-mutant tumors.

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