Christopher J. Lord

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

This paper develops a model to predict resistance to synthetic lethal therapies by integrating protein-protein interaction networks with molecular profiles from CRISPR screens.

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.

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.

LOX inhibition disrupts a collagen-integrin-MYC axis in ILC, halting tumor growth and metastasis with minimal toxicity, offering a new therapeutic strategy.

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 that sequential ATR and PARP inhibition can overcome acquired resistance to DNA damaging agents in pancreatic ductal adenocarcinoma.

This study identifies non-canonical NF-κB signalling as a therapeutic target in CYLD cutaneous syndrome and shows that IKK inhibition reduces tumor viability in patient-derived models.

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.