C. J. Lord

CDK12 Loss Promotes Prostate Cancer Development While Exposing Vulnerabilities to Paralog-Based Synthetic Lethality

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.

PARP inhibitors enhance reovirus-mediated cell killing through the death-inducing signaling complex (DISC) with an associated NF-kappa B-regulated immune response.

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

CDK4/6 inhibition and dsRNA sensor agonism co-operate to enhance anti-cancer effects through ER stress and immune modulation of tumour cells

MND1 and PSMC3IP control PARP inhibitor sensitivity in mitotic cells

This study shows that PSMC3IP and MND1 depletion increases PARP inhibitor sensitivity in mitotic cells through impaired D-loop formation and homology-directed repair.

Integrative analysis of large-scale loss-of-function screens identifies robust cancer-associated genetic interactions

The paper identifies robust cancer-associated genetic interactions across multiple studies and finds that protein-protein interactions are enriched among these interactions.

Genome-wide and high-density CRISPR-Cas9 screens identify point mutations in PARP1 causing PARP inhibitor resistance

The paper identifies PARP1 point mutations causing PARP inhibitor resistance through CRISPR-Cas9 screens and shows their impact on PARP1 trapping and chemotherapy sensitivity.

A compendium of co-regulated protein complexes in breast cancer reveals collateral loss events

The paper identifies 258 protein complexes in breast cancer and finds that mutations in one subunit often lead to reduced expression of other complex members, a phenomenon observed in proteomic but not transcriptomic data.

CancerGD: a resource for identifying and interpreting genetic dependencies in cancer

CancerGD identifies and interprets genetic dependencies in cancer by integrating genotypic profiling with loss-of-function screens in tumor cell lines.