Patrick D. McGillivray

Loss of extracellular matrix-integrin signaling switches off YAP/TEAD and lets prostate adenocarcinoma organoids turn neuroendocrine; LATS inhibition reverses it, and combined YAP, NOTCH and AR inhibition fully reprograms them.

NIMBus identifies mutational hotspots by integrating mutation data with genomic features to account for heterogeneity, revealing known drivers and regulatory disruptions in cancer.

The paper develops a custom ENCODE annotation for cancer genomics, highlighting TF-RBP interactions and network rewiring during oncogenesis, and validates findings using experimental assays.

The paper introduces the Cancer LncRNA Census (CLC), a curated resource of lncRNAs with causative roles in cancer, and shows their genomic and evolutionary features.

ActivePathways integrates multivariate omics data to identify enriched pathways, revealing cancer driver genes and prognostic pathways in breast cancer.

The paper analyzes 2500 cancer genomes to assess the molecular functional impact of mutations, finding that some putative passenger variants may influence gene activity and contribute to cancer phenotypes.

ALoFT annotates and predicts the disease-causing potential of loss-of-function variants across different genetic contexts and populations.