David W. Cescon

The paper investigates the mutational signature of CX5461, a photosensitiser, when combined with UVA light, showing increased SNV burden only in co-exposed cells.

The paper identifies synthetic dosage lethality targets for PLK1-overexpressing cancers using genome-wide screens and validates key hits to show their therapeutic potential.

This study identifies KIFC1 as a therapeutic vulnerability in lung cancers with centrosome amplification by showing its role in mitigating mitotic stress.

The paper develops a method to simulate cell-free chromatin for epigenetic biomarker discovery, showing it better reflects tissue chromatin features than plasma-derived samples.

The paper introduces KuLGaP, a selective measure to assess therapy response in patient-derived xenografts by comparing treatment and control arms, improving accuracy over existing methods.

The paper develops Xeva, an open-source tool for analyzing PDX pharmacogenomic data, finding that few genes and pathways show passage-specific changes.

This study identifies metabolic adaptations in taxane-resistant triple-negative breast cancer cells that lead to epigenetic vulnerabilities, specifically through altered methionine metabolism and H3K27me3 redistribution.

The paper identifies gene isoform-based biomarkers predictive of drug response in breast cancer using pharmacogenomic data from CCLE and GDSC.