Trever Grant Bivona

This study develops small molecules that activate the tumor suppressor kinase LKB1 and shows their therapeutic benefits in cancer cell lines.

This study identifies DNAJC17 as an essential JDP that activates HSP70 to regulate RNA splicing and G2-M progression through structural domains.

The paper uses spatiotemporal photocatalytic proximity labeling to track dynamic EGFR interactomes both extracellularly and intracellularly upon EGF activation.

This study shows RB1 loss in EGFR mutant lung cancer leads to reversible lineage plasticity, accelerating resistance to EGFR TKI therapy through non-genetic mechanisms.

This study uses single-cell lineage tracing and RNAseq to identify pre-existing resistant tumor subclones in lung cancer models and their transcriptional programs, revealing mechanisms of therapy resistance.

This study shows that BRAFV600E-driven lung cancer requires ERBB receptor signaling via ligand-mediated activation, and combined inhibition of BRAFV600E and ERBB improves therapeutic outcomes.

This study shows that CDK4/6 upregulation causes DNA replication stress and genomic instability, leading to resistance to EGFR inhibitors in lung cancer, and suggests combining CDK4/6 and EGFR inhibitors as a treatment.

The paper identifies a myeloid-mesenchymal crosstalk pathway involving Arg1 and ornithine that drives profibrotic metabolism in lung fibrosis.

This paper introduces PERCEPTION, a framework using single-cell transcriptomics to predict cancer treatment response and resistance, outperforming bulk expression-based methods in clinical trials.