T. G. Bivona

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

This study shows that oncogenic protein condensates suppress RTK signaling and modulate drug tolerance in ALK-driven cancers by sequestering adapter proteins and enabling paracrine survival signals.

This study identifies PDK1 as a driver of osimertinib resistance in NSCLC, showing its inhibition sensitizes resistant cells and correlates with disease progression.

This study identifies a FAK-YAP signaling axis that drives drug-tolerant persister cells and residual disease in lung cancer, showing that inhibiting this axis improves tumor response to targeted therapies.

The paper tracks tumor evolution in a mouse model using lineage tracing and single-cell RNA-seq, revealing plasticity, fitness-associated programs, and stereotypical evolutionary trajectories.

The paper uses single-cell lineage tracing and RNA-seq to identify diverse metastatic behaviors and their drivers in lung cancer xenografts in mice.

The paper constructs a tyrosine kinase protein interaction map, revealing EGFR network oncogenesis in 19% of EGFR wild-type lung cancers, which is targetable with EGFR inhibitors.

This study identifies membraneless protein granules formed by RTK oncoproteins that activate RAS/MAPK signaling independently of lipid membranes in cancer.

This study uses longitudinal single-cell RNA sequencing to reveal therapy-induced adaptations in lung cancer, identifying cell state transitions and pathways associated with treatment response and resistance.

The paper identifies co-occurring RAS-MAPK pathway alterations in MET exon 14 skipping mutation positive lung cancers that limit response to MET inhibitors and suggests combining MET and MEK inhibitors to overcome resistance.

The paper identifies epigenetic drivers of esophageal squamous cell carcinoma through multi-omics analysis, revealing hypomethylation patterns and non-canonical WNT signaling activation.

This study identifies ETV4 and CCNE1 as targets of the CIC-DUX4 fusion oncoprotein, showing their roles in sarcoma metastasis and tumor growth, and highlights therapeutic strategies targeting the CCNE-CDK2 complex.

The paper identifies PDHK1 as a synthetic-essential gene in PTEN-deficient cells and cancers, showing its upregulation drives aerobic glycolysis and correlates with poor patient survival.

This paper develops a computational framework to predict dynamic polytherapy switching strategies to address tumor heterogeneity and evolution in lung adenocarcinoma.