V. Olivas

CDK4 or CDK6 upregulation induces DNA replication stress and genomic instability to cause EGFR targeted therapy resistance in lung cancer

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.

3-Phosphoinositide-dependent kinase 1 drives acquired resistance to osimertinib

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

A focal adhesion kinase-YAP signaling axis drives drug tolerant persister cells and residual disease in lung cancer

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.

Targeted cancer therapy induces APOBEC fuelling the evolution of drug resistance

This study shows that targeted cancer therapy induces APOBEC-mediated mutagenesis, promoting drug resistance by increasing genetic diversity through mechanisms involving NF-κB activation and reduced DNA repair.

Deficiency of the splicing factor RBM10 limits EGFR inhibitor response in EGFR mutant lung cancer

This study shows that RBM10 deficiency reduces EGFR inhibitor efficacy in EGFR mutant lung cancer by altering Bcl-x splicing and apoptosis, and that co-inhibiting Bcl-xL can overcome this resistance.

A tyrosine kinase protein interaction map reveals targetable EGFR network oncogenesis in lung cancer

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.

The CIC-DUX4 fusion oncoprotein drives metastasis and tumor growth via distinct downstream regulatory programs and therapeutic targets in sarcoma

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.

Synthetic essentiality of metabolic regulator PDHK1 in PTEN-deficient cells and cancers

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.

Novel computational method for predicting polytherapy switching strategies to overcome tumor heterogeneity and evolution

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