C. M. Blakely

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.

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.

Heterogeneity and targeted therapy-induced adaptations in lung cancer revealed by longitudinal single-cell RNA sequencing

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.

Co-occurring alterations in the RAS-MAPK pathway limit response to MET inhibitor treatment in MET exon 14 skipping mutation positive lung cancer

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.

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.