J. K. Rotow

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.

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.