Vincent Haddad

TL;DR: Final OS data from IMPRESS are supportive of earlier PFS results and are sufficient to warn physicians against the continuation of treatment with first-generation EGFR tyrosine kinase inhibitors beyond radiologic disease progression when chemotherapy is initiated.

TL;DR: Evidence is provided that chronic stress hormones promote EGFR TKI resistance via β2-AR signaling by an LKB1/CREB (cyclic adenosine 3′,5′-monophosphate response element–binding protein)/IL-6–dependent mechanism and suggest that combinations of β-blockers with EG FR TKIs merit further investigation as a strategy to abrogate resistance.

TL;DR: HGF/c-MET pathway mediates VEGFR inhibitor resistance and vascular remodeling in NSCLC and in patients with cancer receiving VEGfr TKIs, high pretreatment HGF plasma levels correlated with poorer survival.

TL;DR: BICR analysis of IPASS data support the original, investigator-assessed results, and EGFR mutation-positive status remains a significant predictor of response to first-line TKI therapy.