Abstract

Epidermal Growth Factor Receptor (EGFR) exon 19 deletions and L858R mutations are oncogenic drivers in a subset of non-small cell lung cancers (NSCLC). While tyrosine kinase inhibitor (TKI) therapies against mutant EGFR have significantly improved response rates and progression free survival (PFS) compared to cytotoxic chemotherapy for patients with metastatic EGFR-mutated NSCLC, responses to therapy are incomplete and resistance to EGFR-targeted therapies is inevitable. Somatic and copy-number alterations in cell cycle genes concurrent with EGFR mutations have been suggested to play a role in EGFR-TKI resistance, however this has not been completely characterized.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call