title: Unravelling signal escape through maintained EGFR activation in advanced non-small cell lung cancer (NSCLC): new treatment options.
abstract: The discovery of activating epidermal growth factor receptor (EGFR) mutations has opened up a new era in the development of more effective treatments for patients with non-small cell lung cancer (NSCLC). However, patients withEGFR-activating mutated NSCLC treated with EGFR tyrosine kinase inhibitors (TKIs) ultimately develop acquired resistance (AR). Among known cases of patients with AR, 70% of the mechanisms involved in the development of AR to EGFR TKI have been identified and may be categorised as either secondaryEGFRmutations such as theT790Mmutation, activation of bypass track signalling pathways such as MET amplification, or histologic transformation.EGFR-mutant NSCLC tumours maintain oncogenic addiction to the EGFR pathway beyond progression with EGFR TKI. Clinical strategies that can be implemented in daily clinical practice to potentially overcome this resistance and prolong the outcome in this subgroup of patients are presented.
authors.affiliation: Medical Oncology Department , Gustave Roussy, Université Paris-Saclay , Villejuif , France.
authors.forename: Jordi
authors.initials: J
authors.lastname: Remon
authors.affiliation: Medical Oncology Department, Gustave Roussy, Université Paris-Saclay, Villejuif, France; Paris Sud University, Orsay, France.
authors.forename: Benjamin
authors.initials: B
authors.lastname: Besse
keywords: ACQUIRED RESISTANCE; EGFR MUTANT; EGFR TKI; OSIMERTINIB; lung cancer