The continued EGFR-TKI with cytotoxic chemotherapy at progression—poison or medicine?

EGFR tyrosine kinase inhibitors (TKI) have shown the efficacy in treatment of lung cancer patients with EGFR sensitizing mutations, and their use has led to a doubling of progression-free survival (PFS) and a lengthening of overall survival (OS) by more than 2 years. However, the emergence of resistance is inevitable, which creates new challenges for the management of patients with EGFR-mutant lung cancer (1). As several approaches after the development of resistance have been suggested, one of them is the continuation of EGFR-TKI with local therapy to aggravated lesions if necessary (2). This recommendation is based on some studies which showed the survival benefits by the continuation of EGFR-TKI compared with switching to cytotoxic chemotherapy (3,4). It implies that EGFR-TKI still has a role on the control of the EGFR-mutant lung cancer despite acquired resistance to EGFR-TKI. This phenomenon may be contributed by the capability of EGFR-TKI-sensitive clones to grow fast if EGFR-TKI removed and the relatively slow growth rate of resistant clones (5)