Does c-Met remain a rational target for therapy in patients with EGFR TKI-resistant non-small cell lung cancer?

Cytotoxic chemotherapy, the historical standard treatment for non-small cell lung cancer (NSCLC), has reached a therapeutic plateau [1]. In recent years, molecularly targeted agents designed to inhibit abnormally activated signaling pathways that can promote oncogenesis have had a significant impact on how NSCLC is treated and patient outcomes. Consequently, the greatest advances in targeted therapy for NSCLC have been made with agents that inhibit other targets, notably epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK).

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