An advanced c-MET-amplified NSCLC patient that was treated with crizotinib

c-MET is a tyrosine kinase receptor, which is encoded in part by mesenchymal-epidermal transition (MET) exon 14. Mutations in the MET gene can cause increased c-MET signaling and oncogenic stimulation. Although c-MET mutation is rare, it is a targetable driver mutation. Although the guidelines do not recommend routine screening before treatment decision, there are drugs that can be used in patients who have c-MET mutation or amplification.

We present a metastatic c-MET-amplified non-small cell lung cancer (NSCLC) patient who was treated with crizotinib. He was not eligible for chemotherapy because of poor performance score; c-MET amplification was investigated after the other common driver mutations were negative.

After c-MET amplification was shown, crizotinib 250 mg BID was started. A partial response was achieved with the initiation of crizotinib, and his performance score improved after treatment.

We presented a metastatic c-MET-amplified NSCLC patient, who was not eligible for standard platin doublet chemotherapy, to emphasize the importance of investigating all driver mutations, including c-MET amplification especially in patients who cannot tolerate cytotoxic chemotherapy.