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To date, several studies have described the mechanism of resistance to first‐ or second‐generation anaplastic lymphoma kinase (ALK) inhibitors. Secondary  ALK  mutations,  ALK  gene amplification, and other bypass signal activations (i.e.,  KRAS  mutation,  EGFR  mutation, amplification of  KIT , and increased autophosphorylation of EGFR) are known as resistance mechanisms. However, little has been previously reported on acquired resistance mechanisms to lorlatinib. Here, we report a case of a patient with  ALK ‐positive lung adenocarcinoma that acquired resistance to lorlatinib during treatment for brain metastasis and showed histological transformation to squamous cell carcinoma with  MET  amplification. We also review the previous literature on the resistance mechanism to ALK inhibitors.

Transformation from adenocarcinoma to squamous cell lung carcinoma with MET amplification after lorlatinib resistance: A case report