Transformation from adenocarcinoma to squamous cell lung carcinoma with MET amplification after lorlatinib resistance: A case report. Issue 5 (21st January 2021)

• Record Type: Journal Article
• Authors: Ueda, Shoko; Shukuya, Takehito; Hayashi, Takuo; Suzuki, Mario; Kondo, Akihide; Arai, Yuta; Takeshige, Tomohito; Ninomiya, Hironori; Takahashi, Kazuhisa
• Is Part Of: Thoracic cancer. Volume 12:Issue 5(2021)
• Page Start: 715
• Page End: 719
• Publication Date: 2021-01-21
• Subjects: Anaplastic lymphoma kinase -- lorlatinib -- lung cancer -- squamous cell lung cancer transformation; Chest -- Cancer -- Periodicals; Chest -- Cancer -- Treatment -- Periodicals; Chest -- Surgery -- Periodicals; 616.99494005
• DOI: 10.1111/1759-7714.13829
• Languages: English
• ISSNs: 1759-7706

Abstract

Abstract: 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. Abstract : Little has been 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.