Open AccessTransformation from adenocarcinoma to squamous cell lung carcinoma with MET amplification after lorlatinib resistance: A case report
Author(s) -
Ueda Shoko,
Shukuya Takehito,
Hayashi Takuo,
Suzuki Mario,
Kondo Akihide,
Arai Yuta,
Takeshige Tomohito,
Ninomiya Hironori,
Takahashi Kazuhisa
Publication year - 2021
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13829
Subject(s) - medicine , anaplastic lymphoma kinase , cancer research , adenocarcinoma , mutation , kras , acquired resistance , lung cancer , transformation (genetics) , gene duplication , cancer , gene , pathology , biology , genetics , malignant pleural effusion , colorectal cancer
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.