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Transformation from adenocarcinoma to squamous cell lung carcinoma with MET amplification after lorlatinib resistance: A case report.
- Source :
-
Thoracic cancer [Thorac Cancer] 2021 Mar; Vol. 12 (5), pp. 715-719. Date of Electronic Publication: 2021 Jan 21. - Publication Year :
- 2021
-
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.<br /> (© 2021 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.)
- Subjects :
- Adenocarcinoma pathology
Aminopyridines pharmacology
Carcinoma, Non-Small-Cell Lung pathology
Drug Resistance, Neoplasm
Female
Humans
Lactams pharmacology
Middle Aged
Pyrazoles pharmacology
Adenocarcinoma drug therapy
Aminopyridines therapeutic use
Carcinoma, Non-Small-Cell Lung drug therapy
Lactams therapeutic use
Pyrazoles therapeutic use
Subjects
Details
- Language :
- English
- ISSN :
- 1759-7714
- Volume :
- 12
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Thoracic cancer
- Publication Type :
- Academic Journal
- Accession number :
- 33475256
- Full Text :
- https://doi.org/10.1111/1759-7714.13829