Crizotinib Treatment for Lorlatinib-resistant MET-amplified EML4-ALK-fusion Positive Advanced Lung Adenocarcinoma: A Case Report.
10.3779/j.issn.1009-3419.2024.102.37
- Author:
Xinyi WANG
1
;
Ning MU
1
;
Mei LIU
1
;
Yue XU
1
;
Shengnan WU
1
;
Huan LV
1
;
Chunhua MA
1
Author Information
1. Department of Oncology 5, Tianjin Union Medical Center, The First Affiliated Hospital of Nankai University, Tianjin 300121, China.
- Publication Type:English Abstract
- Keywords:
ALK gene fusion;
Crizotinib;
Lorlatinib;
Lung neoplasms;
MET amplification;
Molecularly targeted therapy
- MeSH:
Humans;
Adenocarcinoma/genetics*;
Adenocarcinoma of Lung/genetics*;
Aminopyridines/therapeutic use*;
Crizotinib/therapeutic use*;
Drug Resistance, Neoplasm/drug effects*;
Lactams/therapeutic use*;
Lung Neoplasms/genetics*;
Oncogene Proteins, Fusion/metabolism*;
Protein Kinase Inhibitors/therapeutic use*;
Proto-Oncogene Proteins c-met/metabolism*;
Pyrazoles/therapeutic use*
- From:
Chinese Journal of Lung Cancer
2024;27(12):956-960
- CountryChina
- Language:Chinese
-
Abstract:
Lung cancer is a major cause of cancer-related mortality worldwide. Among patients with non-small cell lung cancer (NSCLC), approximately 3%-7% harbor anaplastic lymphoma kinase (ALK) gene fusions. In recent years, multiple tyrosine kinase inhibitors (TKIs) have significantly improved the survival of patients with metastatic ALK-positive NSCLC. However, disease progression due to resistance remains a challenge. This article retrospectively analyzes a case of advanced lung adenocarcinoma with the echinoderm microtubule associated protein like 4 (EML4)-ALK fusion variant 3 (V3). The patient developed resistance to Lorlatinib treatment accompanied by mesenchymal-epithelial transition factor (MET) amplification. Effective tumor control was achieved with the combined use of Crizotinib and Lorlatinib, providing a valuable reference for further exploration of treatment strategies following resistance to ALK-TKIs in clinical practice.
.
