Non-small-cell lung cancer: how to manage MET exon 14 skipping mutant disease

被引：8

作者：

Blaquier, Juan Bautista ^{[1
]}

Recondo, Gonzalo ^{[1
]}

机构：

[1] Ctr Med Educ & Clin Res CEMIC, Thorac Oncol Unit, Med Oncol, Buenos Aires, Argentina

来源：

DRUGS IN CONTEXT | 2022年 / 11卷

关键词：

acquired resistance; exon 14 skipping mutations; MET; next-generation sequencing; non-small-cell lung cancer; target therapy; SOMATIC MUTATIONS; ACQUIRED-RESISTANCE; C-MET; ANTITUMOR-ACTIVITY; KINASE DOMAIN; GROWTH-FACTOR; AMPLIFICATION; INHIBITORS; CARCINOMA; CRIZOTINIB;

D O I：

10.7573/dic.2022-2-2

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Several oncogenic mechanisms have been identified for MET, including MET amplification, fusions, mutations in the tyrosine kinase domain and exon 14 skipping alterations. MET exon 14 mutations are found in about 3-5% of non-small-cell lung cancers. Dysregulation of the MET receptor leads to cell proliferation and survival by activation of the PI3K-AKT-TOR and RAS-RAF-MET-ERK canonical pathways. Targeting the MET tyrosine kinase domain in the setting of MET exon 14 mutations using effective MET tyrosine kinase inhibitors is a current targeted therapy option for patients with metastatic lung cancer. In this Review, we focus on the management of patients with MET exon 14 skipping alterations by addressing the biology of the MET receptor and exon 14 skipping mutations, current treatment strategies, and sequential treatment options based on resistance mechanisms to MET inhibitors in patients with non-small-cell lung cancer.

引用

页数：10

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