Impact of MET alterations on targeted therapy with EGFR-tyrosine kinase inhibitors for EGFR-mutant lung cancer

被引：0
作者：
Zhe Zhang
Sen Yang
Qiming Wang
机构：
[1] The Affiliated Cancer Hospital of Zhengzhou University,Department of Internal Medicine
[2] Henan Cancer Hospital,undefined
来源：
Biomarker Research | / 7卷
关键词：
MET amplification; EGFR-TKIs; Resistance; Non-small cell lung cancer;
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摘要：
EGFR-tyrosine kinase inhibitors (EGFR-TKIs) have achieved remarkable outcomes in the treatment of patients with EGFR-mutant non-small-cell lung cancer, but acquired resistance is still the main factor restricting their long-term use. In addition to the T790 M mutation of EGFR, amplification of the MET (or c-MET) gene has long been recognized as an important resistance mechanism for first- or second-generation EGFR-TKIs. Recent studies suggest that a key mechanism of acquired resistance to third-generation EGFR-TKIs (such as osimertinib) may be MET amplification and/or protein overactivation, especially when they are used as a first-line treatment. Therefore, in patients resistant to first-generation EGFR-TKIs caused by MET amplification and/or protein overactivation, the combination of osimertinib with MET or MEK inhibitors may be considered.
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