scholarly journals A case of EGFR mutant lung adenocarcinoma that acquired resistance to EGFR-tyrosine kinase inhibitors with MET amplification and epithelial-to-mesenchymal transition

2015 ◽  
pp. 783 ◽  
Author(s):  
Seigo Miyoshi ◽  
Takahide Kato ◽  
Hitoshi Katayama ◽  
Ryoji Ito ◽  
Takafumi Okura ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Tyrosine Kinase Inhibitors ◽  
Epithelial To Mesenchymal Transition ◽  
Kinase Inhibitors ◽  
Acquired Resistance ◽  
Mesenchymal Transition ◽  
Met Amplification ◽  
Egfr Tyrosine Kinase Inhibitors ◽  
Egfr Mutant

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

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Zhe Zhang ◽  
Sen Yang ◽  
Qiming Wang
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Acquired Resistance ◽  
Egfr Tyrosine Kinase ◽  
Met Amplification ◽  
Egfr Tyrosine Kinase Inhibitors ◽  
Egfr Mutant ◽  
Egfr Tkis

AbstractEGFR-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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