Acquired Resistance to EGFR Tyrosine Kinase Inhibitors is Associated With Low Efficacy of Radiation Therapy for Brain Metastases From EGFR-mutant Lung Adenocarcinoma

2012 ◽  
Vol 84 (3) ◽  
pp. S102
Author(s):  
H. Hirata ◽  
K. Nakamura ◽  
N. Kunitake ◽  
Y. Shioyama ◽  
T. Sasaki ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Brain Metastases ◽  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Acquired Resistance ◽  
Egfr Tyrosine Kinase ◽  
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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