MET is a member of the receptor tyrosine kinase and proto-oncogene playing a major role in tumor development and metastasis. MET mutations have been reported in up to 3.3% of low-grade gliomas and 2.2% of glioblastomas. MET E168D mutation is located in a conserved domain containing the ligand binding site. In vitro studies have shown that E168D may be associated with higher ligand affinity and higher susceptibility to c-Met inhibitors in lung cancer. The predictive and prognostic significance of MET mutations in brain tumors is unclear and needs to be further studied. Correlation with other clinical and laboratory findings is recommended.
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