The MET p. E168D mutation has been reported in various tumors including lung cancer according to the COSMIC database. Some studies indicate that this mutation may be associated with higher affinity for ligand, HGF. In vitro studies in cell lines with cells expressing MET p.E168D may show increased sensitivity to MET inhibitor. According to ClinVar, this particular variant is a likely benign germline variant (https://preview.ncbi.nlm.nih.gov/clinvar/variation/41627/). The clinical significance of this variant remains to be fully elucidated.

MET is a member of the receptor tyrosine kinase and proto-oncogene playing a major role in tumor development and metastasis. MET E168D has been previously reported in papillary thyroid carcinoma. This mutation is located in the SEMA domain containing the ligand binding site. In vitro study has shown that E168D alters MET functionality in lung cancer. The prognostic and predictive significance of MET mutations in thyroid cancer is not clear and correlation with other clinical and laboratory findings is necessary. Of note, this variant is reported as a likely benign germline variant in ClinVar (https://preview.ncbi.nlm.nih.gov/clinvar/variation/41627/).

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 1% of primary prostate cancers and up to 4.4% of metastatic prostate cancers. Studies have suggested that overexpression of c-MET and aberrant activation of the HGF/c-MET axis in prostate cancer is a relatively late event in tumor progression seen in advanced stages of the disease. MET E168D mutation is located in the SEMA domain containing the ligand binding site. The prognostic and predictive significance of MET mutations in prostate cancer is not clear and correlation with other clinical and laboratory findings is necessary.

MET is a member of the receptor tyrosine kinase and proto-oncogene playing a major role in tumor development and metastasis. Mutations in MET have been reported in 4-9% of cutaneous melanoma. MET E168D has not been reported in melanomas. This 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 prognostic and predictive significance of MET mutations in melanoma is not clear and correlation with other clinical and laboratory findings is necessary.

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 ~2% of colon cancers. 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 prognostic and predictive significance of MET mutations in colon cancer is not clear and correlation with other clinical and laboratory findings is necessary.

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.