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MET E168D
GeneMET
Variantmissense
Amino Acid ChangeE168D
Transcript ID (GRCh37/hg19)ENST00000318493
Codon168
Exon2
Germline/Somatic?Somatic
Pertinent Negative In
Tumor TypePrimary Site
See All Pertinent Negatives

Interpretations

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Tier 3
MET
Variants
MET E168D
Primary Sites
Lung
Tumor Types
Adenocarcinoma
Interpretation

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.

Last updated: 2019-02-22 18:05:13 UTC
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Tier 3
MET
Variants
MET E168D
Primary Sites
Thyroid
Tumor Types
Papillary Carcinoma
Interpretation

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/).

Last updated: 2018-10-05 18:06:21 UTC
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Tier 3
MET
Variants
MET E168D
Primary Sites
Prostate
Tumor Types
Adenocarcinoma
Carcinoma
Interpretation

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.

Last updated: 2016-10-23 22:02:16 UTC
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Tier 3
MET
Variants
MET E168D
Primary Sites
Skin
Tumor Types
Melanoma
Interpretation

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.

Last updated: 2016-11-04 01:04:05 UTC
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Tier 3
MET
Variants
MET E168D
Primary Sites
Colon
Rectum
Tumor Types
Adenocarcinoma
Interpretation

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.

Last updated: 2017-04-10 19:03:06 UTC
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Tier 3
MET
Variants
MET E168D
Primary Sites
Brain
Tumor Types
Glioblastoma
Astrocytoma, Anaplastic
Astrocytoma, Pilocytic
Interpretation

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.

Last updated: 2017-04-17 22:58:40 UTC
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Disclaimer: You assume full responsibility for all risks associated with using this PMKB website. The Englander Institute for Precision Medicine at Weill Cornell Medicine makes no guarantee of the comprehensiveness, reliability or accuracy of the information on this website and assumes no responsibility for errors in the information associated with this web site. Healthcare providers and patients must integrate all clinical and laboratory findings as well as information from a variety of sources before deciding on appropriate clinical care options.


When using PMKB, please cite: Huang et al., JAMIA 2017


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