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Interpretation 225
Tier 3
MET
Variants
MET T1010I
Primary Sites
Brain
Tumor Types
Glioblastoma
Interpretation

MET is frequently overexpressed in glioblastomas (GBM), and some gliomas show hepatocyte growth factor (HGF) autocrine activation of the MET signaling pathway. Several studies have found that HGF and MET are expressed at higher levels in human gliomas than in control brain tissue, and that expression levels correlate with tumor grade. Some studies have shown that the HGF expression in high-grade (WHO Grade III-IV) tumors was significantly higher than in low-grade (WHO I-II) tumors. Similarly, coexpression of HGF and MET is observed more frequently in Grade IV GBM than in low-grade glioma, consistent with the contribution of an HGF/MET autocrine loop to malignant progression in these tumors. However, MET sequence alterations have been rare. The p.T1010I mutation, in the cytoplasmic juxtamembrane domain of MET has been reported in some tumor types and also has been reported as a germline variant present in less than 1% of the general population. Its role in tumor development and progression continues to be studied. The utility of MET pathway inhibitors also continues to be explored.

Citations
  1. Zenali M, et al. Retrospective Review of MET Gene Mutations. Oncoscience 2015;2(5):533-41
  2. Awad AJ, et al. Targeting MET for glioma therapy. Neurosurg Focus 2014;37(6):E10
  3. Neklason DW, et al. Activating mutation in MET oncogene in familial colorectal cancer. BMC Cancer 2011;11():424
  4. Ma PC, et al. c-MET mutational analysis in small cell lung cancer: novel juxtamembrane domain mutations regulating cytoskeletal functions. Cancer Res 2003;63(19):6272-81
Last updated: 2020-07-24 14:51:29 UTC
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When using PMKB, please cite: Huang et al., JAMIA 2017


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