MET

Reference work entry

Abstract

The receptor tyrosine kinase MET activates numerous cellular signaling pathways after binding with its ligand, hepatocyte growth factor (HGF). MET is involved in a wide range of biological processes and is critical for tissue homeostasis under physiological conditions. MET is also a known oncogene that is abnormally activated in many human cancers by mutation, protein overexpression or amplification. Furthermore, MET is implicated as a common mechanism of resistance to targeted therapies such as EGFR inhibitors. In this review, we describe the biology of MET, the mechanisms by which it becomes an oncogenic driver, its role as a target in cancer medicine, and emerging biomarkers to select patients for MET-targeted therapy. Pre-clinical and clinical data for anti-MET therapies to date are then summarized.

Keywords

Acquired TKI resistance Biomarker Cell scatter Crizotinib Gene amplification Hepatocyte growth factor (HGF) Hereditary papillary renal cell carcinoma Mesenchymal-epithelial transition (MET) receptor Oncogene Tivantinib 

References

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Copyright information

© Springer Science+Business Media New York 2017

Authors and Affiliations

  1. 1.Division of Hematology and OncologyColumbia University Medical CenterNew YorkUSA
  2. 2.Department of MedicineAlbert Einstein College of Medicine/Montefiore Medical CenterBronxUSA

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