MET

Ramsey Asmar, Balazs Halmos

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The receptor tyrosine kinase METactivates 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.

Original languageEnglish (US)
Title of host publicationCancer Therapeutic Targets
PublisherSpringer New York
Pages773-786
Number of pages14
Volume2-2
ISBN (Electronic)9781441907172
ISBN (Print)9781441907165
DOIs
StatePublished - Jan 1 2017

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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

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Asmar, R., & Halmos, B. (2017). MET. In Cancer Therapeutic Targets (Vol. 2-2, pp. 773-786). Springer New York. https://doi.org/10.1007/978-1-4419-0717-2_87