title: [A simple view on lung cancer biology: the MET pathway].
abstract: MET is a cell membrane tyrosine kinase receptor for its ligand the hepatocyte growth factor (HGF), also called scatter factor (SF). MET conveys mitogenic, motogenic and proangiogenic signals, important during embryonic development and during the development of cancer. Activation of the HGF-MET pathway seems to be associated with a poor prognosis in lung cancer. Activation in lung cancer may be related to several molecular anomalies: ligand overexpression, receptor overexpression, genomic amplification or MET mutation. In MET amplified or mutated lung cancer, MET may be an important oncogene, as the tumor appears "MET addicted". In other lung cancers, MET may be implicated in tumour progression by tissue invasion and formation of metastases. MET amplification is also a mechanism known to be implicated in 20% of secondary resistance to EGFR inhibitors in patients presenting EGFR mutated lung cancer. Different strategies of MET inhibition in lung cancer are being studied, particularly in EGFR mutated lung cancer. In this review we discuss the structure of the MET receptor, the activated pathways, the main genomic anomalies in lung cancer and the development of MET inhibitors.
authors.affiliation: Service de pneumologie et réanimation, hôpital Tenon, Assistance Publique-Hôpitaux de Paris, 4 rue de La-Chine, Paris cedex 20, France.
authors.forename: A-M
authors.initials: AM
authors.lastname: Ruppert
authors.forename: M
authors.initials: M
authors.lastname: Beau-Faller
authors.forename: L
authors.initials: L
authors.lastname: Belmont
authors.forename: A
authors.initials: A
authors.lastname: Lavolé
authors.forename: V
authors.initials: V
authors.lastname: Gounant
authors.forename: J
authors.initials: J
authors.lastname: Cadranel
authors.forename: M
authors.initials: M
authors.lastname: Wislez
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D002455:Cell Division; D018450:Disease Progression; D004789:Enzyme Activation; D005784:Gene Amplification; D017228:Hepatocyte Growth Factor / Q000502:physiology; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000201:enzymology* / Q000473:pathology; D008958:Models, Molecular; D058990:Molecular Targeted Therapy; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D009857:Oncogenes; D011379:Prognosis; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D017434:Protein Structure, Tertiary; D019859:Proto-Oncogene Proteins c-met / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction
chemical_list: D000970:Antineoplastic Agents; D009363:Neoplasm Proteins; D047428:Protein Kinase Inhibitors; D017228:Hepatocyte Growth Factor; C491743:MET protein, human; D019859:Proto-Oncogene Proteins c-met