KIT and KIT: from biology to clinical use |
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| Authors: | Curtit Elsa Mansi Laura Viel Erika Dobi Erion Chaigneau Loïc Nguyen Thierry Pivot Xavier Blay Jean-Yves Kalbacher Elsa |
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| Institution: | 1. CHU Jean-Minjoz, 3, boulevard Fleming, 25030 Besançon Cedex, France;2. Hôpital édouard-Herriot, unité Inserm 453, centre Léon-Bérard, 69003 Lyon, France;1. Institut Gustave Roussy, Villejuif, France;2. The Royal Marsden NHS Foundation Trust, London, United Kingdom;1. Immunisation Department, Public Health England, London, UK;2. Meningococcal Reference Unit, Public Health England, Manchester, UK;3. GlaxoSmithKline Vaccines, Siena, Italy;4. Médecins Sans Frontières, Nukus, Uzbekistan;5. St George''s University of London, London, UK;1. The University of Texas, MD Anderson Cancer Center, Houston, TX, USA;2. Centre Hospitalier Universitaire de Grenoble, Grenoble, France;3. Johannes Wesling Klinikum Minden, University of Bochum, Germany;4. Mayo Clinic, Scottsdale, AZ, USA;5. Gilead Sciences, Inc., Foster City, CA, USA;6. The Oncology Institute of Hope and Innovation, Santa Ana, CA, USA;7. Department of Clinical Haematology and Bone Marrow Transplantation, Royal Melbourne Hospital, Victoria, Australia;1. Department of Geological Sciences, POB 112120, University of Florida, Gainesville, FL 32611, USA;2. Laboratoire des Sciences du Climat et de l''Environnement, LSCE/IPSL, CNRS-CEA-UVSQ, Université de Paris-Saclay, F-91198 Gif-sur-Yvette, France;3. Godwin Laboratory for Palaeoclimate Research, Department of Earth Sciences, University of Cambridge, Cambridge CB2 3EQ, UK;4. Institute of Geological Sciences and Oeschger Centre for Climate Change Research, University of Bern, Baltzerstrasse 1+3, CH-3012 Bern, Switzerland |
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| Abstract: | Scientific knowledge on gastrointestinal stromal tumors (GIST) has highly progressed over the last 10 years. The molecular bases of oncogenic transformation, KIT activating mutations, were identified in 1998 by Hirota et al. The product of KIT proto-oncogene, KIT protein, is a transmembrane receptor with tyrosine kinase activity. Tyrosine kinase inhibitors targeting these mutated activated kinases, namely imatinib and more recently sunitinib, nilotinib, masitinib or sorafenib, have deeply modified GIST prognosis. Molecular biology in GIST is now becoming a routine tool for treatment selection. In patients with advanced GIST, imatinib should be given until progression, and then, other tyrosine kinase inhibitors targeting KIT should be used. In the adjuvant setting, the optimal duration of imatinib treatment remains unknown. |
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| Keywords: | KIT imatinib sunitinib tumeurs stromales gastro-intestinales récepteur tyrosine kinase KIT imatinib sunitinib gastrointestinal stromal tumors tyrosine kinase receptor |
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