title: [Which platform to support a personalized lung cancer treatment?].
abstract: Considerable progress has been achieved in the understanding of lung cancer biology. Molecular driver mutations have been identified and different targeted therapies have been developed. Thus, the management of small size biopsies is essential and needs a strong collaboration between the different medical partners, particularly pulmonologist, pathologist, molecular biologist and oncologist. The aim is to optimise histological and molecular analyses allowing patients access to novel biotherapies. The French National Cancer Institute set up platforms for molecular genetics at university hospitals with expertise in molecular and pathological analysis. Mutational status of EGFR is analyzed routinely in non-small lung cancer. Treatment with EGFR inhibitors as first line therapy is limited to lung cancer patients harboring an EGFR mutation. More recently, ALK rearrangements have been identified as a rare driver mutation in lung cancer. Crizotinib, an ALK inhibitor is a new therapeutic standard in ALK rearranged tumors. Other biomarkers as RAS, BRAF, HER2 or PIK3CA have potential clinical relevance with possible approval of novel tailored treatment and will be discussed in this report. The project "BIOMARQUEURS France" will underscore the results of the French platform of more than 15 000 French patients.
authors.affiliation: Assistance Publique-Hôpitaux de Paris, hôpital Tenon, service de pneumologie et réanimation, 4, rue de la Chine, 75970 Paris Cedex 20, France.
authors.forename: Anne-Marie
authors.initials: AM
authors.lastname: Ruppert
authors.forename: Martine
authors.initials: M
authors.lastname: Antoine
authors.forename: Michèle
authors.initials: M
authors.lastname: Beau-Faller
authors.forename: Jacques
authors.initials: J
authors.lastname: Cadranel
authors.forename: Marie
authors.initials: M
authors.lastname: Wislez
mesh_terms: D000077548:Anaplastic Lymphoma Kinase; D001706:Biopsy; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D058534:Class I Phosphatidylinositol 3-Kinases; D000077547:Crizotinib; D066246:ErbB Receptors / Q000037:antagonists & inhibitors; D005602:France; D018773:Genes, erbB-1 / Q000235:genetics; D018734:Genes, erbB-2 / Q000235:genetics; D011905:Genes, ras / Q000235:genetics; D005819:Genetic Markers / Q000235:genetics; D006801:Humans; D008168:Lung / Q000473:pathology; D008175:Lung Neoplasms / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D058990:Molecular Targeted Therapy / Q000379:methods*; D009154:Mutation / Q000235:genetics* / Q000502:physiology; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics; D057285:Precision Medicine / Q000379:methods*; D016730:Program Development; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics; D011720:Pyrazoles / Q000627:therapeutic use; D011725:Pyridines / Q000627:therapeutic use; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics
chemical_list: C522504:EML4-ALK fusion protein, human; D005819:Genetic Markers; D015514:Oncogene Proteins, Fusion; D011720:Pyrazoles; D011725:Pyridines; D000077547:Crizotinib; D019869:Phosphatidylinositol 3-Kinases; D058534:Class I Phosphatidylinositol 3-Kinases; C484760:PIK3CA protein, human; C000626173:ALK protein, human; D000077548:Anaplastic Lymphoma Kinase; D066246:ErbB Receptors; D020794:Receptor Protein-Tyrosine Kinases; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf