title: PROFILing non-small-cell lung cancer patients for treatment with crizotinib according to anaplastic lymphoma kinase abnormalities: translating science into medicine.
abstract: BACKGROUND
  In the recent years, the growing attention to the molecular background of non-small-cell lung cancer (NSCLC) led to the identification of different molecular subtypes according to genetic abnormalities driving the disease development and progression. Whereas the addicted pathways were successfully inhibited (such as the mutant epidermal growth factor receptor), clinicians have witnessed a dramatic survival improvement. In this regard, the molecular portrait of adenocarcinoma was recently enriched by the identification of a specific patients' subgroup characterized by abnormalities in the anaplastic lymphoma kinase (ALK), with unclear prognostic features but impressive response to specific inhibitors.
  
  
  METHODS
  In this article, updated data derived from the development and the use of crizotinib (the most advanced in development among tyrosine kinase ALK inhibitors) in comparison with standard second-line chemotherapy for patients affected by ALK-altered NSCLC are reviewed.
  
  
  CONCLUSIONS
  Taking into account the available data, pretreated NSCLC patients carrying the ALK-translocation require a selected targeted therapy which significantly improves activity, efficacy and symptoms control versus chemotherapy. In this context, the identification of this disease entity and the availability of such impressive therapeutic targeting represent a further step toward the understanding of the molecular complexity behind the adenocarcinoma of the lung.
authors.affiliation: University of Verona, Azienda Ospedaliera Universitaria Integrata, G.B. Rossi Academic Hospital, Medical Oncology, P.zza L.A. Scuro 10, 37124, Verona, Italy.
authors.forename: Sara
authors.initials: S
authors.lastname: Pilotto
authors.forename: Umberto
authors.initials: U
authors.lastname: Peretti
authors.forename: Silvia
authors.initials: S
authors.lastname: Novello
authors.forename: Giulio
authors.initials: G
authors.lastname: Rossi
authors.forename: Michele
authors.initials: M
authors.lastname: Milella
authors.forename: Matteo
authors.initials: M
authors.lastname: Giaj Levra
authors.forename: Ludovica
authors.initials: L
authors.lastname: Ciuffreda
authors.forename: Francesco
authors.initials: F
authors.lastname: Massari
authors.forename: Matteo
authors.initials: M
authors.lastname: Brunelli
authors.forename: Giampaolo
authors.initials: G
authors.lastname: Tortora
authors.forename: Emilio
authors.initials: E
authors.lastname: Bria
mesh_terms: D000077548:Anaplastic Lymphoma Kinase; D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D000077547:Crizotinib; D020869:Gene Expression Profiling; D020022:Genetic Predisposition to Disease; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D058990:Molecular Targeted Therapy; D010641:Phenotype; D057285:Precision Medicine; D011237:Predictive Value of Tests; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011720:Pyrazoles / Q000627:therapeutic use*; D011725:Pyridines / Q000627:therapeutic use*; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D057170:Translational Research, Biomedical; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D047428:Protein Kinase Inhibitors; D011720:Pyrazoles; D011725:Pyridines; D000077547:Crizotinib; C000626173:ALK protein, human; D000077548:Anaplastic Lymphoma Kinase; D020794:Receptor Protein-Tyrosine Kinases