ALK-mutated non-small-cell lung cancer: a new strategy for cancer treatment

Lung. 2012 Aug;190(4):381-8. doi: 10.1007/s00408-012-9391-y. Epub 2012 May 15.


The anaplastic lymphoma kinase (ALK) tyrosine kinase (TK) receptor has emerged recently as a potentially relevant biomarker and therapeutic target in solid and hematologic tumors. A variety of alterations in the ALK gene, such as mutations, overexpression, amplification, translocations, or other structural rearrangements, have been implicated in human cancer tumorigenesis. In this article we review the potential role that ALK may have in lung tumor origin, the methodology to detect the different molecular alterations, and the most important clinical aspects of ALK alterations in NSCLC patients.

Publication types

  • Review

MeSH terms

  • Anaplastic Lymphoma Kinase
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Crizotinib
  • Gene Amplification
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics*
  • Mutation / genetics*
  • Protein Kinase Inhibitors / therapeutic use*
  • Pyrazoles / therapeutic use
  • Pyridines / therapeutic use
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Translocation, Genetic


  • Protein Kinase Inhibitors
  • Pyrazoles
  • Pyridines
  • Crizotinib
  • ALK protein, human
  • Anaplastic Lymphoma Kinase
  • Receptor Protein-Tyrosine Kinases