New targets in advanced NSCLC: EML4-ALK

Clin Adv Hematol Oncol. 2011 Mar;9(3):207-14.


Targeted therapies aimed at inhibiting oncogenic tyrosine kinases are becoming commonplace in the treatment of cancer. The EML4-ALK fusion gene was first identified as a potentially targetable oncogenic driver in non-small cell lung cancer in 2007. A small molecule ALK inhibitor, crizotinib, may now be on the verge of approval by the US Food and Drug Administration for the treatment of ALK-rearranged lung cancer. Here we review the discovery of EML4-ALK, the development of clinical diagnostics for ALK rearrangements, the clinical epidemiology of lung cancers driven by EML4-ALK, and ongoing ALK inhibitor-based clinical trials.

Publication types

  • Review

MeSH terms

  • Carcinoma, Non-Small-Cell Lung* / diagnosis
  • Carcinoma, Non-Small-Cell Lung* / epidemiology
  • Carcinoma, Non-Small-Cell Lung* / genetics
  • Carcinoma, Non-Small-Cell Lung* / metabolism
  • Carcinoma, Non-Small-Cell Lung* / therapy
  • Crizotinib
  • Genetic Therapy
  • Humans
  • Lung Neoplasms* / diagnosis
  • Lung Neoplasms* / epidemiology
  • Lung Neoplasms* / genetics
  • Lung Neoplasms* / metabolism
  • Lung Neoplasms* / therapy
  • Oncogene Proteins, Fusion / genetics*
  • Oncogene Proteins, Fusion / metabolism
  • Pyrazoles / therapeutic use
  • Pyridines / therapeutic use


  • EML4-ALK fusion protein, human
  • Oncogene Proteins, Fusion
  • Pyrazoles
  • Pyridines
  • Crizotinib