The biology and treatment of EML4-ALK non-small cell lung cancer

Eur J Cancer. 2010 Jul;46(10):1773-80. doi: 10.1016/j.ejca.2010.04.002. Epub 2010 Apr 24.

Abstract

The fusion between echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) has recently been identified in a subset of non-small cell lung cancers (NSCLCs). EML4-ALK is most often detected in never smokers with lung cancer and has unique pathologic features. EML4-ALK is oncogenic both in vitro and in vivo and ALK kinase inhibitors are quite effective in pre-clinical model systems. More recently ALK inhibitors have entered clinical development and remarkably clinical efficacy has been observed in NSCLC patients harbouring EML4-ALK translocations. This review will focus on the biology, clinical characteristics, diagnosis and treatment of EML4-ALK NSCLC.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Anaplastic Lymphoma Kinase
  • Antineoplastic Agents / therapeutic use
  • Carcinoma, Non-Small-Cell Lung / diagnosis
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / therapy
  • Enzyme Inhibitors / therapeutic use
  • Gene Rearrangement
  • Humans
  • In Situ Hybridization, Fluorescence
  • Lung Neoplasms / diagnosis
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / therapy
  • Mutation
  • Oncogene Proteins, Fusion / genetics*
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Receptor Protein-Tyrosine Kinases
  • Reverse Transcriptase Polymerase Chain Reaction
  • Smoking / genetics
  • Translocation, Genetic

Substances

  • Antineoplastic Agents
  • EML4-ALK fusion protein, human
  • Enzyme Inhibitors
  • Oncogene Proteins, Fusion
  • ALK protein, human
  • Anaplastic Lymphoma Kinase
  • Protein-Tyrosine Kinases
  • Receptor Protein-Tyrosine Kinases