[Treatment of advanced non-small-cell lung cancer with driver mutations]

Dtsch Med Wochenschr. 2015 Mar;140(5):323-8. doi: 10.1055/s-0041-100759. Epub 2015 Mar 3.
[Article in German]

Abstract

Advanced non-small-cell lung cancer is no longer one disease but the collective name for different diseases defined by clinical, histological, immunohistochemical and, to an increasing extent, molecular biomarkers. This article deals with the treatment options we gained by identifying so called driver mutations in a growing subset of these cancers. For patients whose tumors are characterized by a targetable molecular alteration such as an activating EGFR-Mutation, an ALK-translocation or a ROS1-rearrangement, we see prolonged survival and oral treatments with tyrosine kinase inhibitors demonstrate superiority to chemotherapy in terms of response (remission rate), progression free survival and quality of life. We provide a review of the literature and discuss the status quo of the diagnostic need and the therapeutic options in Germany and Europe.

Publication types

  • 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 / mortality
  • Carcinoma, Non-Small-Cell Lung / therapy*
  • DNA Mutational Analysis*
  • ErbB Receptors / genetics
  • Gene Rearrangement
  • Humans
  • Lung Neoplasms / diagnosis
  • Lung Neoplasms / genetics
  • Lung Neoplasms / mortality
  • Lung Neoplasms / therapy*
  • Molecular Targeted Therapy*
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Protein-Tyrosine Kinases / genetics
  • Proto-Oncogene Proteins / genetics
  • Receptor Protein-Tyrosine Kinases / genetics
  • Survival Rate
  • Translocation, Genetic

Substances

  • Antineoplastic Agents
  • Proto-Oncogene Proteins
  • ALK protein, human
  • Anaplastic Lymphoma Kinase
  • EGFR protein, human
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • ROS1 protein, human
  • Receptor Protein-Tyrosine Kinases