Between 10 and 15 % of non-small cell lung cancers (NSCLC) proliferate due to the presence of a so-called driver mutation. This molecular alteration allows the cancer to continue to proliferate and can be deliberately inhibited. In addition to mutations in the epidermal growth factor receptor gene (EGFR) and translocations between the echinoderm microtubule-associated protein-like 4 gene (EML 4) and the anaplastic lymphoma kinase gene (ALK), this applies to ROS1 gene translocations. For the former two alterations, many inhibitors are already available, whereas for ROS1 and other driving mutations the evidence is sparse due to the rare occurrence of these mutations in NSCLC.
- Heigener, D. F.
- Horn, M.
- Reck, M.
Keywords
- Antineoplastic Agents/administration & dosage
- Biomarkers, Tumor/*antagonists & inhibitors/genetics
- Carcinoma, Non-Small-Cell Lung/*drug therapy/*genetics
- Evidence-Based Medicine
- Humans
- Lung Neoplasms/*drug therapy/*genetics
- Molecular Targeted Therapy/*methods
- Precision Medicine/methods
- Treatment Outcome
- Anaplastic lymphoma kinase
- Carcinoma, non-small-cell lung
- EGFR protein, human
- Mutation, driver
- ROS1 protein, human
