Zusammenfassung
Ein Anteil von 10 bis 15 % der nichtkleinzelligen Lungenkarzinome (NSCLC) proliferiert auf der Basis einer sogenannten Treibermutation. Diese molekulare Alteration hält das maligne Potenzial aufrecht und ist gezielt blockierbar. Neben Mutationen in EGFR, dem Gen des „epidermal growth factor receptor“, betrifft dies Translokationen zwischen den Genen des „echinoderm microtubule-associated protein-like 4“ (EML4) und der anaplastischen Lymphomkinase (ALK) sowie die Alteration im ROS1-Gen. Für die ersten beiden Alterationen stehen mittlerweile mehrere Generationen von Inhibitoren zur Verfügung. Für ROS1 und weitere Treibermutationen ist die Datenlage zurzeit noch recht spärlich, da sie beim NSCLC sehr selten vorkommen.
Abstract
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.
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D.F. Heigener und M. Reck erhielten Honorare für Vorträge und für das Mitwirken an Advisory Boards sowie Reisekostenerstattungen von Hoffmann-La Roche, Boehringer Ingelheim, Pfizer, Novartis, AstraZeneca, MSD und Bristol-Myers Squibb. M. Horn gibt an, dass kein Interessenkonflikt besteht.
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M. Wehling, Mannheim
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Heigener, D.F., Horn, M. & Reck, M. Targeted Therapy und Precision Medicine. Internist 57, 1243–1249 (2016). https://doi.org/10.1007/s00108-016-0121-z
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DOI: https://doi.org/10.1007/s00108-016-0121-z
Schlüsselwörter
- Nichtkleinzelliges Lungenkarzinom
- EGFR-Protein, human
- Anaplastische Lymphomkinase
- ROS1-Protein, human
- Treibermutation