Targeting ALK, ROS1, and BRAF Kinases
作者： Robert C. Doebele , D. Ross Camidge
DOI: 10.1097/JTO.0B013E31826DF05E
关键词: Cancer research 、 Oncogene 、 Adenocarcinoma 、 Mutation 、 Receptor Protein-Tyrosine Kinases 、 Medicine 、 ROS1 、 Cancer cell 、 Lung cancer 、 Cell
摘要: Cancer cells demonstrate numerous genetic aberrations. Despite this complexity, it is hypothesized that cancer are often addicted to a single oncogenic driver such inhibition of target would lead cell death.1 Data collected from patients with adenocarcinoma by the Lung Mutation Consortium (LCMC) significant number harboring distinct drivers, many which may be amenable targeted therapies.2 Two current areas intense investigation match therapies growing list selected oncogene aberrations in NSCLC and also understand mechanisms resistance these so can overcome or potentially delayed new drugs drug combinations.
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