作者: J Tanizaki , I Okamoto , K Takezawa , K Sakai , K Azuma
DOI: 10.1038/BJC.2011.586
关键词:
摘要: Lung cancer is the leading cause of deaths worldwide. Given successful development tyrosine kinase inhibitors (TKIs) that target epidermal growth factor receptor (EGFR) for treatment individuals with lung positive EGFR mutations (Paez et al, 2004), identification other kinases implicated in would be expected to facilitate new molecularly targeted therapies. A potential driver mutation was recently identified 5 10% cases non-small-cell (NSCLC): fusion echinoderm microtubule-associated protein-like 4 gene (EML4) anaplastic lymphoma (ALK), which results production a protein (EML4–ALK) (Soda 2007; Shaw 2009; Sasaki 2010). Early-phase clinical trials have revealed TKIs ALK show marked efficacy patients EML4–ALK (Kwak However, not all benefit from such treatment, response these agents thus differing even among who harbour this same molecular abnormality. We now investigated possible reasons variability ALK-TKIs use human NSCLC cell lines EML4–ALK.