Patient-reported outcomes in a phase II study of alectinib

The ALK fusion gene, NPM-ALK , was originally identified in a case of anaplastic large cell lymphoma in 1994, and the EML4 -ALK fusion gene was discovered in non-small cell lung cancer (NSCLC) by Drs Soda and Mano in 2007.1 2 This was the first report of identification of a fusion gene in NSCLC. The incidence, according to this first report, of EML4-ALK fusion gene in NSCLC is 6.7%.2 EML4-ALK encodes a transforming fusion kinase, which is a promising therapeutic target for ALK fusion gene-positive (hereinafter ALK-positive) NSCLC. Several fusion partners for ALK other than EML4 , such as KIF5B , TFG and  KCL1 , have also been reported in NSCLC.3 ALK fusion genes have also been detected in several solid tumours other than NSCLC, such as renal cell carcinoma, colon cancer, breast cancer, ovarian cancer, pancreas cancer and inflammatory myofibroblastic tumours,3 4 and ALK inhibitors have been shown to be effective for these cancers also harbouring the fusion gene, similar to the case for EML4-ALK- positive NSCLC.4 5Crizotinib is the first ALK inhibitor that was initially developed as a MET inhibitor and is also known as an ROS inhibitor.6 The phase III PROFILE 1014 trial was conducted to comparatively evaluate the safety and efficacy of crizotinib as a first-line treatment agent for patients with ALK-positive NSCLC.7 Progression-free survival (PFS) was significantly longer in the crizotinib arm than in the conventional chemotherapy arm …