Current evidence in support of the second-generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor alectinib for the treatment of non-small cell lung cancer positive for ALK translocation

Abstract

Treatment for advanced non-small cell lung cancer (NSCLC) depends on the molecular characteristics of the tumor. Mutations of the epidermal growth factor receptor ( EGFR ) gene are present in ~32% of Asians and ~7% of individuals of other ethnic groups with NSCLC (1), and rearrangements of the anaplastic lymphoma kinase ( ALK ) gene have been detected in ~3% to 5% of NSCLC tumors (2-4). The echinoderm microtubule-associated protein-like 4 ( EML4 ) gene is the most common fusion partner of ALK in NSCLC, and the fusion gene exists in several variants with different breakpoints within EML4 . NSCLC tumors that harbor ALK fusion genes are oncogene addicted and therefore usually sensitive to treatment with ALK tyrosine kinase inhibitors ( ALK -TKIs).