Emerging resistance pathways in lung cancer: what has ROS-1 taught us?
Molecular characterization of non-small cell lung cancer (NSCLC) and implications for treatment and prognosis are increasingly important. Selection of molecularly targeted systemic therapy is commonly based on clonal oncogenic drivers of which epidermal growth factor receptor (EGFR) and the fusion gene echinoderm microtubule-associated protein-like 4 anaplastic lymphoma kinase (EMLA4-ALK) are examples established in clinical practice. The former, found in approximately 10–15% of patients with NSCLC in the western world, is more prevalent in adenocarcinoma, non/light smokers, younger females, and patients of far eastern descent (1). Patients with EMLA4-ALK translocated tumors share similar clinical characteristics but are less prevalent (2). Several other rarer candidate driver mutations, including ROS proto-oncogene 1, receptor tyrosine kinase (ROS-1), are also implicated in NSCLC (3).