Tackling ALK in non-small cell lung cancer: the role of novel inhibitors

Lung cancer remains one of the deadliest neoplasms worldwide, with less than 18% of patients alive five years after diagnosis (1); non-small cell lung cancer (NSCLC) accounts for 85% of all lung cancers (2). Notably, NSCLC is not a single pathological entity, but it is rather a mixture of malignancies different in terms of histology and molecular patterns, differentially impacting upon disease outcomes. Several genetic events lead to the expression of molecularly altered tyrosine kinase receptors (TKRs) and signaling proteins that, while conferring decisive oncogenic potential to malignant cells, represent suitable and crucial therapeutic targets. In addition to mutations occurring in EGFR, KRAS, BRAF and other genes (3), recent interest has been conferred to gene fusions determining the aberrant expression of proteins, which generates similar profiles of oncogenic addiction (4)