Targeted oncology
-
The anaplastic lymphoma kinase (ALK) fusion gene is a key oncogenic driver in a subset of patients with advanced non-small cell lung cancer (NSCLC). Oncogenic fusion genes, including echinoderm microtubule-associated protein-like 4 (EML4) and ALK, have been detected in approximately 2-7 % of NSCLC patients. Fluorescence in situ hybridization (FISH) is the recommended method for detecting ALK gene rearrangement. ⋯ Treatment-related adverse events, predominantly restricted to the gastrointestinal and visual systems, are generally self-limiting or easily managed. Crizotinib is a new standard of care for patients with advanced, ALK-positive, NSCLC. In this review, we will discuss the discovery of ALK rearrangements, the clinical epidemiology of lung cancer driven by ALK, the clinical data for ALK-targeted therapy in NSCLC, and ongoing ALK inhibitor-based clinical trials.
-
Non-small cell lung cancer (NSCLC) has recently been associated with interesting molecular characteristics that have important implications in carcinogenesis and response to targeted therapies. Targeted therapies, if given to a patient subpopulation enriched by the presence of relevant molecular targets, can often abrogate cell signaling that perpetuates cancer progression. For instance, several molecular alterations have been defined as "driver mutations," such as mutations in EGFR and EML4-ALK fusion gene. ⋯ These first steps towards personalized medicine represent a shift in the management of NSCLC. Indeed, NSCLC should no longer be viewed as one common generic tumor but rather as a collection of more rare diseases with different biological behaviors and different sensitivities to targeted treatments. We are now clearly entering an era of personalized medicine for NSCLC cancers, and the development of molecular profiling technologies to assess DNA provides the potential to tailored medical care.