It was only 3 years ago that an acquired translocation of EML4 with ALK leading to the expression of an EML4-ALK oncoprotein in non-small cell lung cancer (NSCLC) was reported. Tumor cells expressing EML4-ALK are "addicted" to its continued function. Now, crizotinib, an oral ALK inhibitor, is demonstrated to provide dramatic clinical benefit with little toxicity in patients having such advanced NSCLC, and a mechanism of clinical resistance to crizotinib is identified. Such therapy "targeted" at oncogenic proteins provides "personalized" medicine and prompts genome-wide mutation analysis of human tumors to find other therapeutic targets. © 2010 Elsevier Inc.
Gerber, D. E., & Minna, J. D. (2010, December 14). ALK Inhibition for Non-Small Cell Lung Cancer: From Discovery to Therapy in Record Time. Cancer Cell. https://doi.org/10.1016/j.ccr.2010.11.033