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Review
. 2010 Dec 14;18(6):548-51.
doi: 10.1016/j.ccr.2010.11.033.

ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time

David E Gerber  1 , John D Minna
Affiliations
Review

ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time

David E Gerber et al. Cancer Cell. .

Abstract

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.

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