| Literature DB >> 21156280 |
David E Gerber1, John D Minna.
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.Entities:
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Year: 2010 PMID: 21156280 PMCID: PMC3110762 DOI: 10.1016/j.ccr.2010.11.033
Source DB: PubMed Journal: Cancer Cell ISSN: 1535-6108 Impact factor: 31.743