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.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Gerber DE,Minna JDdoi
10.1016/j.ccr.2010.11.033subject
Has Abstractpub_date
2010-12-14 00:00:00pages
548-51issue
6eissn
1535-6108issn
1878-3686pii
S1535-6108(10)00491-5journal_volume
18pub_type
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