Journal
CANCER CELL
Volume 18, Issue 6, Pages 548-551Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2010.11.033
Keywords
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Funding
- Lung Cancer SPORE NCI [P50CA70907]
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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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