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

First Author  Gerber DE Year  2010
Journal  Cancer Cell Volume  18
Issue  6 Pages  548-51
PubMed ID  21156280 Mgi Jnum  J:167436
Mgi Id  MGI:4868290 Doi  10.1016/j.ccr.2010.11.033
Citation  Gerber DE, et al. (2010) ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time. Cancer Cell 18(6):548-51
abstractText  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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