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PMID: 21156280 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Review

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

Cancer cell ·Vol. 18 ·No. 6 ·2010-12-14 ·Pages 548-51

Gerber DE, Minna JD

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.

MeSH Terms
Anaplastic Lymphoma Kinase Carcinoma, Non-Small-Cell Lung/drug therapy Clinical Trials as Topic Drug Discovery Humans Lung Neoplasms/drug therapy Protein Kinase Inhibitors/therapeutic use Protein-Tyrosine Kinases/antagonists & inhibitors Receptor Protein-Tyrosine Kinases Translational Research, Biomedical
Chemicals
Protein Kinase Inhibitors ALK protein, human Anaplastic Lymphoma Kinase Protein-Tyrosine Kinases Receptor Protein-Tyrosine Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Gerber David E
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, 75390, USA. david.gerber@utsouthwestern.edu
Minna John D
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Article Info
Journal
Cancer cell
Abbr.
Cancer Cell
ISSN
1878-3686
Published
2010-12-14
Pages
548-51
Language
English
Region
United States
NLM ID
101130617
PMCID
PMC3110762
Subset
IM
Grants
NCI NIH HHS · P50 CA070907 · United States
NCI NIH HHS · P50 CA070907-14 · United States
NCI NIH HHS · P50CA70907 · United States
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