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EML4-ALK Fusion Gene and Efficacy of an ALK Kinase Inhibitor in Lung Cancer

Clinical Cancer Research · 2008 · Vol. 14(13) · pp. 4275–4283

Jussi Koivunen✉(Center for Neuro-Oncology)Craig H. Mermel(Massachusetts Institute of Technology)Kreshnik Zejnullahu(Center for Neuro-Oncology)Carly MurphyEugene Lifshits(Massachusetts General Hospital)Alison J. Holmes(Center for Neuro-Oncology)Hwan Geun Choi(Harvard University)Young Tae Kim(Sungkyunkwan University)Derek Y. Chiang(Broad Institute)Roman K. Thomas(Max Planck Institute for Metabolism Research)Jinseon Lee(Samsung Medical Center)William G. Richards(Brigham and Women's Hospital)David J. Sugarbaker(Brigham and Women's Hospital)Christopher T. Ducko(Brigham and Women's Hospital)Neal I. LindemanJudith Marcoux(Center for Neuro-Oncology)Jeffrey A. Engelman(Massachusetts General Hospital)Nathanael S. Gray(Harvard University)Charles LeeMatthew Meyerson(Center for Neuro-Oncology)Pasi A. Jänne(Center for Neuro-Oncology)

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Abstract

EML4-ALK is found in the minority of NSCLC. ALK kinase inhibitors alone or in combination may nevertheless be clinically effective treatments for NSCLC patients whose tumors contain EML4-ALK.

Lung Cancer Treatments and Mutations PI3K/AKT/mTOR signaling in cancer Lung Cancer Research StudiesCancer researchEpidermal growth factor receptorProtein kinase BCell growthCell cultureCrizotinibLung cancerKinaseBiologyALK inhibitor

MeSH terms

AgedAntineoplastic AgentsCarcinoma, Non-Small-Cell LungEnzyme InhibitorsFemaleHumansLung NeoplasmsMaleMiddle AgedOncogene Proteins, FusionGene Expression Regulation, EnzymologicApoptosisErb-b2 Receptor Tyrosine KinasesReceptor, ErbB-2Cell Line, Tumor

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Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers