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ALK-driven tumors and targeted therapy: focus on crizotinib

Authors Murga-Zamalloa C, Lim M

Received 10 January 2014

Accepted for publication 5 February 2014

Published 20 March 2014 Volume 2014:7 Pages 87—94


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Carlos Murga-Zamalloa, Megan S Lim

Department of Pathology, University of Michigan, Ann Arbor, MI, USA

Abstract: Receptor tyrosine kinases have emerged as promising therapeutic targets for a diverse set of tumors. Overactivation of the tyrosine kinase anaplastic lymphoma kinase (ALK) has been reported in several types of malignancies such as anaplastic large cell lymphoma, inflammatory myofibroblastic tumor, neuroblastoma, and non-small-cell lung carcinoma. Further characterization of the molecular role of ALK has revealed an oncogenic signaling signature that results in tumor dependence on ALK. ALK-positive tumors display a different behavior than their ALK-negative counterparts; however, the specific role of ALK in some of these tumors remains to be elucidated. Although more studies are required to establish selective targeting of ALK as a definitive therapeutic option, initial trials have shown extraordinary results in the majority of cases.

Keywords: lymphoma, therapy, kinase, pathobiology

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