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Targeted inhibition in tumors with ALK dependency

Authors Kwak E, Clark J, Shaw A

Received 13 March 2012

Accepted for publication 23 October 2012

Published 10 January 2013 Volume 2013:4 Pages 1—8

DOI https://doi.org/10.2147/LCTT.S16313

Review by Single-blind

Peer reviewer comments 4


Eunice L Kwak, Jeffrey W Clark, Alice T Shaw

Massachusetts General Hospital Cancer Center, Boston, MA, USA

Abstract: The oncogenic function of gene translocations involving the anaplastic lymphoma kinase (ALK) was first reported in rare subtypes of non-Hodgkin's lymphoma almost two decades ago. More recently, aberrant ALK signaling was found to be an oncogenic driver in subsets of non-small cell lung cancer (NSCLC), particularly in patients with little or no tobacco smoking history. The advent of molecularly targeted therapies that inhibit ALK has allowed the pairing of ALK inhibitors such as crizotinib as treatment for ALK-positive NSCLC, yielding dramatic responses and long-term disease control. The clinicopathologic features of ALK-driven NSCLC, the clinical development of ALK inhibitors, and the genetic determinants of acquired resistance to ALK inhibition are among the topics covered in this review.

Keywords: targeted inhibition, tumors, ALK dependency

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