Targeted inhibition in tumors with ALK dependency

Eunice L Kwak, Jeffrey W Clark, Alice T ShawMassachusetts General Hospital Cancer Center, Boston, MA, USAAbstract: 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...

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Main Authors: Kwak EL, Clark JW, Shaw AT
Format: Article
Language:English
Published: Dove Medical Press 2013-01-01
Series:Lung Cancer: Targets and Therapy
Online Access:http://www.dovepress.com/targeted-inhibition-in-tumors-with-alk-dependency-a11914
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author Kwak EL
Clark JW
Shaw AT
author_facet Kwak EL
Clark JW
Shaw AT
author_sort Kwak EL
collection DOAJ
description Eunice L Kwak, Jeffrey W Clark, Alice T ShawMassachusetts General Hospital Cancer Center, Boston, MA, USAAbstract: 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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spelling doaj.art-47647a89cdb9463a8e88b0b7ed4428452022-12-21T21:20:59ZengDove Medical PressLung Cancer: Targets and Therapy1179-27282013-01-012013default18Targeted inhibition in tumors with ALK dependencyKwak ELClark JWShaw ATEunice L Kwak, Jeffrey W Clark, Alice T ShawMassachusetts General Hospital Cancer Center, Boston, MA, USAAbstract: 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 dependencyhttp://www.dovepress.com/targeted-inhibition-in-tumors-with-alk-dependency-a11914
spellingShingle Kwak EL
Clark JW
Shaw AT
Targeted inhibition in tumors with ALK dependency
Lung Cancer: Targets and Therapy
title Targeted inhibition in tumors with ALK dependency
title_full Targeted inhibition in tumors with ALK dependency
title_fullStr Targeted inhibition in tumors with ALK dependency
title_full_unstemmed Targeted inhibition in tumors with ALK dependency
title_short Targeted inhibition in tumors with ALK dependency
title_sort targeted inhibition in tumors with alk dependency
url http://www.dovepress.com/targeted-inhibition-in-tumors-with-alk-dependency-a11914
work_keys_str_mv AT kwakel targetedinhibitionintumorswithalkdependency
AT clarkjw targetedinhibitionintumorswithalkdependency
AT shawat targetedinhibitionintumorswithalkdependency