Please use this identifier to cite or link to this item:
Title: Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs
Authors: Bayliss, Richard
Choi, Jene
Fennell, Dean A.
Fry, Andrew M.
Richards, Mark W.
First Published: 11-Jan-2016
Publisher: Springer Verlag for Birkhäuser Basel
Citation: Cellular and Molecular Life Sciences, 2016, 73 (6), pp. 1209-1224
Abstract: A fusion between the EML4 (echinoderm microtubule-associated protein-like) and ALK (anaplastic lymphoma kinase) genes was identified in non-small cell lung cancer (NSCLC) in 2007 and there has been rapid progress in applying this knowledge to the benefit of patients. However, we have a poor understanding of EML4 and ALK biology and there are many challenges to devising the optimal strategy for treating EML4-ALK NSCLC patients. In this review, we describe the biology of EML4 and ALK, explain the main features of EML4-ALK fusion proteins and outline the therapies that target EML4-ALK. In particular, we highlight the recent advances in our understanding of the structures of EML proteins, describe the molecular mechanisms of resistance to ALK inhibitors and assess current thinking about combinations of ALK drugs with inhibitors that target other kinases or Hsp90.
DOI Link: 10.1007/s00018-015-2117-6
ISSN: 1420-682X
eISSN: 1420-9071
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © the authors, 2016. This is an open-access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Appears in Collections:Published Articles, Dept. of Molecular and Cell Biology

Files in This Item:
File Description SizeFormat 
Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs.pdfPublished (publisher PDF)3.11 MBAdobe PDFView/Open

Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.