Bayliss, R orcid.org/0000-0003-0604-2773, Choi, J, Fennell, DA et al. (2 more authors) (2016) Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs. Cellular and Molecular Life Sciences, 73 (6). pp. 1209-1224. ISSN 1420-682X
Abstract
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.
Metadata
Item Type: | Article |
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Authors/Creators: |
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Copyright, Publisher and Additional Information: | © The Author(s) 2016. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
Keywords: | Fusion; Oncogene; Lung cancer; Kinase; Structural biology |
Dates: |
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Institution: | The University of Leeds |
Academic Units: | The University of Leeds > Faculty of Biological Sciences (Leeds) > School of Molecular and Cellular Biology (Leeds) |
Depositing User: | Symplectic Publications |
Date Deposited: | 09 Dec 2016 16:33 |
Last Modified: | 09 Dec 2016 16:37 |
Published Version: | http://doi.org/10.1007/s00018-015-2117-6 |
Status: | Published |
Publisher: | Springer Verlag |
Identification Number: | 10.1007/s00018-015-2117-6 |
Related URLs: | |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:109342 |