Specific inhibition of members of the EGFR (epidermal growth factor receptor) family, particularly EGFR and HER2 (human epidermal growth factor receptor 2), are an important therapeutic strategy in many human cancers. Compared with classical chemotherapy, these targeted therapeutics are very specific and initially effective, but acquired resistance against these targeted therapies is a recurring threat. A growing body of recent work has highlighted a pseudokinase in the EGFR family, HER3, and its ligand, NRG (neuregulin β1), to be of importance in models of resistant cancers, as well as in patients. In the present article, we describe some of the roles in which HER3 can mediate acquired resistance and discuss the current efforts to target HER3 itself in cancer.
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August 2014
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Conference Article|
August 11 2014
A role for the pseudokinase HER3 in the acquired resistance against EGFR- and HER2-directed targeted therapy
Jeroen Claus;
Jeroen Claus
1
*Cancer Research UK, London Research Institute, Lincoln's Inn Fields, London WC2A 3LY, U.K.
1To whom correspondence should be addressed (emailjeroen.claus@cancer.org.uk).
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Gargi Patel;
Gargi Patel
†Richard Dimbleby Department of Cancer Research, Randall Division and Division of Cancer Studies, Kings College London, Guy's Medical School Campus, London SE1 1UL, U.K.
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Tony Ng;
Tony Ng
†Richard Dimbleby Department of Cancer Research, Randall Division and Division of Cancer Studies, Kings College London, Guy's Medical School Campus, London SE1 1UL, U.K.
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Peter J. Parker
Peter J. Parker
*Cancer Research UK, London Research Institute, Lincoln's Inn Fields, London WC2A 3LY, U.K.
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Publisher: Portland Press Ltd
Received:
February 14 2014
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2014 Biochemical Society
2014
Biochem Soc Trans (2014) 42 (4): 831–836.
Article history
Received:
February 14 2014
Citation
Jeroen Claus, Gargi Patel, Tony Ng, Peter J. Parker; A role for the pseudokinase HER3 in the acquired resistance against EGFR- and HER2-directed targeted therapy. Biochem Soc Trans 1 August 2014; 42 (4): 831–836. doi: https://doi.org/10.1042/BST20140043
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