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Drug Discov Today. 2017 Jan;22(1):72-84. doi: 10.1016/j.drudis.2016.07.010. Epub 2016 Jul 21.

Exploiting receptor tyrosine kinase co-activation for cancer therapy.

Author information

1
Translational Bioinformatics and Cancer Systems Biology Laboratory, Division of Medical Oncology, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: aikchoon.tan@ucdenver.edu.
2
Division of Cancer Biology, The Institute of Cancer Research, London SW3 6JB, UK.
3
Division of Cancer Biology, The Institute of Cancer Research, London SW3 6JB, UK. Electronic address: paul.huang@icr.ac.uk.

Abstract

Studies over the past decade have shown that many cancers have evolved receptor tyrosine kinase (RTK) co-activation as a mechanism to drive tumour progression and limit the lethal effects of therapy. This review summarises the general principles of RTK co-activation and discusses approaches to exploit this phenomenon in cancer therapy and drug discovery. Computational strategies to predict kinase co-dependencies by integrating drug screening data and kinase inhibitor selectivity profiles will also be described. We offer a perspective on the implications of RTK co-activation on tumour heterogeneity and cancer evolution and conclude by surveying emerging computational and experimental approaches that will provide insights into RTK co-activation biology and deliver new developments in effective cancer therapies.

PMID:
27452454
PMCID:
PMC5346155
DOI:
10.1016/j.drudis.2016.07.010
[Indexed for MEDLINE]
Free PMC Article

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