Journal
DRUG DISCOVERY TODAY
Volume 22, Issue 1, Pages 72-84Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.drudis.2016.07.010
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Funding
- Institute of Cancer Research (ICR)
- Cancer Research UK [C36478/A19281]
- Margaret T. Grohne Family Foundation
- Royal Society International Exchanges Scheme
- NATIONAL CANCER INSTITUTE [P50CA058187] Funding Source: NIH RePORTER
- Cancer Research UK [19281] Funding Source: researchfish
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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.
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