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Cancers 2015, 7(3), 1758-1784;

Targeting RTK Signaling Pathways in Cancer

The John van Geest Cancer Research Centre, School of Science and Technology, Nottingham Trent University, Clifton Lane, NG11 8NS Nottingham, UK
Academic Editor: Vita Golubovskaya
Received: 4 May 2015 / Revised: 24 August 2015 / Accepted: 26 August 2015 / Published: 3 September 2015
(This article belongs to the Special Issue Cancer Cell Proliferation)
Full-Text   |   PDF [821 KB, uploaded 3 September 2015]   |  


The RAS/MAP kinase and the RAS/PI3K/AKT pathways play a key role in the regulation of proliferation, differentiation and survival. The induction of these pathways depends on Receptor Tyrosine Kinases (RTKs) that are activated upon ligand binding. In cancer, constitutive and aberrant activations of components of those pathways result in increased proliferation, survival and metastasis. For instance, mutations affecting RTKs, Ras, B-Raf, PI3K and AKT are common in perpetuating the malignancy of several types of cancers and from different tissue origins. Therefore, these signaling pathways became prime targets for cancer therapy. This review aims to provide an overview about the most frequently encountered mutations, the pathogenesis that results from such mutations and the known therapeutic strategies developed to counteract their aberrant functions. View Full-Text
Keywords: RTK; MAP kinase; PI3K; AKT; small molecule inhibitors; cancer RTK; MAP kinase; PI3K; AKT; small molecule inhibitors; cancer

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Regad, T. Targeting RTK Signaling Pathways in Cancer. Cancers 2015, 7, 1758-1784.

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