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Sunitinib: the antiangiogenic effects and beyond

Authors Hao Z, Sadek I

Received 7 May 2016

Accepted for publication 2 August 2016

Published 8 September 2016 Volume 2016:9 Pages 5495—5505

DOI https://doi.org/10.2147/OTT.S112242

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Manfred Beleut

Peer reviewer comments 2

Editor who approved publication: Dr William Cho


Zhonglin Hao, Ibrahim Sadek

Department of Medicine, Section of Hematology and Oncology, Georgia Cancer Center, Medical College of Georgia, Augusta University, Augusta, GA, USA

Abstract: As a multitargeted kinase inhibitor, sunitinib has carved its way into demonstrating itself as a most effective tyrosine kinase inhibitor in the treatment of metastatic renal cell carcinoma. Mechanistically, sunitinib inhibits multiple receptor tyrosine kinases, especially those involved in angiogenesis, that is, vascular endothelial growth factor receptor, platelet-derived growth factor receptor, and proto-oncogene cKIT. Sunitinib has also been implicated in enhancing cancer invasiveness and metastasis. Mechanisms of resistance are poorly understood, but both intrinsic and acquired mechanisms are thought to be involved. While the side effects are manageable, sunitinib, like many other tyrosine kinase inhibitors, can be associated with serious toxicities that require careful management including frequent dose reductions. Although still in the early stage, emerging evidence points to an immunomodulatory role for sunitinib. It is also likely to contribute to the overall outcomes, especially those seen in metastatic renal cell carcinoma, and such effects are thought to be mediated by the proto-oncogene cKIT receptor. Combination with other modalities such as stereotactic body radiation therapy, therapeutic vaccines, and checkpoint inhibitors is being pursued for improved efficacy.

Keywords: sunitinib, angiogenesis, MDSC, cancer

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