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Impact of tivozanib on patient outcomes in treatment of advanced renal cell carcinoma

Authors Yalcin S, Lacin S

Received 20 February 2019

Accepted for publication 13 June 2019

Published 16 August 2019 Volume 2019:11 Pages 7779—7785

DOI https://doi.org/10.2147/CMAR.S206105

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Professor Nakshatri


Suayib Yalcin,1 Sahin Lacin2

1Hacettepe University Institute of Cancer, Department of Medical Oncology, Ankara, Turkey; 2University of Health Sciences, Diyarbakir Gazi Yasargil Training and Research Hospital, Department of Medical Oncology, Diyarbakir, Turkey

Correspondence: Suayib Yalcin
Hacettepe University Institute of Cancer, Department Of Medical Oncology, Faculty of Medicine, Ankara 006100, Sihhiye, Turkey
Email syalcin@hacettepe.edu.tr

Abstract: Renal cell carcinoma (RCC) is the most common type of kidney malignancy, and the clear-cell subtype represents the majority of RCCs. RCC is a heterogeneous disease in terms of genetic and histological features which determine the behavior of the disease. The von Hippel–Lindau (VHL) is a tumor suppressor gene and mutations of this gene are seen in 95% of clear-cell RCCs. Inactivation of VHL causes the accumulation of hypoxia-inducible factor-1 (HIF-1), and in turn, accumulation of HIF-1 induces overexpression of vascular endothelial growth factor (VEGF); the increase in VEGF expression makes RCC a highly vascularized tumor, and forms the rationale for antiVEGF treatment. In the past decade, improvement in the survival of RCC patients has been observed due to new effective therapies, such as antiVEGF and mammalian target of rapamycin (mTOR) targeting agents and immune checkpoint inhibitors. The majority of VEGF targeted agents are not just selective to VEGF receptors, but usually also have inhibitory effects on other kinases, such as c-KIT and FLT3. Tivozanib is an extremely potent and selective tyrosine kinase inhibitor (TKI) of VEGFR-1, 2, and 3, with a relatively long half-life, that is approved by the European Commission for the treatment of advanced/metastatic RCC. Tivozanib, at very low serum concentration can inhibit phosphorylation of VEGFR −1, −2, and −3 tyrosine kinase activity. This article summarizes the clinical data on tivozanib in the treatment of advanced/metastatic RCC.

Keywords: renal cell carcinoma, vascular endothelial growth factor, tyrosine kinase inhibitors, tivozanib, clear-cell carcinoma


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