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H. Xin, C. Zhang, A. Herrmann, Y. Du, R. Figlin and H. Yu, “Sunitinib Inhibition of Stat3 Induces Renal Cell Carcinoma Tumor Cell Apoptosis and Reduces Immunosuppressive Cells,” Cancer Research, Vol. 69, No. 6, 2009, pp. 2506-2513. doi:10.1158/0008-5472.CAN-08-4323

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• TITLE: Current Perspectives on Sunitinib Targeted Therapy for Tumors

  AUTHORS: Karolin Kamel Abdel-Aziz

  KEYWORDS: Platelet-Derived Growth Factor (PDGF), Cytochrome P450 Enzyme (CYP3A4), Dose-Limiting Toxicities (DLTs), Hepatocyte Growth Factor (HGF), Tyrosine Kinases (TKs)

  JOURNAL NAME: Journal of Cancer Therapy, Vol.2 No.4, October 12, 2011

  ABSTRACT: This review highlights therapeutic agents from recent cancer therapeutic trials showing the greatest potential for further clinical use for sunitinib in the near future. In fact, sunitinib is one of multi-tyrosine kinase inhibitors; tyrosine kinases are enzymes, which transfer phosphate groups from ATP to the hydroxyl group of tyrosine residues on signal transduction molecules. Phosphorylation of signal transduction molecules, in turn, induces dramatic changes in tumor growth, including activation of angiogenesis and DNA synthesis. Therefore, sustain efforts have been directed for developing inhibitors for angiogenesis, which is the marginal process for tumor growth and development through targeting TKs. Almost if not all angiogenesis inhibitors target the vascular endothelial growth factor (VEGF) signaling pathway.