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• W2315513215 abstract "Background: The vascular endothelium growth factor (VEGF) pathway plays a pivotal role in angiogenesis. Axitinib (AG-013736), a potent small molecule receptor tyrosine kinase inhibitor highly selective for VEGF receptor 1, 2 and 3, is currently being tested in Phase II/III clinical trials for the treatment of solid tumors and has been approved as a second-line treatment for renal cell carcinoma (RCC). The hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (c-Met) pathway has also been shown to play an important role in tumor vascularization, as well as epithelial to mesenchymal transition (EMT), metastatization, and acquired resistance. Crizotinib (PF-02341066), a potent and selective inhibitor of anaplastic lymphoma kinase (ALK) and c-Met kinase, has been approved for the treatment of advanced ALK-positive non-small cell lung cancer. The aim of this study was to assess the combinational effect of axitinib and crizotinib in two models of RCC with differing degrees of c-Met expression and sensitivity to anti-angiogenic agents. We hypothesized that the combination would provide greater anti-tumor and anti-angiogenesis efficacy compared to single-agents. Methods: Human high c-Met expressing 786-O and low c-Met expressing RP-01 (developed from a skin metastasis of a patient with sporadic clear cell RCC) xenografts were inoculated into SCID mice (8/group). After approximately 6 weeks of tumor growth, mice were treated with vehicle, axitinib (36 mg/kg, 2x/day, oral gavage), crizotinib (25 mg/kg, 1x/day, oral gavage), or axitinib plus crizotinib. Once tumor volume of vehicle mice reached 200 mm2, mice were sacrificed and tumor tissue was excised and analyzed. A sunitinib-resistant RP-01 model was also developed through continued in vivo exposure to sunitinib (60 mg/kg, 1x/day, oral gavage) to further test the different responses to treatments and to evaluate the possible role of c-Met in sunitinib resistance. Compounds were kindly provided by Pfizer. Results: We observed that single-agent crizotinib anti-tumoral activity was strongly related to c-Met expression, inhibiting 786-O tumor growth in vivo, but not RP-01. More interestingly, significant synergistic effects were found with crizotinib and axitinib, whereby enhanced inhibition of 786-O xenograft tumor growth was found (from 17%, axitinib, to 76% combination, p Citation Format: Eric S. Ciamporcero, Kiersten M. Miles, Remi Adelaiye, Stefania Pizzimenti, Giuseppina Barrera, Roberto Pili. Combination of axitinib and crizotinib in renal cell carcinoma models. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1618. doi:10.1158/1538-7445.AM2013-1618" @default.
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• W2315513215 date "2013-04-15" @default.
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• W2315513215 title "Abstract 1618: Combination of axitinib and crizotinib in renal cell carcinoma models." @default.
• W2315513215 doi "https://doi.org/10.1158/1538-7445.am2013-1618" @default.
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