Overcoming the resistance to molecular-targeted therapy for renalcell carcinoma by analyzing of VHL control mechanism in a HIF independent manner
| Project/Area Number |
23890093
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腎細胞癌 / 抗血管新生療法 / VHL / CCL2 / JunB / EphriaB2 |
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| Research Abstract |
We previously reported that the pathway of pVHL-atypical PKC-JunB in a hypoxia-inducible factor (HIF) independent manner contributed to the progression in clear cell renal cell carcinoma (ccRCC), and detected chemokine (C-C motif) ligand-2 (CCL2) as one of a downstream effector of it. To obtain findings of overcoming resistance to existing anti-VEGF therapies, the purpose of this research is to investigate the utility of CCL2 as a novel therapeutic target in ccRCC. In this study, we evaluated CCL2 expression in ccRCC clinical specimens, and confirmed that CCL2 expression involved in tumor growthand vascularization in xenograft derived from ccRCC cell lines. Moreover, we confirmed the anti-tumor effect of CCL2 neutralization antibodies to xenograft derived from ccRCC clinical specimens and cell lines. These results suggest that CCL2 could be a potential therapeutic target in ccRCC.
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Report
(3 results)
Research Products
(4 results)
