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VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases.

Abstract : Tumor growth depends on blood supply, requiring the development of new vessels, and vascular endothelial growth factor (VEGF) plays a central role in neoangiogenic processes. For this reason, VEGF represents a target for the development of new therapeutic antiangiogenic molecules. Clinical trials using anti-VEGF mAbs such as bevacizumab have validated the efficacy of this therapeutic approach but have also revealed adverse effects. Here we report that a VEGF-derived immunogen, consisting of a heterocomplex of a murine (m)VEGF and keyhole limpet hemocyanin, called "mVEGF kinoid," triggered a strong Ab immune response in mice. The anti-VEGF Abs inhibited both the proliferation of human umbilical vein endothelial cells cultured in the presence of mVEGF and the binding of mVEGF to its receptor-2 Flk-1. In mVEGF kinoid-immunized BALB/c mice challenged with syngeneic CT26 colorectal tumor cells, the number and size of lung metastases were significantly decreased. In human (h)VEGF kinoid-immunized BALB/c mice, high levels of serum Abs to hVEGF were present, and purified IgG from these mice decreased by > or =50% the tumor growth of human A673 rhabdomyosarcoma cells and HT29 colon carcinoma xenografted in Swiss nude and NOD/SCID mice, respectively. Tumor cell growth inhibition was similar to that observed in mice receiving therapeutic doses of bevacizumab. These experiments suggest that a therapeutic vaccine containing VEGF kinoid may represent a strategy for safely combating VEGF-dependent neovascularization and metastases occurring in malignant tumors.
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https://www.hal.inserm.fr/inserm-00180303
Contributor : Marie Garcia <>
Submitted on : Thursday, October 18, 2007 - 4:15:29 PM
Last modification on : Wednesday, October 14, 2020 - 4:09:08 AM

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Farhad Haghighi Rad, Hélène Le Buanec, Sébastien Paturance, Patrick Larcier, Philippe Genne, et al.. VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases.. Proceedings of the National Academy of Sciences of the United States of America , National Academy of Sciences, 2007, 104 (8), pp.2837-42. ⟨10.1073/pnas.0611022104⟩. ⟨inserm-00180303⟩

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