[血管生成因子抗独特型抗体对肿瘤进展的调节]。

N Ortéga, F Jonca, S Vincent, C Favard, B Malavaud, N Bertrand, C Mazerolles, P Richmann, Y Pouliquen, J P Sarrammon, M M Ruchoux, J Plouët
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引用次数: 0

摘要

我们利用抗独特型策略设计了模拟血管内皮生长因子(VEGF)或成纤维细胞生长因子2 (FGF2)生物学效应的循环探针。VEGF受体KDR/flk-1的激活诱导内皮细胞增殖,但不诱导其迁移,而FGF受体FGF- r1的激活则产生相反的结果。在移植了肿瘤碎片的裸鼠中,长期递送KDR/flk-1激动剂,而不是FGF-R1,增加了肿瘤体积。镜下检查显示血管增生和癌细胞增生。相比之下,正常组织中细胞增殖无差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Modulation of the tumoral progression by anti-idiotypic antibodies of angiogenesis factors].

We took advantage of the anti-idiotypic strategy to design circulating probes mimicking the biological effects of VEGF (vascular endothelial growth factor) or FGF2 (fibroblast growth factor 2). The activation of the VEGF receptor KDR/flk-1 induced endothelial cell proliferation but not their migration, whereas that of the FGF receptor FGF-R1 gave opposite results. The long lasting delivery of KDR/flk-1 agonists, but not that of FGF-R1, in nude mice grafted with tumor fragments enhanced the tumor volume. Microscopic examination showed an increase in both the vascularization and the proliferation of cancer cells. In contrast, no difference in cell proliferation was observed within normal tissues.

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