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
{"title":"[Modulation of the tumoral progression by anti-idiotypic antibodies of angiogenesis factors].","authors":"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","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":10555,"journal":{"name":"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie","volume":"319 5","pages":"411-5"},"PeriodicalIF":0.0000,"publicationDate":"1996-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Comptes rendus de l'Academie des sciences. Serie III, Sciences de la vie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.