OBJECTIVE: To evaluate the potential effect of bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF), on the angiogenesis and tumor growth of retinoblastoma in vitro and in vivo. METHODS: The antiangiogenic effects of bevacizumab were evaluated in a coculture of a Y-79 human retinoblastoma cell line and a human umbilical vein endothelial cell line by means of a cell proliferation assay kit and a VEGF enzyme-linked immunosorbent assay. The Y-79 xenotransplanted nude mice were treated with bevacizumab intraperitoneally twice weekly for 4 weeks, during which each tumor was measured once a week. The mice were then euthanized, and the weight of each tumor and its microvessel density were determined via CD34 immunohistochemical staining. RESULTS: The mean (standard error of the mean) increased human umbilical vein endothelial cell proliferation, when cocultured with Y-79 (156% [1%]), was suppressed 58% (5%) by the blockage of VEGF induced by bevacizumab. By causing a 2-fold reduction in microvessel density in the Y-79 xenograft model, bevacizumab induced a 75% reduction in the growth of the retinoblastomas without producing significant systemic toxicity. Conclusions and Clinical Relevance Treatment with bevacizumab suppressed the angiogenesis and growth of retinoblastoma in vitro and in vivo. Bevacizumab is likely to be of benefit in the treatment of retinoblastoma.
OBJECTIVE: To evaluate the potential effect of bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF), on the angiogenesis and tumor growth of retinoblastoma in vitro and in vivo. METHODS: The antiangiogenic effects of bevacizumab were evaluated in a coculture of a Y-79 humanretinoblastoma cell line and a human umbilical vein endothelial cell line by means of a cell proliferation assay kit and a VEGF enzyme-linked immunosorbent assay. The Y-79 xenotransplanted nude mice were treated with bevacizumab intraperitoneally twice weekly for 4 weeks, during which each tumor was measured once a week. The mice were then euthanized, and the weight of each tumor and its microvessel density were determined via CD34 immunohistochemical staining. RESULTS: The mean (standard error of the mean) increased human umbilical vein endothelial cell proliferation, when cocultured with Y-79 (156% [1%]), was suppressed 58% (5%) by the blockage of VEGF induced by bevacizumab. By causing a 2-fold reduction in microvessel density in the Y-79 xenograft model, bevacizumab induced a 75% reduction in the growth of the retinoblastomas without producing significant systemic toxicity. Conclusions and Clinical Relevance Treatment with bevacizumab suppressed the angiogenesis and growth of retinoblastoma in vitro and in vivo. Bevacizumab is likely to be of benefit in the treatment of retinoblastoma.
Authors: Amir R Hajrasouliha; Toshinari Funaki; Zahra Sadrai; Takaaki Hattori; Sunil K Chauhan; Reza Dana Journal: Invest Ophthalmol Vis Sci Date: 2012-03-09 Impact factor: 4.799
Authors: F Rodjan; P de Graaf; P van der Valk; A C Moll; J P A Kuijer; D L Knol; J A Castelijns; P J W Pouwels Journal: AJNR Am J Neuroradiol Date: 2012-05-24 Impact factor: 3.825