Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: Anti-tumor effects of a human VEGFR-2-based DNA vaccine in mouse models | Genetic Vaccines and Therapy BioMed Central Research Anti-tumor effects of a human VEGFR-2-based DNA vaccine in mouse models Ke Xief Rui-Zhen BaR Yang Wuf Quan Liu Kang Liu and Yu-Quan Wei Open Access Address State Key Laboratory of Biotherapy and Cancer Center West China Hospital West China Medical School Sichuan University Guo Xue Xiang No 37 Chengdu Sichuan 610041 PR China Email Ke Xie - mei97@ Rui-Zhen Bai - Yang Wu - stillwy@ Quan Liu - liuquan621@ Kang Liu - tonkanl@ Yu-Quan Wei - yuquawei@ Corresponding author fEqual contributors Published 21 June 2009 Received 13 April 2009 Genetic Vaccines and Therapy 2009 7 10 doi 1479-0556-7-10 Accepted 21 June 2009 This article is available from http content 7 1 10 2009 Xie et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Vascular endothelial growth factor VEGF and its receptor VEGFR-2 Flk-1 KDR play a key role in tumor angiogenesis. Blocking the VEGF-VEGFR-2 pathway may inhibit tumor growth. Here we used human VEGFR-2 as a model antigen to explore the feasibility of immunotherapy with a plasmid DNA vaccine based on a xenogeneic homologue of this receptor. Methods The protective effects and therapeutic anti-tumor immunity mediated by the DNA vaccine were investigated in mouse models. Anti-angiogenesis effects were detected by immunohistochemical staining and the alginate-encapsulate tumor cell assay. The mechanism of action of the DNA vaccine was primarily explored by detection of auto-antibodies and CTL activity. Results The DNA vaccine elicited a strong protective and therapeutic anti-tumor immunity through an anti-angiogenesis mechanism in mouse models .
