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Tumors require blood supply and, to overcome this restriction, induce angiogenesis. Vascular endothelial growth factor ( VEGF ) plays an important role in this process, which explains the great number of antiangiogenic therapies targeting  VEGF . The research and development of targeted therapy has led to the approval of bevacizumab, a humanized anti‐ VEGF  monoclonal antibody ( mA b), in clinical settings. However, side effects have been reported, usually as a consequence of bolus‐dose administration of the antibody. This limitation could be circumvented through the use of anti‐idiotype (Id) antibodies. In the present study, we evaluated the efficacy of an active  VEGF ‐binding immune response generated by an anti‐bevacizumab idiotype  mA b, 10.D7. The 10.D7 anti‐Id  mA b vaccination led to detectable levels of  VEGF ‐binding anti‐anti‐Id antibodies. In order to examine whether this humoral immune response could have implications for tumor development, 10.D7‐immunized mice were challenged with B16‐F10 tumor cells. Mice immunized with 10.D7 anti‐Id  mA b revealed reduced tumor growth when compared to control groups. Histological analyses of tumor sections from 10.D7‐immunized mice showed increased necrotic areas, decreased  CD 31‐positive vascular density and reduced  CD 68‐positive cell infiltration. Our results encourage further therapeutic studies, particularly if one considers that the anti‐Id therapeutic vaccination maintains stable levels of  VEGF ‐binding antibodies, which might be useful in the control of tumor relapse.

Anti‐bevacizumab idiotype antibody vaccination is effective in inducing vascular endothelial growth factor‐binding response, impairing tumor outgrowth