Angiogenesis (the formation of new blood vessels from pre-existing blood vessels) plays an important role in the growth and spread of tumors. Angiogenesis is regulated by a balance of activators and inhibitors. One of the angiogenic activators is the vascular endothelial growth factor (VEGF, also referred to as VEGF-A). Over the past decade, several angiogenesis inhibitors have been discovered and implemented in the therapy of cancer patients. Bevacizumab (a humanized monoclonal antibody that inhibits VEGF-A) has been shown to improve survival in different tumor types in first and second line therapy when given in various chemotherapy combinations. Furthermore, research has shown a survival benefit of continued VEGF suppression with bevacizumab beyond first progression in metastatic colorectal cancer. So although repeated use of bevacizumab as a chronic therapy is much desired, currently this is not feasible because of substantial disadvantages of bevacizumab therapy. First, since bevacizumab only offers temporary VEGF neutralization, it needs frequent repeated administration. Secondly, bevacizumab is an intravenous therapy, which requires hospitalization on each administration. Third, bevacizumab has very high production costs. These specific drawbacks of longer term monoclonal antibody therapy could be circumvented by the use of a therapeutic cancer vaccine targeting VEGF. A vaccine is able to induce sustained VEGF suppression and can be administered via an intramuscular (IM) injection. In addition, a vaccine will likely inhibit VEGF more effectively as compared to bevacizumab, because a vaccine induces a polyclonal antibody response, resulting in higher avidity binding. Furthermore, it is believed that endogenous antibodies have a better tumor penetrating capacity, as compared to exogenously administered antibodies. The vaccine hVEGF26-104 is a truncated synthetic peptide mimic of the VEGF protein and consists of 79 amino acids (residue 26-104). The vaccine contains an antigen that directs the body's own polyclonal antibody response towards the active site of the endogenous VEGF molecule. After binding of the antibodies to endogenous VEGF this hormone will no longer be able to bind to its receptors (VEGFR1 and VEGFR2) and consequently will no longer exert its pro-angiogenic effect. To enhance the immune response, RFASE, which belongs to the adjuvant group of sulpholipopolysaccharides, will be used as an adjuvant.