Our finding is in keeping with this idea since GLEA2 was immunogenic in some patients only during or after but not prior to radiation. In the future, radiation may significantly improve the results of immunotherapy for tumors located in the CNS. Modulating the tumor immunoresponse can contribute to overcome the current shortcomings of immunotherapy. Our results provide also evidence that the analysis of antigen seroreactivity may be useful for monitoring tumor development under treatment. The immune system may be ideally suited to identify even subtle changes in tumor development that cannot be picked up by other approaches. Future developments can combine the power of imaging technology and the sensitivity of approaches that utilize the immune system for tumor detection. Detection and monitoring of human tumors by seroreactivity of Notopterol antigens is, however, still in its infancy. Out of the over 2000 antigens known to be immunogenic in human tumor patients, only very few have been analyzed for the course of their seroreactivity during tumor progression under treatment. There are no studies that follow the antigen reactivity during the progress of human brain tumors. Surpassing the scope of our study, an optimized monitoring of brain tumor development under treatment would require an extended number of immunogenic antigens that yet need to be Nitisinone identified. Our study does not focus on the question why radiation results in increased GLEA2 seroreactivity. One obvious explanation is the release of GLEA2 as the result of cell destruction due to radiation. The increased GLEA2 seroreactivity found in glioblastoma patients at the time of surgery may also be caused by necrosis that is typically associated with human glioblastoma. Alternatively, GLEA2 may also be presented via MHC class I on the surface of glioblastoma cells. However, MHC class I antigen presentation is remarkably inefficient. This may be overcome by radiation that both enhance degradation of cellular proteins and MHC class I expression. Independent of the molecular mechanisms, the study indicates that radiation increases the antibody response against GLEA2 in glioma patients.