Tumor vascular normalization induced by antiangiogenic therapy such as bevacizumab (BEV) is a promising strategy to remodel tumor microenvironment. However, this effect is transient and finally vanished because of inevitable adaptive therapy resistance. In this study, we found that targeting tumor glycolysis activator PFKFB3 is a novel potential strategy to enhance BEV therapy efficacy and prolonged vascular normalization in glioblastoma. IVIM parameters are much better than DCE-MRI as alternative translatable imaging biomarkers for evaluating tumor response and monitoring vascular normalization.
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