Abstract
Advanced MR imaging methods have an essential role in classification, grading, follow-up and therapeutic management in patients with brain tumors. With the introduction of new therapeutic options, the challenge for better tissue characterization and diagnosis increase, calling for new reliable non-invasive imaging methods. In the current study we evaluated the added value of a combined protocol of blood oxygen level dependent (BOLD) imaging during hyperoxic challenge (termed hemodynamic response imaging (HRI)) in an orthotopic mouse model for glioblastoma under anti-angiogenic treatment with B20-4.1.1, an anti-VEGF antibody. In glioblastoma tumors, the elevated HRI indicated progressive angiogenesis as further confirmed by histology. In the current glioblastoma model, B20-treatment caused delayed tumor progression with no significant changes in HRI yet with slightly reduced tumor vascularity as indicated by histology. Furthermore, fewer apoptotic cells and higher proliferation index were detected in the B20-treated tumors compared to control-treated tumors. In conclusion, HRI provides an easy, safe and contrast agent free method for the assessment of the brain hemodynamic function, an additionally important clinical information.
Highlights
Glioblastoma is the most common primary malignant brain tumor with two-year survival rates of less than 30%
In the current study we evaluated the added value of a combined protocol of blood oxygen level dependent (BOLD) imaging during hyperoxic challenge (termed hemodynamic response imaging (HRI)) in an orthotopic mouse model for glioblastoma under anti-angiogenic treatment with B20-4.1.1, an antiVEGF antibody
Hemodynamic Response Imaging (HRI)- a method based on changes in the BOLD-Magnetic resonance images (MRI) signal caused by hyperoxia, was evaluated in a mouse model of glioblastoma treated with anti-angiogenic therapy
Summary
Glioblastoma is the most common primary malignant brain tumor with two-year survival rates of less than 30%. Significant research efforts have focused on the use of anti-angiogenic therapies for the treatment of glioblastoma These drugs have the potential to normalize abnormal tumor vasculature structurally and functionally, reduce the risk of hemorrhage, enhance the penetration of concurrently administered chemotherapy and improve the efficacy of cytotoxic drugs and radiation by alleviating hypoxia [3, 4]. Bevacizumab (Avastin), a monoclonal antibody that inactivates vascular endothelial growth factor (VEGF), was lately approved by the US Food and Drug Administration for treatment of recurrent glioblastoma. It reduces MRI enhancement, and provides benefit by controlling peritumoral edema and improving clinical performance. Besides angiogenesis [1], phenomena such as vascular co-option and vascular mimicry were evident in glioblastoma, especially following antiangiogenic therapies [5]
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