Angiogenesis is a fundamental physiological process to form new blood vessel to support cancer growth and development by providing nutrients and oxygen. It occurs for almost all solid tumors such as glioblastoma(GBM) and thus anti-angiogenesis therapeutics are increasingly applied to treat various cancers. GBM is the most aggressive primary malignant brain tumor in humans with a 5-year survival rate under 5% and median overall survival of only 12–14 months . GBM features rich vascularization due to the high expression of various pro-angiogenic factors, which makes anti-angiogenesis as an attractively newly emerging targeted therapy strategy of GBM, although the standard treatments of GBM are still surgical operation, radiotherapy, and chemotherapy at present.

For instance, vascular endothelial growth factor inhibitor, bevacizumab, has been the sole anti-angiogenesis targeted therapeutic licensed by the FDA for use in GBM. In order to discover more effective anticancer agents, multi-targeted tyrosine kinase inhibitors (TKIs), such as Sunitinib, are being under clinical investigations owing to their antitumor capabilities via the pathways of anti-angiogenesis as well as anti-proliferation. Sunitinib (marketed as Sutent by Pfizer, and previously known as SU11248) is an oral, small-molecule, multi-targeted TKI that was approved by the FDA for the treatment of renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST) on January 26, 2006. Sunitinib was the first cancer drug simultaneously approved for two different indications. Sunitinib as antiangiogenic therapeutic has already been used to treat renal carcinoma, gastrointestinal stromal tumors, lung cancer, and other solid tumors.

Xiao bao at Fudan University Shanghai Cancer Center, Shanghai, published an article aimed to monitor early treatment response of Sunitinib in U87MG models mimicking glioblastoma multiforme by longitudinal ¹⁸F-FLT microPET/CT imaging. Immunohistochemistry results show

representative tumor sections of haematoxylin and eosin (H&E), CD31, and Ki-67 staining for the control and Sunitinib groups on days 0,1,3,7,and13 after therapy. CD31-positive staining was broadly observed in all untreated tumor sections, which demonstrated relatively abundant microvessel density (MVD). Ater Sunitinib treatment, the MVD level in tumor sections decreased remarkably, which indicated effective anti-angiogenic activity of the drug.

Reference:

Early Monitoring Antiangiogenesis Treatment Response of Sunitinib in U87MG Tumor Xenograft by (18)F-FLT MicroPET/CT Imaging. Biomed Res Int. 2013;2013:218578.