Skip to main content
Fig. 1 | Journal of Hematology & Oncology

Fig. 1

From: The brain-penetrating CXCR4 antagonist, PRX177561, increases the antitumor effects of bevacizumab and sunitinib in preclinical models of human glioblastoma

Fig. 1

Anti-angiogenic therapies induce the expression of CXCR4 and SDF1α in experimental glioblastomas (1). a Graphical distribution of tumor weights at the end of treatment cycle of 35 days (mean ± standard deviation, (SD)). Each column included ten tumors. b Size-based grouping of representative U87-derived tumors from animals of control (three tumors) or treated (three tumors) with sunitinib or bevacizumab. c Western blot evaluation of single three tissue extracts from smaller and larger tumors in each group of treatment. Each lane was loaded with 100 μg of protein. CXCR4, TGFβRI, Ang2, and Ang1 expression was normalized versus actin. d Statistical analyses of correlation performed among the levels of CXCR4 (adjusted densitometric units by western blots normalized versus actin) and tumor weight for all 30 tissues (ten tissue extracts for three treatments). e Statistical analyses of correlation performed on untreated tumors (ten tissue extracts). f Statistical analyses of correlation performed on bevacizumab treated tumors (ten tissue extracts). g Statistical analyses of correlation performed on sunitinib treated tumors (ten tissue extracts). h, i Histological appearance (h) and CXCR4 and Tie2 expression (i) in untreated and treated with bevacizumab or sunitinib U87 xenografts with resolution of ×100, ×200, and ×400

Back to article page