Fig. 1: Tumor and vasculature responses to AAD in CRC and NPC. | Cell Death & Disease

Fig. 1: Tumor and vasculature responses to AAD in CRC and NPC.

From: Lenvatinib for effectively treating antiangiogenic drug-resistant nasopharyngeal carcinoma

Fig. 1

AC Tumor growth (A) and tumor weights (B) were measured in CRC and NPC xenografts receiving vehicle or anti-VEGF treatment. The tumor inhibition ratios were calculated (C) (n = 6 mice per group). D Representative micrographs of Ki67+ proliferative cells and cleaved caspase-3+ apoptotic cells in vehicle- or anti-VEGF-treated CRC and NPC tumors. Scale bar = 50 μm. Quantification of Ki67+, cleaved caspase-3+ signals, and proliferation/apoptosis index (PA index) in vehicle- or anti-VEGF-treated CRC and NPC cancers (n = 8 random fields per group). E Representative micrographs of CD31+ microvessels and CA9+ hypoxic areas in vehicle- or anti-VEGF-treated CRC and NPC tumors. Scale bar in upper panel = 100 μm, scale bar in lower panel = 50 μm. Quantification of CD31+ tumor vessel parameters and CA9+ signals in vehicle- or anti-VEGF-treated CRC and NPC tumors (n = 8 random fields per group). FH Tumor growth (F) and tumor weights (G) were measured in CRC and NPC xenografts receiving vehicle or sunitinib treatment. The tumor inhibition ratios were calculated (H) (n = 6 mice per group). ***P < 0.001. NS not significant. Data presented as mean ± SD.

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