Figure 6
Figure 6. Imatinib reduces MCL tumor growth and angiogenesis of SOX11-positive MCL xenograft tumors. (A-B) Left panel, Tumor growth represented by tumor volumes (mm3) at the indicated days PI of Z138 and JEKO1 SOX11-positive xenografts treated with IP injections of imatinib (n = 5, n = 9) (green) or vehicle PBS (n = 5, n = 9) (blue) and SOX11-knockdown xenografts treated with IP of vehicle PBS (n = 5, n = 8) (yellow). Right panel, Graph displaying tumor volumes (mm3) at the time of tissue harvest, comparing imatinib (green) vs vehicle PBS (blue) treated SOX11-positive xenografts and (yellow) vehicle PBS-treated SOX11-knockdown xenografts. Compared with vehicle PBS, imatinib treatment significantly suppressed tumor growth of the SOX11-positive xenografts observed during follow-up (400 mm3 vs 1330 mm3, P < 1 × 10−4, and 490 mm3 vs 1400 mm3, P < 1 × 10−4 in Z138 and JEKO1, respectively) and ex vivo measurements (450 mm3 vs 2000 mm3, P = .008, and 630 mm3 vs 2400 mm3, P = .0004 in Z138 and JEKO1, respectively). (C) Top panel, Macroscopic appearance and consecutive histological sections from representative SOX11-positive (n = 14) and SOX11-knockdown xenograft tumors (n = 13) upon imatinib or vehicle PBS treatment. Immunohistochemical stainings were performed with a specific antibody anti-human SOX11 (×40) and an anti-mouse CD31 (×20). Bottom panel, Graph displaying the percentage of density of CD31-positive MVD areas in Z138 and JEKO1 xenograft tumors in (green) imatinib or (blue) vehicle PBS-treated SOX11-positive xenografts and (yellow) vehicle PBS-treated SOX11-knockdown xenografts, delineated by the presence of CD31-positive staining. Bar plot represents the mean percentage ± SD. P-val are shown. The significance of difference was determined by independent sample Student t test. PI, postinoculation.

Imatinib reduces MCL tumor growth and angiogenesis of SOX11-positive MCL xenograft tumors. (A-B) Left panel, Tumor growth represented by tumor volumes (mm3) at the indicated days PI of Z138 and JEKO1 SOX11-positive xenografts treated with IP injections of imatinib (n = 5, n = 9) (green) or vehicle PBS (n = 5, n = 9) (blue) and SOX11-knockdown xenografts treated with IP of vehicle PBS (n = 5, n = 8) (yellow). Right panel, Graph displaying tumor volumes (mm3) at the time of tissue harvest, comparing imatinib (green) vs vehicle PBS (blue) treated SOX11-positive xenografts and (yellow) vehicle PBS-treated SOX11-knockdown xenografts. Compared with vehicle PBS, imatinib treatment significantly suppressed tumor growth of the SOX11-positive xenografts observed during follow-up (400 mm3 vs 1330 mm3, P < 1 × 10−4, and 490 mm3 vs 1400 mm3, P < 1 × 10−4 in Z138 and JEKO1, respectively) and ex vivo measurements (450 mm3 vs 2000 mm3, P = .008, and 630 mm3 vs 2400 mm3, P = .0004 in Z138 and JEKO1, respectively). (C) Top panel, Macroscopic appearance and consecutive histological sections from representative SOX11-positive (n = 14) and SOX11-knockdown xenograft tumors (n = 13) upon imatinib or vehicle PBS treatment. Immunohistochemical stainings were performed with a specific antibody anti-human SOX11 (×40) and an anti-mouse CD31 (×20). Bottom panel, Graph displaying the percentage of density of CD31-positive MVD areas in Z138 and JEKO1 xenograft tumors in (green) imatinib or (blue) vehicle PBS-treated SOX11-positive xenografts and (yellow) vehicle PBS-treated SOX11-knockdown xenografts, delineated by the presence of CD31-positive staining. Bar plot represents the mean percentage ± SD. P-val are shown. The significance of difference was determined by independent sample Student t test. PI, postinoculation.

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