Basic Research
Copyright ©The Author(s) 2004.
World J Gastroenterol. Dec 15, 2004; 10(24): 3583-3589
Published online Dec 15, 2004. doi: 10.3748/wjg.v10.i24.3583
Figure 1
Figure 1 Expression of p53 protein before (-) and after infec-tion with Ad-p53 (+) in pancreatic cancer cell lines.
Figure 2
Figure 2 Decreased in vitro growth rate in pancreatic cancer cell lines 24 h after infection with Ad-p53. Data points repre-sent means from 9 samples of viable cells in three indepen-dent experiments; bars, SD.
Figure 3
Figure 3 Percentage of apoptotic cells of human and rat pan-creatic carcinoma cell lines either infected with Ad-CD con-trol vector or Ad-p53 (MOI 1) 24 h prior ± 5-FU chemotherapy (5 µg/mL) given for 48 h. Points represent means from 9 samples in three independent experiments; bars, 95%CI.
Figure 4
Figure 4 Gel electrophoresis for PCR products from DSL6A tumors removed from Lewis rats 24 h following the last treatment. (P) positive control, vector DNA; (N) negative con-trol (RT minus control); (C) Ad-CD control virus treated tu-mor (Ad-CD); (T) Ad-p53 infected tumor.
Figure 5
Figure 5 Efficacy of Ad-p53 infection and 5-FU as single agents vs the combination of both on tumor growth of Lewis rats challenged with DSL6A tumor cells. Arrowheads indicate treat-ment application. 1All animals were killed after 6 cycles of therapy because the tumor size was above 600 mm2.
Figure 6
Figure 6 Ad-p53 mediated sensitisation of tumors to apoptosis in response to 5-FU in vivo. Formalin-fixed tissue sections were analyzed by TUNEL labelling. Original magnification × 200.