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d Changes of relative mean vessel density of rapamycin.
(D) Quantification of the mean vessel density demonstrates a significantly higher vessel density in the control group, **P < 0.001.
Mean vessel density (MVD) increases from normal cervical tissue, through low- and high-grade CIN to SCC.
(D) Quantification of the mean vessel density in tumor sections demonstrates a highly significant decrease in vessel density in the therapy group, **P < 0.001.
Immunohistochemistry with CD-31 and Ki67 resulted in a reduction in endothelial cells (and therefore mean vessel density and cell proliferation), pointing to a decrease in oxygen consumption and demand.
Mean vessel density was reduced in Imatinib-treated animals.
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Mean vessel densities were quantified as the average number of CD31+ vessels in a minimum of 10 non-adjacent 40× fields.
7 Compared with subcutaneous tumours of syngeneic origin, KPC tumours demonstrated a desmoplastic stroma and lower mean vessel densities, thus limiting the accumulation of the active gemcitabine triphosphate (dFdCTP).
Rapamycin led to tumour growth delay associated with increased relative vessel size (8.5 to 10.3, P = 0.045) and decreased mean relative vessel density (0.27 to 0.22, P = 0.0015).
This was in line with immunohistology, demonstrating a highly significant decrease in mean blood vessel density in tumors of the therapy group (Figure 5D; CD31-positive area: control group, 3.35 ± 0.112%; therapy group, 0.99 ± 0.324%; **P < 0.001).
While the mean lymphatic vessel density was highest in the 3 week old MFP tumours, the 5 week old SC tumours demonstrated the highest mean lymphatic vessel area.
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