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. 2013 May 11;4(6):830–843. doi: 10.18632/oncotarget.971

Table 4. Effects of mTOR and PI3K inhibitors on the constitutive release of angioregulatory mediators by primary human AML cells.

Soluble mediator Rapamycin Temsirolimus GDC-0941 3-MA
CXCL8 96.5 %
0.4737
103.0 %
0.8218
66.0 %
0.0004
93.5 %
0.1502
CXCL9 76.0 %
0.2048
69.0 %
0.0317
50.0 %
0.0047
32.5 %
0.0009
CXCL10 50.5
0.0003
52.0
0.0002
53.0
0.0007
29.0
0.0001
CXCL11 70.5
0.0226
81.0
0.183
56.5
0.0311
35.0
0.0005
Ang-1 89.0
0.0270
89.0
0.0195
76.0
<0.0001
71.0
<0.0001
Ang-2 97.0
0.3164
88.0
0.1682
85.0
0.0006
79.0
0.0014
VEGF 64.0
0.1665
41.0
0.0051
51.0
0.0255
86.0
0.5621
HGF 75.0
0.0020
72.0
0.0001
57.5
<0.0001
57.0
<0.0001
MMP-2 96.0
0.1640
70.5
0.0123
54.3
0.0002
58.5
0.0009
MMP-9 64.5
0.0004
60.0
0.0010
59.0
<0.0001
83.5
0.0207

The results are presented as the median % inhibition (upper value) of mediators released after drug treatment compared to levels in control cultures without drugs. The corresponding p-value (lower value) is shown where statistically significant differences are marked in bold. The drugs were tested at the following concentrations: rapamycin 1.0 μM, temsirolimus 0.1 μM, GDC-0941 1.0 μM and 3-MA 1.0 mM).