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. 2007 Mar 8;109(12):5411–5421. doi: 10.1182/blood-2006-06-032490

Table 2.

Effect of IM treatment on Bcr-Abl kinase activity and downstream signaling pathways in CD34+ cells expressing low and high levels of Bcr-Abl: percentage inhibition with IM treatment

IM, μM MIG R1
BAlo
BAhi
0.10 1.00 0.10 1.00 0.10 1.00
P-Bcr-Abl, n = 3* NE NE 68.7 ± 7.6 91.8 ± 6.8 55.2 ± 9.3 97.5 ± 6.1
P-Akt, n = 3 −45.5 ± 41.7 −23.12 ± 32.1 12.5 ± 16 29.1 ± 28.9 44.5 ± 9.0 80.2 ± 4.7
P-MAPK, n = 3* 8.5 ± 28.3 −9.34 ± 4.7 69.6 ± 21.4 58 ± 28.5 66.2 ± 5.5 85.6 ± 2.8
P-STAT5, n = 4* −28 ± 36 −32 ± 39 66.6 ± 13.1 73.5 ± 11.5 67.2 ± 5.4 94.2 ± 2.5
Bcl-XL, n = 3 −2.03 ± 10.72 −13.59 ± 23.66 23.98 ± 31.93 0.51 ± 43.17 36.38 ± 8.20 53.8 ± 4.6
Mcl-1, n = 2 −46.41 ± 67.25 −109.0 ± 103.9 61.05 ± 17.89 54.97 ± 7.9 71.82 ± 3.8 89.15 ± 4.77

Results are expressed as percentage relative to untreated control cells. Differences related to Bcr-Abl expression levels and IM exposure were analyzed using 2-way ANOVA; values are mean ± SEM.

*

P < .001[AU21] for IM-treated versus untreated cells.

P < .05 for IM-treated versus untreated cells.

P = .01 for BAlo versus BAhi cells.