Figure 1
Figure 1. Conditioned medium of IM-resistant LAMA cells confers IM and NI resistance to IM-naive LAMA cells. (A) CM of IM-resistant (R) clones protects IM-naive LAMA cells from IM- and NI-induced apoptosis. Percentage of viable cells after treatment is shown relative to no treatment controls. Bars represent mean ± SD of 3 independent experiments using CM of the 3 R and 3 UR clones (10, 14, and 25, respectively); ** P < .001 (1-way ANOVA, Bonferroni adjustment for multiple comparisons). (B) 25R-CM and patient no. 1–derived CM protects IM-naive, CD34+-enriched progenitors of patients with first-diagnosis CML (n = 3; patients no. 3, 4, and 8). Primary progenitor cells were exposed to 10 μM NI for 72 hours in the presence of 25UR-CM (as control), 25R-CM, or IM-resistant patient no. 1–derived CM (▪) and then placed into semisolid Methocult medium. Emerging colonies were counted. Bars represent fold increased colony formation ± SD by 25R-CM (⊡), or patient no. 1–derived CM (▪) relative to 25UR control treatment.

Conditioned medium of IM-resistant LAMA cells confers IM and NI resistance to IM-naive LAMA cells. (A) CM of IM-resistant (R) clones protects IM-naive LAMA cells from IM- and NI-induced apoptosis. Percentage of viable cells after treatment is shown relative to no treatment controls. Bars represent mean ± SD of 3 independent experiments using CM of the 3 R and 3 UR clones (10, 14, and 25, respectively); ** P < .001 (1-way ANOVA, Bonferroni adjustment for multiple comparisons). (B) 25R-CM and patient no. 1–derived CM protects IM-naive, CD34+-enriched progenitors of patients with first-diagnosis CML (n = 3; patients no. 3, 4, and 8). Primary progenitor cells were exposed to 10 μM NI for 72 hours in the presence of 25UR-CM (as control), 25R-CM, or IM-resistant patient no. 1–derived CM (▪) and then placed into semisolid Methocult medium. Emerging colonies were counted. Bars represent fold increased colony formation ± SD by 25R-CM (⊡), or patient no. 1–derived CM (▪) relative to 25UR control treatment.

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