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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Mol Cancer Ther. 2015 Apr 3;14(6):1376–1384. doi: 10.1158/1535-7163.MCT-15-0036

Figure 1. BV-resistant ALCL and HL in vitro cell models.

Figure 1

Proliferation experiments were performed in duplicate wells and averaged over 2 separate experiments, and a repeated measures ANOVA model is applied to show that time, group, and their interactions are all very significant (Panel A and B). Viable cells counts were performed by hemocytometer with methylene blue. Panel A: L428 and L428-R were seeded at 100,000 cells per well and incubated with BV at 80 μg/ml. L428-R cells are able to proliferate at this concentration whereas L428 can not. (p < 0.0001). Panel B: Karpas-299 and Karpas-R were seeded at 40,000 cells per well and incubated with BV at 30 ng/ml. Karpas-R cells are able to prliferate at this concentration whereas Karpas-299 can not (p < 0.0003). MTS assays were performed in triplicate wells and averaged over 3 separate experiments, and cells were seeded in 96-well plates at 5,000 cells (L428) and 10,000 cells (Karpas-299) per well. Panel C: A four-parameter log-logistic model was fitted to assess inhibitory effect of L428-P and L428-R, respectively. The estimated IC50 (standard error)s are 27.46 (4.76) and 236.08 (22.15) respectively. Panel D: A four-parameter log-logistic model was fitted to assess inhibitory effect of Karpas-P and Karpas-R, respectively. The estimated IC50 (standard error)s are 0.0029 (0.021) and 19.45 (1.87) respectively.