Figure 5.
Figure 5. Low doses of CDDO-Im and bortezomib/proteasome inhibitor PS-341 trigger synergistic anti-MM activity in patient MM cells. (A) CD138+ MM patient cells (patient nos. 1-3) were treated with CDDO-Im (80 nM), bortezomib (2 nM), or CDDO-Im + bortezomib for 24 hours and assessed for viability using MTT assays. Values are mean ± SD of triplicate samples, P = .05; experiments were repeated 2 times with similar results. (B) CD138+ MM patient cells (patient nos. 1-3) were treated with CDDO-Im (80 nM), bortezomib (2 nM), or CDDO-Im + bortezomib for 24 hours and assessed for apoptosis by DNA fragmentation assays. Values are the mean ± SD of triplicate samples, P = .06; experiments were repeated 3 times with similar results. (C) Normal lymphocytes from 4 healthy donors were treated with CDDO-Im (80 nM) + bortezomib (2 nM) for 24 hours, and viability was assessed by an MTT assay. Results are the mean ± SD of 3 independent experiments, with P = .31 using Jonchkeere-Tepstra (J-T) test for trend.

Low doses of CDDO-Im and bortezomib/proteasome inhibitor PS-341 trigger synergistic anti-MM activity in patient MM cells. (A) CD138+ MM patient cells (patient nos. 1-3) were treated with CDDO-Im (80 nM), bortezomib (2 nM), or CDDO-Im + bortezomib for 24 hours and assessed for viability using MTT assays. Values are mean ± SD of triplicate samples, P = .05; experiments were repeated 2 times with similar results. (B) CD138+ MM patient cells (patient nos. 1-3) were treated with CDDO-Im (80 nM), bortezomib (2 nM), or CDDO-Im + bortezomib for 24 hours and assessed for apoptosis by DNA fragmentation assays. Values are the mean ± SD of triplicate samples, P = .06; experiments were repeated 3 times with similar results. (C) Normal lymphocytes from 4 healthy donors were treated with CDDO-Im (80 nM) + bortezomib (2 nM) for 24 hours, and viability was assessed by an MTT assay. Results are the mean ± SD of 3 independent experiments, with P = .31 using Jonchkeere-Tepstra (J-T) test for trend.

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