Figure 4
The BH3-mimetic ABT-737 sensitizes B-NHL cells expressing high levels of Bcl-2 and Bcl-xL to rituximab-induced apoptosis. (A) Resistant B-NHL cells were incubated for 48 hours with cross-linked rituximab (Rc), the pharmacologic BH3-mimetic ABT-737 (100 nM for Jeko-1 and HT cells, 5 nM for Sc-1 cells), or both. The fraction of cells with apoptotic DNA fragmentation was quantified flow cytometrically; mean values plus SD of 3 independent experiments are shown. (B) Resistant B-NHL cells were incubated for 24 hours with staurosporine (STS, 25 nM), the pharmacologic BH3-mimetic ABT-737 (100 nM for Jeko-1 and HT cells, 5 nM for Sc-1 cells), or both. The fraction of cells with apoptotic DNA fragmentation was quantified flow cytometrically; mean values plus SD of 3 independent experiments are shown.

The BH3-mimetic ABT-737 sensitizes B-NHL cells expressing high levels of Bcl-2 and Bcl-xL to rituximab-induced apoptosis. (A) Resistant B-NHL cells were incubated for 48 hours with cross-linked rituximab (Rc), the pharmacologic BH3-mimetic ABT-737 (100 nM for Jeko-1 and HT cells, 5 nM for Sc-1 cells), or both. The fraction of cells with apoptotic DNA fragmentation was quantified flow cytometrically; mean values plus SD of 3 independent experiments are shown. (B) Resistant B-NHL cells were incubated for 24 hours with staurosporine (STS, 25 nM), the pharmacologic BH3-mimetic ABT-737 (100 nM for Jeko-1 and HT cells, 5 nM for Sc-1 cells), or both. The fraction of cells with apoptotic DNA fragmentation was quantified flow cytometrically; mean values plus SD of 3 independent experiments are shown.

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