Fig. 6: Implications of BCR inhibition in HR-mediated DSBs repair in CRISPR/Cas9-edited clones and primary CLLs. | Leukemia

Fig. 6: Implications of BCR inhibition in HR-mediated DSBs repair in CRISPR/Cas9-edited clones and primary CLLs.

From: CRISPR/Cas9-generated models uncover therapeutic vulnerabilities of del(11q) CLL cells to dual BCR and PARP inhibition

Fig. 6

a HG3WT, HG3-del(11q) and HG3-del(11q) ATMKO cells were treated with olaparib, ibrutinib and/or bendamustine and cell viability was assessed by MTT assay 72 h later. Surviving fraction is expressed relative to untreated controls and data are presented as the mean ± SD of two independent experiments. b Primary CLL cells were seeded in co-culture with HS-5 bone marrow stromal cells, 1.5 μg/mL CpG and 50 ng/mL IL-2 and treated with the indicated doses of olaparib, ibrutinib and/or bendamustine for 5 days. Normalized surviving fraction is expressed relative to untreated cells. c Tail moment quantification of neutral comet assays in HG3WT (blue) and HG3-del(11q) ATMKO (red) clones 16 h after olaparib (5 μM), ibrutinib (5 μM) and/or bendamustine (50 μM). Data are shown as the mean values ± SD of at least 50 comets analyzed per condition in three independent experiments.

Back to article page