Fig. 2: Evaluation of double-strand breaks signaling and repair in del(11q)/ATM-deficient CLL cells. | Leukemia

Fig. 2: Evaluation of double-strand breaks signaling and repair in del(11q)/ATM-deficient CLL cells.

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

Fig. 2

a Left panel: representative images of γH2AX foci formation (red) in HG3WT, HG3-del(11q) and HG3-del(11q) ATMKO clones. Upper panel shows non-irradiated (−IR) HG3 cells and lower panel represents HG3 clones 1 h after 2 Gy irradiation (+IR). Right panel: quantification of the number of γH2AX foci per cell 1 h after irradiation. Data are represented as the mean values ± SD of three independent experiments. At least 75 cells per experiment were counted. b Quantification of the number of γH2AX foci per cell 1 h after irradiation in primary CLL samples stimulated to proliferate for 24 h before IR (2 Gy). Groups are stratified based on ATMWT (n = 8) ATM monoallelic (n = 6) or biallelic (n = 4) defects in CLL samples. At least 75 cells per patient were counted. Primary samples used in this experiment are detailed in Supplementary Table 1. c Left panel: representative images of the neutral comet assay experiment in HG3WT, HG3-del(11q) and HG3-del(11q) ATMKO clones. Upper images show non-irradiated HG3 comets, middle panel represents comets right after 40 Gy irradiation and lower images present comets 3 h after 40 Gy irradiation, when HG3WT were able to repair the IR-generated DNA damage. Right panel: tail moment quantification of neutral comet assays in HG3WT, HG3-del(11q) and HG3-del(11q) ATMKO clones 3 h after 40 Gy irradiation. Data represent the mean values ± SD of at least 50 comets analyzed per condition in three independent experiments.

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