Fig. 1: RIPK3 does not play a critical role in the development or therapeutic response in MYC-driven lymphomas.

a Kaplan–Meier survival curves of Eμ-Myc (n = 37, median survival of 118 days), Eμ-Myc;Ripk3^+/− (n = 54, median survival of 97 days) or Eμ-Myc;Ripk3^−/− (n = 80, median survival of 97 days) mice. The difference in survival between mice of the different the genotypes was not significant (log-rank (Mantel–Cox) test). b Stacked bar graph showing the percentages of pro/pre-B (B220⁺sIg⁻), B (B220⁺sIg⁺) and mixed pre-B/B cell lymphomas observed for Eμ-Myc (n = 34), Eμ-Myc;Ripk3^+/− (n = 6) and Eμ-Myc;Ripk3^−/− (n = 13). The difference in surface marker phenotype between lymphomas of the different genotypes was not significant (repeated measures one-way ANOVA, with the Geisser–Greenhouse correction). c–f Eμ-Myc lymphoma cell lines with wt p53, AF47A and AH15A, transduced with expression constructs for Cas9 and sgRNAs targeting Ripk3 (RIPK3 KO) or transduced with an empty vector (EV) were treated with increasing concentrations of etoposide (0–10 μM) (c), paclitaxel (0–10 μM) (d), dexamethasone (0–50 μM) (e) for 48 h, or (f) with S63845 (0–10 μM) for 24 h. Cell viability was assessed using Annexin V plus PI staining and FACS analysis. The frequency of Annexin V⁻PI⁻ cells was normalised to control (DMSO treated) cells (Viability (% untreated)). Means ± SD for three independent experiments are shown.