Fig. 2

Functional ex vivo studies showing doxorubicin resistance and sensitivity to DDR inhibition in TP53 mutant cells from peritoneal effusion. a WST-1 viability assay of primary ascitic fluid BL cells and KM-H2 cells treated with DMSO and doxorubicin 500 nM for 24 h. The percentage of viable cells after treatment in each cell line was normalized to its own untreated (DMSO) control. b Western blot analysis of BL TP53 mutant primary cells and TP53 wild type HL-derived KM-H2 cells showing p21 induction in KM-H2 cells after doxorubicin (doxo) treatment (500 nM for 6 and 24 h). c Western blot analysis of BL TP53 mutant primary cells and TP53 wild type HL-derived KM-H2 cells showing relative overexpression of pCHK1 S345 and pH2AX S139 in primary BL TP53 mutant BL cells, compared to TP53 wild type KM-H2 cells. d–i Immunocytochemistry for p-CHK1 S345, p-H2AX S139, in cultured primary cells from peritoneal fluid (d, e), the bulky mass (f, g), and KM-H2 cells (g, h) confirming western blot findings (×400). j WST-1 viability assay of primary BL cells from ascitic fluid and KM-H2 cells treated with DMSO and PF-0477736 250 nM for 24 h. The percentage of viable cells after treatment in each cell line was normalized to its own untreated (DMSO) control. k Western blot assay of TP53 mutant primary BL cells from ascitic fluid and TP53 wild type HL-derived KM-H2 cells showing pH2AX S139 induction in primary BL cells after PF-0477736 treatment (250 nM for 24 h).