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. 2023 Nov 22;9(47):eadg2263. doi: 10.1126/sciadv.adg2263

Fig. 3. ATM loss drives sensitivity to inhibitors of PARP, ATR, and DNA-PK in bladder cancer preclinical models.

Fig. 3.

(A) Immunofluorescence images showing radiation-induced Rad51 foci formation in ATM-deleted and WT ATM KU19-19 bladder cancer cells. (B) Quantification of radiation-induced Rad51 foci shows no difference in ATM-deleted compared to WT ATM KU19-19 cells. Data are displayed as means ± SD, n = 5, ***P < 0.001 and ****P < 0.0001. (C to G) Cell survival curves for WT ATM and ATM-deleted human and mouse bladder cancer cell lines following olaparib treatment. There was a significant increase in olaparib sensitivity in ATM-deleted cells compared to WT ATM lines across all models (see also fig. S8). (H to L) Cell survival curves for WT ATM and ATM-deleted human and mouse bladder cancer cell lines following berzosertib treatment. There was a significant increase in berzosertib sensitivity in ATM-deleted cells compared to WT ATM lines across nearly all models. (M) Cell survival curves for WT ATM and ATM-deleted bladder cancer cells following nedisertib treatment.