Fig. 1: Fusion-positive ARMS cells are sensitive to pharmacological ATR inhibition.
From: Therapeutic targeting of ATR in alveolar rhabdomyosarcoma
a Schematic of the DNA damage response pathway and small molecule inhibitor targeting proteins involved. DSB = Double Strand Break, SSB = Single Strand Break. b Heatmap showing sensitivity of ARMS (FP-RMS), Ewing sarcoma (EWS), ERMS (FN-RMS), and primary myoblast control cells (Ctrl) to the different DNA damage response inhibitors (blue indicates high sensitivity and red low sensitivity as defined by the rank of IC50 values). c Dose-response curves of cell viability for FP-RMS cell lines treated with the ATR inhibitor AZD6738 compared to primary myoblasts (n = 3). d IC50 values for FP-RMS, EWS, FN-RMS and Ctrl cells treated with AZD6738 (P = 4.10 × 10−3; 6.00 × 10−4; 6.30 × 10−3 for EWS, FP-RMS and FN-RMS vs Ctrl, respectively; from left to right, n = 8, 6, 5, and 5 biologically independent cells). e Dose-response curves of cell viability for FP-RMS cell lines treated with the ATR inhibitor BAY 1895344 compared to primary myoblasts (n = 3). f IC50 values for FP-RMS, EWS, FN-RMS and Ctrl cells treated with BAY 1895344 (P = 2.31 × 10−4; 4.59 × 10−5; 0.116 for EWS, FP-RMS and FN-RMS vs Ctrl, respectively; from left to right, n = 8, 6, 5, and 5 biologically independent cells). All statistical analyses correspond to two-sided student’s t-test; data presented as mean value ± error bars representing standard deviation.
