Fig. 1. Genetic alterations in SPOP and ERG are synthetic sick.

a Distribution of genetic alterations in SPOP and ERG across 333 primary prostate cancers in TCGA database^3,8,9. b 3D growth of mouse prostate epithelial organoids derived from C57BL/6 mice over-expressing the indicated SPOP and ERG species (bar represents 20 µm) (n = 3, technical replicates). Representative bright-field pictures and hematoxylin and eosin (H&E) stained sections are shown. c In vivo growth of VCaP xenografts over-expressing the indicated SPOP species in immune-compromised mice (each group, n = 10). d Immunoblot of VCaP cells overexpressing the indicated SPOP species and corresponding quantification of the indicated protein levels depicted as a heatmap. Protein expression changes were normalized to β-ACTIN and Control cell line, (n = 2). e Tumor growth kinetics of xenografts established from LuCaP-147 PDX (SPOP-Y83C) stably overexpressing ΔERG or Control vector (each group, n = 10). Corresponding immunoblot and quantification are depicted as a heatmap. Protein expression changes were normalized to Vinculin (VCL) and Control cell line. f Dose–response curve of VCaP cells overexpressing the indicated SPOP species and treated with the ETS-inhibitor YK-4-279. All error bars, mean + s.e.m. P-values were determined by one-way ANOVA (b) or two-way ANOVA (c, e, f) with multiple comparisons and adjusted using Benjamini–Hochberg post-test ****P < 0.0001. Molecular weights are indicated in kilodaltons (kDa). Source data are provided as a Source Data File.