Figure 1 from The Proteogenomics of Prostate Cancer Radioresistance

The genomic landscape of CF- and HF-resistant prostate cancer cells. A, Schematic of experimental design and workflow. B, Somatic SNV count for CF- vs. HF-resistant cells. CF-resistant cells gained twice more SNVs than HF (P = 0.1; Mann–Whitney U test). C, SNVs in cancer driver genes. Presented are all driver genes that are predicted to be strongly influenced by SNVs. Considered are SNVs that were identified in all three replicates for each cell type. Top, single-base substitution types. Bottom, the predicted annotation. D, Gained SNVs converged on partly similar cancer mutational signatures. Most signatures of known etiology, irrespective of the treatment schedule, are associated with defective DNA mismatch repair. Signature etiologies: SBS5, unknown; SBS26 and SBS15, defective DNA mismatch repair; SBS1, spontaneous deamination of 5-methylcytosine; SBS14, concurrent polymerase epsilon mutation and defective DNA mismatch repair; SBS20, concurrent POLD1 mutations and defective DNA mismatch repair; SBS44, defective DNA mismatch repair. E, Somatic SV counts for CF- and HF-resistant cells. The number of somatic SVs is similar between CF- and HF-resistant cells (P = 1; Mann–Whitney U test). F, Distinct SVs in CF-resistant cells compared to HF across the genome. Considered are SVs that were identified in all three replicates for each cell type. Chromosome numbers are presented on the x-axis. The colored lines represent types of SVs: DEL, deletion; DUP, duplication; INV, inversion; TRA, translocation. G, Fusion transcripts that were identified in either CF- and/or HF-resistant cells. Purple, the fusion transcript was identified; white, the fusion transcript was not identified. The results are presented for three replicates for each cell line.