KDR and neoplasm: PTIM models of PCB490–3 (Fig. 4a, Additional file 27: Table S13), PCB490–4 (Fig. 4b, Additional file 27: Table S13), and PCB490–5 with integrated RNA-seq data (Fig. 4c, Additional file 27: Table S13) indicated common efficacious mechanisms across the heterogeneous tumor sites: epigenetic modifiers (HDAC, EHMT), PI3K/mTOR inhibition, and VEGF (KDR) signaling inhibition.