NSC12 elicits antitumor activity in WM. (A) Enrichment plots of AKT-, STAT3, MAPK-related genes in primary WM patients’ derived CD19⁺ cells, as shown by performing GSEA (P < .05; FDR < 2 5%), using a publicly available data set (GEO6691). BCWM.1, MWCL.1, MEC.1 cells (B) or primary WM patients’ derived CD19⁺ cells (n. 3) (C), and normal PBMCs (D) were exposed to increasing concentrations of NSC12 (0.1 to 10 μM) for 48 hours. Cell survival was evaluated by MTT assay. Average of triplicate experiments ± standard deviation (SD) is shown. (E) BCWM.1 and MWCL.1 cells were exposed to NSC12 (6 μM) for 12 hours and subjected to wide transcriptome profiling, showing a significant inhibition of FGFR-signaling–related gene sets, as shown by performing GSEA (P < .05; FDR < 25%). (F) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 6 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-phoshpo(p)-FGFR3, -p-FSR2, -GAPDH. (G) BCWM.1 and MWCL.1 cells were cultured in the presence or absence of NSC12 (0 to 6 μM; 6 hours). WM cells were then harvested, and cell lysates were subjected to western blot using anti-p-AKT, -AKT, -p-GSK3β, -p-6SR, -p-ERK, -ERK, -p-JAK2, -p-STAT3, -GAPDH. MTT, 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide.