Fig. 2

IFNa and TKI effects on mRNA and protein expression in cell lines and patient PBMCs. BCR-ABL-positive (blue) or JAK2V617F-positive (red) cells were treated with 1 μM imatinib (BCR-ABL) or ruxolitinib (JAK2V617F) or 100 U/ml IFNa or a combination of TKI and IFNa for 4 h. a, b mRNA expression of interferon target genes in transduced murine 32D cells or human K562 (BCR-ABL) or HEL (JAK2V617F) cells, shown as mean values ± SD as a percentage of GAPDH expression. *p < 0.05, **p < 0.01, ***p < 0.001. 32D cells were WEHI starved for 24 h before starting the experiment. c Western blot analysis of the canonical IFNa and oncogene-triggered signaling after TKI and/or IFNa treatment (4 h). The indicated antibodies were used, and GAPDH served as the loading control. d STAT1 expression and tyrosine phosphorylation (pY-STAT1) after 4 h of TKI and/or IFNa treatment in K562 and HEL cells