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. 2013 Mar;98(3):404–408. doi: 10.3324/haematol.2012.067959

Figure 1.

Figure 1.

Ruxolitinib is active against Ba/F3 cells transformed by ETV6-JAK2. (A) KG1A cells (which contain FGFR1OP2-FGFR1) and Ba/F3 cells transformed to IL3-independence by the fusion genes ETV6-JAK2, SPTBN1-FLT3, ZMYM2-FGFR1 or BCR-ABL1 were exposed to ruxolitinib for 48 h. Values are means +/− SE of 3 independent experiments. (B) Expression as a percentage of Day 0 MTS reading (where line crosses y-axis at 100%) indicates a net reduction in numbers of Ba/F3-ETV6-JAK2 cells over 48 h. Values are means +/− SE of 2 independent experiments. (C) Treatment of cells with ruxolitinib for 4 h resulted in a dose-dependent reduction in phosphorylation of ETV6-JAK2, ERK, STAT5 and AKT. Translation from an internal methionine results in two isoforms of ETV6-JAK2;2 we found only the larger to be phosphorylated.