Figure 4
Oncogenic tyrosine kinases increase SSA repair. SSA frequency was determined in BaF3 cells transformed with different oncogenic tyrosine kinases. Cells cotransfected with SAGFP and I-SceI expression vector were evaluated by flow cytometry after 48 hours. (A) BaF3 cells transformed with the Tel-ABL (n = 4) and Tel-PDGFR (n = 5) oncogenes were used to measure SSA frequency in response to imatinib (1 μM) treatment, as indicated. (B) BaF3 cells transformed with FLT3-ITD and parental BaF3 cells were used to measure SSA frequency in response to midostaurin (50 nM) treatment, as indicated (n = 3). (C) Parental BaF3.EpoR cells containing the Jak2.V617F mutation or the double mutation, V617F.Y114A, were used to measure SSA frequency (n = 3). (D) HEL cells expressing mutant Jak2.V617F were used to measure SSA frequency in response to a Jak inhibitor (1 μM) (n = 3).

Oncogenic tyrosine kinases increase SSA repair. SSA frequency was determined in BaF3 cells transformed with different oncogenic tyrosine kinases. Cells cotransfected with SAGFP and I-SceI expression vector were evaluated by flow cytometry after 48 hours. (A) BaF3 cells transformed with the Tel-ABL (n = 4) and Tel-PDGFR (n = 5) oncogenes were used to measure SSA frequency in response to imatinib (1 μM) treatment, as indicated. (B) BaF3 cells transformed with FLT3-ITD and parental BaF3 cells were used to measure SSA frequency in response to midostaurin (50 nM) treatment, as indicated (n = 3). (C) Parental BaF3.EpoR cells containing the Jak2.V617F mutation or the double mutation, V617F.Y114A, were used to measure SSA frequency (n = 3). (D) HEL cells expressing mutant Jak2.V617F were used to measure SSA frequency in response to a Jak inhibitor (1 μM) (n = 3).

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