Figure 6.
Figure 6. An antioxidant prevents mutations in BCR/ABL kinase domain and IM resistance in CML cells. Cells from CML-BC patients previously untreated with IM (no resistance detected prior to the experiment) were cultured for 6 weeks in medium supplemented with SCF + GM-CSF in the absence (CML) or presence of IM (CML + IM) or PDTC (CML + PDTC) (similar to that described in Figure 2). ROS levels were examined by fluorescence (Relative fluorescence). Cells were plated in methylcellulose without growth factors in the presence or absence of 2 μM IM, and colonies were counted after 7 days. Results represent percent of IM-resistant cells (mean ± SD). Mutation rate and mutation phenotype in BCR/ABL kinase is shown. Mutations leading to previously described amino acid substitutions are listed (Aa substitutions). *P < .05 and **P < .001 compared with CML group.

An antioxidant prevents mutations in BCR/ABL kinase domain and IM resistance in CML cells. Cells from CML-BC patients previously untreated with IM (no resistance detected prior to the experiment) were cultured for 6 weeks in medium supplemented with SCF + GM-CSF in the absence (CML) or presence of IM (CML + IM) or PDTC (CML + PDTC) (similar to that described in Figure 2). ROS levels were examined by fluorescence (Relative fluorescence). Cells were plated in methylcellulose without growth factors in the presence or absence of 2 μM IM, and colonies were counted after 7 days. Results represent percent of IM-resistant cells (mean ± SD). Mutation rate and mutation phenotype in BCR/ABL kinase is shown. Mutations leading to previously described amino acid substitutions are listed (Aa substitutions). *P < .05 and **P < .001 compared with CML group.

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