Figure 7.
Figure 7. An antioxidant inhibits ROS-induced mutations in BCR/ABL kinase domain in vivo. Leukemia-bearing SCID mice were fed with control chow (▪) or vitamin E-enriched diet (VE diet, ▦). Then, mononuclear cells of SPL and BMC were plated in methylcellulose in the absence of IL-3 (only leukemia cells grow) and the presence or absence of IM, and colonies were counted after 7 days. BCR/ABL kinase domain in IM-resistant cells was amplified by reverse transcriptase-polymerase chain reaction and sequenced. Mutation frequency and the percentages of base substitutions (Mutation phenotype) in the sequence encoding BCR/ABL kinase are shown. Mutations leading to previously described amino acid substitutions in BCR/ABL kinase are listed (Aa substitutions). *P < .01 compared with control chow group.

An antioxidant inhibits ROS-induced mutations in BCR/ABL kinase domain in vivo. Leukemia-bearing SCID mice were fed with control chow (▪) or vitamin E-enriched diet (VE diet, ▦). Then, mononuclear cells of SPL and BMC were plated in methylcellulose in the absence of IL-3 (only leukemia cells grow) and the presence or absence of IM, and colonies were counted after 7 days. BCR/ABL kinase domain in IM-resistant cells was amplified by reverse transcriptase-polymerase chain reaction and sequenced. Mutation frequency and the percentages of base substitutions (Mutation phenotype) in the sequence encoding BCR/ABL kinase are shown. Mutations leading to previously described amino acid substitutions in BCR/ABL kinase are listed (Aa substitutions). *P < .01 compared with control chow group.

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