Figure 6
Figure 6. Cytoplasmic p27 promotes BCR-ABL1–induced leukemia. (A) BM cells from p27−/− and p27CK− mice were transduced with BCR-ABL1 retrovirus, sorted by FACS for GFP+/Lin− cells and plated in methylcellulose in absence of cytokines. Myeloid colony formation of BCR-ABL1–transduced cells was assessed after 8 days. (B) Kaplan-Meier survival analysis of p27+/+ mice transplanted with BCR-ABL1–transduced BM cells from p27−/− and p27CK− mice. (C) WBC and PLT counts and (D) spleen and liver weights of leukemic mice were compared according to genotype. (E) Lineage distributions of GFP+ cells in the BM and spleen of leukemic mice: granulocytes (Gr1+CD11b+), B cells (CD19+), T cells (CD3+), and LKS cells (Lin−c-Kit+Sca1+). Error bars represent standard deviation. (F) Representative histological sections of BM, liver, lung, and spleen from mice transplanted with BCR-ABL1–transduced BM cells from p27−/− and p27CK− mice. Scale bars represent 100 μm. In above experiments, **P < .010.

Cytoplasmic p27 promotes BCR-ABL1–induced leukemia. (A) BM cells from p27−/− and p27CK− mice were transduced with BCR-ABL1 retrovirus, sorted by FACS for GFP+/Lin cells and plated in methylcellulose in absence of cytokines. Myeloid colony formation of BCR-ABL1–transduced cells was assessed after 8 days. (B) Kaplan-Meier survival analysis of p27+/+ mice transplanted with BCR-ABL1–transduced BM cells from p27−/− and p27CK− mice. (C) WBC and PLT counts and (D) spleen and liver weights of leukemic mice were compared according to genotype. (E) Lineage distributions of GFP+ cells in the BM and spleen of leukemic mice: granulocytes (Gr1+CD11b+), B cells (CD19+), T cells (CD3+), and LKS cells (Linc-Kit+Sca1+). Error bars represent standard deviation. (F) Representative histological sections of BM, liver, lung, and spleen from mice transplanted with BCR-ABL1–transduced BM cells from p27−/− and p27CK− mice. Scale bars represent 100 μm. In above experiments, **P < .010.

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