Figure 1
Figure 1. Decitabine induces aneuploidy in p53 deficient Burkitt lymphoma (BL) cells. (A) The BL cell lines Akata, KemI, and KemIII were treated with 2 μM decitabine (Dec) for 48 hours. The cell-cycle distribution was determined by flow cytometry of cells stained with propidium iodide. Cells regarded as aneuploid are indicated by arrows. (B) TP53 status correlates with presence of decitabine-induced aneuploidy of BL cells. Cells were irradiated with 10 Gy of ionizing radiation (γ-IR) and harvested 24 hours after treatment for analysis with Western blot using a monoclonal antibody against p53. The KemI cell line exhibits abnormally high levels of p53 irrespective of DNA damage, which is indicative of a TP53 mutant status. KemIII cells induce p53 after γ-IR treatment, as predicted by cells carrying wild-type TP53. Akata cells do not express p53, as previously shown.32

Decitabine induces aneuploidy in p53 deficient Burkitt lymphoma (BL) cells. (A) The BL cell lines Akata, KemI, and KemIII were treated with 2 μM decitabine (Dec) for 48 hours. The cell-cycle distribution was determined by flow cytometry of cells stained with propidium iodide. Cells regarded as aneuploid are indicated by arrows. (B) TP53 status correlates with presence of decitabine-induced aneuploidy of BL cells. Cells were irradiated with 10 Gy of ionizing radiation (γ-IR) and harvested 24 hours after treatment for analysis with Western blot using a monoclonal antibody against p53. The KemI cell line exhibits abnormally high levels of p53 irrespective of DNA damage, which is indicative of a TP53 mutant status. KemIII cells induce p53 after γ-IR treatment, as predicted by cells carrying wild-type TP53. Akata cells do not express p53, as previously shown.32 

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