Hdac1/2 knock-down accelerates lymphomagenesis. (A-B) Lin⁻ cells from p53^−/− mice transduced with the control vector (CTRL) or vectors carrying an shRNA against Hdac1 or Hdac2 were sorted for GFP positivity and injected into lethally irradiated recipient WT mice. (A) Immunoblot analysis of cells transduced with the indicated retroviral vectors. The arrow indicates HDAC2. The asterisk indicates HDAC1 residual staining from the previous immunoblotting assay. Hdac3 served as a loading control. (B) Leukemia-free survival curves of mice transplanted with p53 null lin⁻ cells transduced with the control vector (CTRL) or a vector carrying an shRNA against Hdac1 (left panel, P < .05) or Hdac2 (right panel, p=ns). (C-D) Eμ-myc fetal liver progenitor cells were transduced with the control vector (CTRL) or vectors carrying an shRNA against Hdac1 or Hdac2 and injected into irradiated recipient PTPRCA mice. (C) Kaplan-Meier survival curves are shown; hdac1 P < .05, hdac2 p=ns. (D) Western blots were performed on FACS-sorted GFP⁺ cell lysates from a control spontaneous Eμ-myc lymphoma (lane 1) and the indicated primary lymphomas with knockdown of HDAC1 (lanes 2 and 3) or HDAC2 (lanes 4-6) and were analyzed for the expression of the indicated HDACs. B-actin was used as a loading control.