Fig. 3: Defective senescence but intact apoptosis accounts for temporarily deeper responses of Suv39h1-deficient lymphomas.

a Ki67, SA-β-gal activity and H3K9me3 IHC analyses of lymphoma sections, plus whole-body fluorescence scans of mice bearing GFP-tagged control;bcl2 or Suv39h1⁻;bcl2 lymphomas. Results show mean percentages of cells positive for the respective markers in situ after a 5-day CTX exposure or those that remained untreated ± s.d. (n = 3 technical replicates per group). b Overall survival of mice bearing Suv39h1⁻;bcl2 (n = 21, red line) or control;bcl2 (n = 24, black line) lymphomas after CTX treatment. c Tumor-free survival (i.e., TTR) of mice bearing Suv39h1⁻ (n = 18, red line) or control (n = 27, black line) lymphomas after CTX treatment. d Eµ-myc transgene-specific PCR in Suv39h1^- and control Eµ-myc lymphomas prepared from bone marrow (BM), lymph-node (LN), or spleen (SP) from untreated mice (as a positive control) and 10 days after CTX treatment. Shown are analyses in mice bearing n = 8 individual lymphomas. Original photomicrographs are presented in Supplementary Fig. 7. e Spleen sections stained for Ki67 and H3K9 in B220-positive lymphomas from Suv39h1⁻ or control mice. Numbers indicate mean percentages of cells positive for the respective marker in situ 10 days after CTX administration ± s.d. (shown are representative photomicrographs of n = 3 biological replicates per group). f Representative whole-body luciferase imaging of mice harboring Suv39h1⁻ vs. control lymphoma (not bcl2-engineered) before treatment as well as 10 and 30 days after CTX treatment (n = 3 biological replicates per group [see also Supplementary Fig. 3d]). All scale bars in this figure represent 50 µm.