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. Author manuscript; available in PMC: 2016 Apr 19.
Published in final edited form as: Nature. 2016 Mar 16;531(7595):471–475. doi: 10.1038/nature17157

Figure 3. 11B3 deletion can accelerate lymphomagenesis through p53-independent mechanisms.

Figure 3

a, Kaplan–Meier lymphoma-free survival curve of recipient mice receiving Vav1-cre;11B3fl/+ or Vav1-cre; 11B3+/+, transduced simultaneously with a mouse Myc cDNA and an shRNA against Trp53 (shp53). n = 8 per genotype. **P < 0.01 (log-rank test). b, The expression levels of Trp53 and p21 after ADR treatment of resulting lymphoma cells as detected by immunoblotting and RT–qPCR, respectively. p21 levels were normalized to untreated Trp53+/+ lymphomas. Shown are representative results (n = 8 per cohort). c, qPCR analysis to determine the percentage of chromosome 11B3 deletion in pre-B cells (transduced cells before transplantation; n = 3) and resulting lymphomas (n = 5) from the experiment in a. ***P < 0.001 (two-tailed t-test).