Skip to main content
. 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

Extended Data Figure 3. 11B3 recombination and lymphomagenesis in Eu-Myc model.

Extended Data Figure 3

a, The extent of 11B3 deletion in peripheral blood cells, as determined by semi-quantitative PCR, in 11B3fl/+ mice crossed to Cd19-cre (left), Mx1-cre (middle) or Vav1-cre (right). Genomic DNA from 11B3+/Δ ES cells was mixed with 11B3fl/+ cells at different ratios (5% or 20%) as a standard. For Mx1-cre, 6–8-week-old mice were treated with polyinosinic:polycytidylic acid (poly(I:C)) (15 mg kg−1 every other day, 7 times) by intraperitoneal injection. b, Partial 11B3 deletion in Vav1-cre;11B3fl/+ pre-B cells as determined by semi-quantitative PCR, indicating incomplete recombination. c, Complete Trp53fl/+ recombination in Vav1-cre;Trp53fl/+ pre-B cells as determined by PCR. d, Tumour-free survival of Eμ-Myc;Vav1-cre;Trp53fl/+ (n = 9), Eμ-Myc;Vav1-cre;11B3fl/+ (n = 12) and Eμ-Myc;Vav1-cre (n = 6) mice shows that 11B3-deleted tumours have longer tumour latency than Trp53-loss-only controls. ***P < 0.001 (log-rank test).