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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 5. Chromosome 11B3 deletion acts beyond Trp53 loss to drive myeloid leukaemia.

Figure 5

a, AML generation by HSPC isolation (Vav1-cre; Trp53fl/fl or Vav1-cre;11B3fl/Trp53fl) co-transduction with a GFP-linked Nf1 shRNA and an mCherry-linked Mll3 shRNA, and transplantation into sublethally irradiated recipients (n = 10 per group). b, Post-transplant, leukaemia-free survival **P < 0.01 (log-rank test). c, Blood smear of moribund mice (b) that is representative of all animals analysed in each genotype (n = 4). d, RNA-seq comparison of chromosome 11 gene-expression levels between the 11B3Δ/Trp53Δ and Trp53Δ/Δ leukaemia generated in b (n = 4). e, Gene set enrichment analysis of genes on chromosome 17p13 in chromosome 17p-deleted human AML compared to those with TP53 mutations but without 17p deletions. FDR, false discovery rate; NES, normalized enrichment score. f, Kaplan–Meier survival curve of secondary transplants from two independent primary leukaemias of each genotype in a, b. n = 5 in each cohort. **P < 0.01 (log-rank test).