Figure 1
Figure 1. Loss of BCL-XL does not delay thymic lymphoma development in p53-deficient mice. (A) Tumor-free survival of p53−/−;Lck-Cre (control; n = 26), p53−/−;Lck-Cre;Bcl-xfl/+ (n = 16, compared with control; P = .6703), and p53−/−;Lck-Cre;Bcl-xfl/fl mice (n = 26; compared with control; P = .3236); mouse cohorts were compared using the log-rank Mantel-Cox test. (B) Incidence (as % of total mice analyzed) of thymic lymphoma, splenomegaly, and other pathologies (eg, sarcoma) in cohorts of p53−/−;Lck-Cre (n = 26), p53−/−;Lck-Cre;Bcl-xfl/+ (n = 16), and p53−/−;Lck-Cre;Bcl-xfl/fl mice (n = 24). (C) Analysis of the proteins indicated by western blotting in primary thymic lymphoma samples from sick p53−/−;Lck-Cre, p53−/−;Lck-Cre;Bcl-xfl/+, and p53−/−;Lck-Cre;Bcl-xfl/fl mice (representative of 6-10 samples for each genotype). Probing for HSP70 was used as a loading control.

Loss of BCL-XL does not delay thymic lymphoma development in p53-deficient mice. (A) Tumor-free survival of p53−/−;Lck-Cre (control; n = 26), p53−/−;Lck-Cre;Bcl-xfl/+ (n = 16, compared with control; P = .6703), and p53−/−;Lck-Cre;Bcl-xfl/fl mice (n = 26; compared with control; P = .3236); mouse cohorts were compared using the log-rank Mantel-Cox test. (B) Incidence (as % of total mice analyzed) of thymic lymphoma, splenomegaly, and other pathologies (eg, sarcoma) in cohorts of p53−/−;Lck-Cre (n = 26), p53−/−;Lck-Cre;Bcl-xfl/+ (n = 16), and p53−/−;Lck-Cre;Bcl-xfl/fl mice (n = 24). (C) Analysis of the proteins indicated by western blotting in primary thymic lymphoma samples from sick p53−/−;Lck-Cre, p53−/−;Lck-Cre;Bcl-xfl/+, and p53−/−;Lck-Cre;Bcl-xfl/fl mice (representative of 6-10 samples for each genotype). Probing for HSP70 was used as a loading control.

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