Acute loss of BCL-XL has no impact on the sustained expansion of p53^−/−thymic lymphomas in mice. (A) Schematic of the experimental protocol (also used for experiments shown in Figure 6). Lymphomas were harvested from p53^−/−;RosaCreERT2 (control), p53^−/−;RosaCreERT2;Bcl-x^fl/+, p53^−/−;RosaCreERT2;Bcl-x^fl/fl, p53^−/−;RosaCreERT2;Mcl-1^fl/+, or p53^−/−;RosaCreERT2;Mcl-1^fl/fl mice (all Ly5.2⁺). Lymphoma cells (3 × 10⁶; 3-6 independent primary lymphoma samples per genotype tested) were injected into 6 C57BL/6-Ly5.1⁺ recipient mice each. Three recipient mice were treated by oral gavage with 4 mg of tamoxifen on days 7 and 8 after lymphoma cell transplantation, and the other 3 recipients were left untreated and served as controls. These mice were then monitored for lymphoma development. The experiment was concluded 90 days after cell transplantation. (B) Lymphoma-free survival of the mice that had been transplanted with lymphoma cells of the genotypes indicated and treated with either tamoxifen (solid lines; to delete the floxed Bcl-x alleles) or had been left untreated (dashed lines; negative control). (C) Analysis of the proteins indicated by western blotting of transplanted thymic lymphoma samples of the indicated genotypes (representative of 3 samples each) that had grown in recipients treated with tamoxifen (tam) or in recipients that had been left untreated (ctrl). Probing for actin was used as a loading control.