Increased frequency and shorter latency of B-cell lymphomagenesis in the absence of casp8 and p53. Kaplan-Meier analysis of the tumor-free survival in cohorts of WT (n = 12), bcasp8−/− (n = 31), CD19Cre;p53fl/fl (n = 10), and bcasp8−/−p53−/− (n = 30) mice. *P = .04 for the log-rank test between survival curves of bcasp8−/−p53−/− and bcasp8−/− mice and **P = .015 for bcasp8−/−p53−/− and CD19Cre;p53fl/fl mice. (B-C) H&E staining of LNs infiltrated with proliferating bcasp8−/−p53−/− tumor cells. Bar indicates 250 μm in panel B and 500 μm in panel C. (D) bcasp8−/−p53−/− lymphomas infiltrating hepatic sinusoids and periportal spaces. Bar indicates 100 μm. (E-G) High magnification showing tumors with high mitotic index. Bar indicates 50 μm. (H) Mitotic index of tumors from WT (n = 5), p53−/− (n = 3), bcasp8−/− (n = 3), and bcasp8−/−p53−/−(n = 3) mice. Ten different fields were counted for each tumor. *Student t test indicated statistical significance. (I-J) Representative anaphase bridges in H&E-stained tumors from bcasp8−/− mice (I) and bcasp8−/−p53−/− mice (J). (K) Representative abnormal multipolar metaphase observed in H&E-stained tumors from bcasp8−/− mice. (L) Representative abnormal asymmetric metaphase observed in H&E-stained tumors from bcasp8−/−p53−/−mice. (M-N) Binucleated tumor cells in blood smear (N) and touch smear from kidney of bcasp8−/− mice. Bar indicates 10 μm in panels I through N.