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. 2009 Aug;11(8):753–762. doi: 10.1593/neo.09466

Figure 2.

Figure 2

Tumor development in Mdm2+/- and Mdm2+/+ pTH-MYCN transgenic mice. Kaplan-Meier survival probability curves plotted for Mdm2+/+/MYCN (solid line) and Mdm2+/-/MYCN (dashed line) transgenics at 200 days of observation. (A) Combined analysis of 110 Mdm2+/- and 117 Mdm2+/+ mice shows a marked increase in median time to death (latency) and an overall decrease in tumor incidence (P < .001) consistent with the hypothesis that Mdm2 contributes directly to tumorigenesis in this model. (B) When analyzed according to sex, no difference in incidence was observed, but a significant increase in latency can be seen (P < .001). (C) For the female mice, an increase in latency but a pronounced decrease in incidence is now seen. No sex-dependent difference in tumor development was observed in the Mdm2+/+ mice (latency 55 days [95% CI, 52–57 days]). Latency was 80 days (95% CI, 65–95 days) for the male Mdm2+/- mice and 71 days (95% CI, 63–78 days) for the female Mdm2+/- mice. Statistical analysis was performed with the SPSS software version (Gradware, Inc., Austin, TX), and both log-rank (Mantel-Cox) and Wilcoxon methods were applied. Comparisons of survival and latency between sexes for each genotype were performed by Cox regression analysis. Mouse totals: Mdmd2+/-, 62 females and 48 males; Mdm2+/+, 58 females and 59 males.