Fig. 2: Lack of Ppif promotes secondary M/D-driven mammary carcinogenesis.

Wild-type (WT) Ppif^−/−, Ripk3^−/− or Mlkl^−/− female C57BL/6J mice were subjected M/D-driven carcinogenesis and analyzed as illustrated in Fig. 1A. Time to secondary disease (TT2) (A), percentage of mice developing secondary lesions (B), secondary tumor growth (C), number of secondary tumors per mouse (D) and number of secondary tumors per mouse normalized to time to death (TTD) (E) are reported. In (A), median TT2, Mantel–Haenszel hazard ratio (HR) with 95% confidence interval (CI), group size (n) and p values (Log-rank) are indicated. Mice succumbing to primary disease without developing a secondary tumor were censored from the analysis. In (B), group size (n) and p values (Fisher’s exact test, compared to WT mice) are indicated. In (C) both individual and average tumor growth are illustrated, with group size (n) and p values (2-way ANOVA, compared to WT mice) reported. In (D and E) results are reported as means ± SEM and individual data points, p values (Kruskal–Wallis, compared to WT mice) are indicated. NR not reached.