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. Author manuscript; available in PMC: 2021 Nov 5.
Published in final edited form as: J Pathol. 2016 Oct;240(2):224–234. doi: 10.1002/path.4770

Figure 4.

Figure 4.

Cdkn2 deletion accelerates skin tumor formation and promotes metastasis in carcinomas induced by mutant p53. (A) Tumor kinetics in mice with the following genotypes: Cdkn2af/f;p53R172H/f (n=22), Cdkn2af/f;p53f/f (n=27), Cdkn2af/f;p53wt/wt (n=30) and Cdkn2awt/wt;p53f/f (n=23). *P< 0.05 for the following comparisons: Cdkn2af/f;p53R172H/f with each of the other groups; Cdkn2af/f;p53f/f with Cdkn2af/f;p53wt/wt. (B) Hematoxylin and eosin staining of primary tumors with the indicated genotypes. Note the spindle appearance of all tumors that lack Cdkn2a, regardless of the p53 status. The lower right panel shows a representative image for a liver metastasis that developed from a tumor induced by deletion of Cdkn2a and activation of p53R172H. (C) Metastasis rates in mice with the indicated genotypes. P<0.05 for comparisons between Cdkn2af/f;p53R172H/f and the rest of the groups.