Figure 1. Cooperation of loss of p53 and αv integrin during SCC development.

(a) Kinetics of SCC development induced by deletion of p53 and αv in stratified epithelia. Percentage of carcinoma-free mice are represented over time in mice with the following genotypes: αv^f/f-p53^wt/wt (black line; n = 26), αv^wt/wt-p53^f/f (purple line; n = 16), αv^f/wt-p53^f/f (green line; n = 20), αv^f/f-p53^f/wt (blue line; n = 34), αv^f/f-p53^f/f (red line; n = 39). p< 0.05 for the following comparisons: αv^f/f-p53^f/f with each of the other groups; αv^f/f-p53^f/wt with αv^f/f-p53^wt/wt and αv^wt/wt-p53^f/f; αv^f/wt-p53^f/f with αv^f/f-p53^wt/wt. (b) Gross appearance of tumors that developed in the skin, mouth, anal epithelium and eyelid of αv^f/f-p53^f/f mice. (c–f) Hematoxylin and eosin staining of the primary phenotypes observed in SCCs that developed in αv^f/f-p53^f/f mice. (g) Quantification of the main phenotypic variants observed in SCCs that lacked both αv and p53 (αv⁻/p53⁻), only αv (αv⁻/p53⁺), or only p53 (αv⁺/p53⁻). (h) Graphical representation of the relative proportion of pseudoglandular/acantholytic SCCs and conventional SCCs in αv⁻/p53⁻, αv⁻/p53⁺, and αv⁺/p53⁻ tumors.