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. 2022 May 9;9:875517. doi: 10.3389/fmed.2022.875517

FIGURE 5.

FIGURE 5

Carcinogen-induced models of cSCC. Schematic representation of the protocols used for (A) Two-stage DMBA/TPA mouse skin carcinogenesis model. DMBA treatment (pink arrows), TPA treatment (green arrows). Typically, a single DMBA treatment (week 1) is followed by sustained TPA treatments up to 20 weeks. From 21 to 52 weeks a follow up of the animals will evaluate tumor formation; (B) UVR-induced mouse skin carcinogenesis model: hairless immunocompetent SKH-1 mice undergo UVR exposure, which typically induces Trp53 mutation. cSCC formation depends on dose and time of exposure. (C) Example of genetically engineered mouse (GEM) models of cSCC. Upper panel: p53 Flox mice and oncogenic HRAS or KRAS expressing mice are mated with transgenic conditional keratinocyte Cre recombinase expressing mice. Cre expression is constitutive under control of a keratin promoter. The offspring with loss of p53 or oncogenic HRAS and KRAS expression spontaneously develop papilloma or cSCC.; lower panel: mating scheme and tumor formation works as described for the upper panel. However, Cre protein is fused with the estrogen receptor (ER), generating a CreERT protein that works only after tamoxifen treatment.