An inducible mouse model for skin cancer reveals distinct roles for gain- and loss-of-function p53 mutations
J. Clin. Invest. Carlos Caulin, et al. 117:1893 doi:10.1172/JCI31721 [Go to this article.]

Figure 1
K-ras activation initiates skin tumor formation. (A) Gross appearance of the epidermal papillomas that developed in the skin of RU486-treated K5Cre*-Ras mice 16 weeks after exposure to TPA. (B) Schematic representation of the LSL–K-ras^G12D allele. The glycine–to–aspartic acid mutation (asterisk) in codon 12 is located in exon 1 (E1). Primers 1 and 2 (P1 and P2) were used for analysis of excision of the stop cassette. (C) Activation of the K-ras^G12D allele in the skin (lanes 1 and 2) and papillomas (lanes 3, 4, and 5) of K5Cre*-Ras mice. Note that the K-ras^G12D allele is only activated in RU486-treated skin (lane 2), but not in untreated mice (lane 1). (D) Hematoxylin and eosin staining of papillomas that developed in K5Cre*-Ras mice. (E and F) Keratin staining in papillomas: double immunofluorescence for K14 (red) and K13 (green) (E) and K14 (red) and K6 (green) (F) on frozen sections obtained from papillomas that developed in K5Cre*-Ras mice. Original magnification, ×40 (D), ×100 (E and F).