• after RU486 and TPA treatment, 30% of mice develop skin carcinomas compared to 5% of Kras^tm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

• following treatment with RU486 and TPA, mice develop more tumors than in Kras^tm4Tyj Trp53^tm1Brn/ Trp53^tm1Brn Tg(KRT5-cre/PGR)1Der mice

• following treatment with RU486 and TPA, conversion to malignant carcinoma is accelerated relative to in Kras^tm4Tyj Trp53^tm1Brn/ Trp53^tm1Brn Tg(KRT5-cre/PGR)1Der mice

• after RU486 and TPA treatment, 60% of tumors that develop are spindle cell carcinomas

• following treatment with RU486 and TPA, mice develop more tumors than in Kras^tm4Tyj Trp53^tm1Brn/ Trp53^tm1Brn Tg(KRT5-cre/PGR)1Der mice

• following treatment with RU486 and TPA, mice develop less tumors than in Kras^tm4Tyj Trp53^tm1Brn/Trp53^tm3Glo Tg(KRT5-cre/PGR)1Der mice

• after RU486 and TPA treatment, carcinomas that develop following treatment with RU486 and TPA are squamous cell carcinomas with abundant keratin pearls and an absence of spindle cells

• following treatment with RU486 and TPA, mice develop less tumors than in Kras^tm4Tyj Trp53^tm1Brn/Trp53^tm3Glo Tg(KRT5-cre/PGR)1Der mice

• 7 to 10 weeks after treatment with RU486 to activate the cre transgene, mice develop epidermal papillomas

• 7 to 10 weeks after treatment with RU486 to activate the cre transgene, mice develop epidermal papillomas

• after RU486 and TPA treatment, mice develop three-fold more tumors than Kras^tm4Tyj Trp53^tm1Brn heterozygotes and Kras^tm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

• after RU486 and TPA treatment, 60% of mice develop metastasis in the lungs and/or lymph nodes compared to no wild-type mice

• after RU486 and TPA treatment, 42% of tumors exhibit aneuplody compared to 23% of Kras^tm4Tyj Trp53^tm1Brn heterozygotes and 20% of Kras^tm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

• after RU486 and TPA treatment, tumors exhibit centrosome amplification in 3% to 5% of tumors cells

• after RU486 and TPA treatment, carcinoma development is accelerated compared to in Kras^tm4Tyj Trp53^tm1Brn heterozygotes and Kras^tm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

• after RU486 and TPA treatment, 90% of mice develop skin carcinomas compared to 30% of Kras^tm4Tyj Trp53^tm1Brn heterozygotes and 5% of Kras^tm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

• after RU486 and TPA treatment, mice develop three-fold more tumors than Kras^tm4Tyj Trp53^tm1Brn heterozygotes and Kras^tm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

• at 2 to 3 months of age

• at 2 to 3 months of age, mice exhibit a roughening of the epidermis

• cells are larger than in wild-type mice and display a senescence phenotype

• following treatment with mifepristonein in utero, mice exhibit an increase in cellular senescence

• at E17.5 following treatment with mifepristonein in utero

• at E17.5 following treatment with mifepristonein in utero

• following treatment with mifepristonein at 8 months of age

• following treatment with mifepristonein at 8 months of age, mice exhibit lordokyphosis that increases with severity as mouse ages

• following treatment with mifepristonein at 8 months of age, mice exhibit severe alopecia

• at E17.5 following treatment with mifepristonein in utero or at 8 months of age

• following treatment with mifepristonein utero, mice exhibit stratified epidermal layer and arrested epidermal morphogenesis

• after application of a topical antiprogestin, RU486, to the forelimbs and chest of newborn pups so that the cre transgene translocates from the cytoplasm to the nucleus of epidermal cells and becomes active, mice developed blisters filled with fluid on the front legs and paws

• blistering occurs within the basal layer of the epidermis