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The study demonstrated that ornithine decarboxylase (ODC) played a crucial role in the development of basal cell carcinomas (BCCs) in Ptch1+/– mice, which are predisposed to these tumors due to mutations in the PTCH gene. Overexpression of ODC in these mice accelerated BCC induction following UVB exposure, while inhibition of ODC through antizyme overexpression or oral administration of the ODC inhibitor α-difluoromethylornithine reduced BCC formation. These findings suggested that targeting ODC could be an effective chemopreventive strategy against BCCs in humans.

The study demonstrated that ornithine decarboxylase (ODC) played a crucial role in the development of basal cell carcinomas (BCCs) in Ptch1+/– mice, which are predisposed to these tumors due to mutations in the patched (PTCH) gene. Overexpression of ODC in these mice accelerated BCC induction following UVB exposure, while inhibition of ODC through antizyme (AZ) overexpression or the use of the ODC inhibitor α-difluoromethylornithine reduced BCC formation. These findings suggested that targeting ODC could be an effective chemopreventive strategy for reducing BCCs in humans.

The study developed a novel in vivo model using transgenic mice to evaluate agents that protect against UVA-induced photoaging. This model used a human elastin promoter linked to a CAT reporter gene to measure elastin gene induction. It showed that PUVA treatment significantly increased promoter activation, which was reduced by sunscreens, particularly those with SPF 15 and UVA filters. The combination sunscreen provided the greatest protection, reducing CAT activity to near baseline levels. This model proved effective for rapidly identifying and comparing compounds that protect against UVA-induced photoaging, despite differences between murine and human skin responses.

The study investigated the effects of dexamethasone (DXME) on mouse skin treated with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). DXME, when applied after TPA, inhibited both the dermal inflammatory reaction and the induction of epidermal ornithine decarboxylase (ODC) activity. During the hyperplastic stage, DXME continued to counteract inflammation but only weakly inhibited ODC induction. Interestingly, in DXME-protected skin, the hyperplastic stage was delayed, and TPA strongly induced ODC activity in the epidermal cell layer before this stage. The study suggested that as the proliferation process was induced, epidermal cells became more sensitive to TPA, potentially becoming less reliant on inflammatory factors for ODC induction.