Fig. 1From: Ablation of epidermal RXRα in cooperation with activated CDK4 and oncogenic NRAS generates spontaneous and acute neonatal UVB induced malignant metastatic melanomasMacroscopic and histological characterization of spontaneous and acute UVB induced melanomas from control and RXRαep−/−|TyrNRAS Q61K|Cdk4R24C/R24C mice. Mice with epidermal-specific Rxrα ablation in combination with Tyr-NRASQ61K and homozygous Cdk4R24C mutations have (a) spontaneous melanocytic growths; (b) larger melanocytic tumors with some degree of ulceration post single neonatal UVB treatment compared to mice with functional Rxrα. Lesions indicated by arrows. Histological analyses of melanocytic tumors from Tyr-NRASQ61K and Cdk4R24C mice and with functional (left panel) and ablated (right panel) Rxrα. Tyr-NRASQ61K /Cdk4R24C mice with epidermal-specific Rxrα ablation have (c) more pigmented lesions with minimal penetration into epidermal basal layer (inset); (d) greater degree of densely pigmented lesions with enhanced penetration into epidermal basal layer after acute neonatal UVB treatment. E, epidermis; D, dermis; HD, hypodermis. Scale bar =50 μm. e, f Increased epidermal thickness, and (g, h) higher radial growth phase (RGP) and vertical growth phase (VGP) of melanocytic tumors in RXRαep−/− |Tyr-NRASQ61K |Cdk4R24C/R24C mice with (e, g) no UVB treatment and (f, h) single UVB treatment relative to their respective controls. Statistical relevance indicated as follows; * = p < 0.05Back to article page