Infrared radiation does not enhance the frequency of ultraviolet radiation-induced skin tumors, but their growth behaviour in mice

• Published in: Experimental dermatology Vol. 20; no. 4; pp. 346 - 350
• Main Authors: Jantschitsch, Christian, Weichenthal, Michael, Maeda, Akira, Proksch, Ehrhardt, Schwarz, Thomas, Schwarz, Agatha
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.04.2011; Blackwell
• Subjects: Animals; Biological and medical sciences; carcinogenesis; Carcinoma, Squamous Cell - etiology; Carcinoma, Squamous Cell - pathology; Cell Proliferation; Cell Transformation, Neoplastic - radiation effects; Dermatology; DNA Damage; Female; Genes, p53 - genetics; infrared radiation; Infrared Rays - adverse effects; Kaplan-Meier Estimate; Ki-67 Antigen - metabolism; Medical sciences; Mice; Mice, Inbred C57BL; Mutation; Neoplasms, Radiation-Induced - etiology; Neoplasms, Radiation-Induced - pathology; Sarcoma - etiology; Sarcoma - pathology; Skin Neoplasms - etiology; Skin Neoplasms - pathology; Sunlight - adverse effects; Tumor Cells, Cultured; ultraviolet radiation; Ultraviolet Rays - adverse effects; Vertebrata; Ultraviolet radiation; Mammalia; Mouse; Dermatology; Animal; Rodentia; Skin; infrared radiation; Malignant tumor; Carcinogenesis; Cancer
• ISSN: 0906-6705; 1600-0625
• DOI: 10.1111/j.1600-0625.2011.01257.x

:  There is increasing concern about the interaction between infrared radiation (IR) and ultraviolet radiation (UVR) with regard to carcinogenesis because prolonged solar exposure is associated with an increased cumulative load not only of UVR but also of IR. We recently demonstrated that IR‐pretreatment reduces UVR‐induced apoptosis. As this might support the survival of UVR‐damaged cells and thus carcinogenesis, we performed an in vivo photocarcinogenesis study. One group of mice were treated with IR prior to each UVR exposure; additional groups were treated with IR or UVR alone. IR alone did not induce skin cancer. UVR‐induced tumor formation was not enhanced in IR‐pretreated mice, but, in contrast, seemed to occur with delay. This correlated with a reduction of p53 mutated clones in the skin. However, once developed, tumors in IR‐pretreated mice grew faster which was confirmed by their enhanced Ki‐67 expression. The enhanced aggressiveness of tumors derived from IR‐pretreated mice was associated with a higher prevalence of sarcomas than epithelial tumors. Hence, the impact of IR on UVR‐induced carcinogenesis has to be interpreted with caution. Although IR may delay the onset of UVR‐induced tumors, it might contribute to a worse outcome by shifting these tumors into a more aggressive phenotype.