Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Carcinogenesis; Light Cancer; Photocancer

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Ultraviolet radiation is the central carcinogen (see carcinogenesis) in the development of epithelial skin tumours. 60-100% of all basal and squamous cell carcinomas have mutations in the p53 gene (see tumour suppressor genes below). In parallel with this is the clinical observation that about 75-80% of basal cell carcinomas mostly occur in chronically sun-exposed skin areas, especially in the head and neck.

General information
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  • The effect of UV rays in the skin on the cell biological and molecular level is manifold (see oncogenes below). To prevent malignant transformation, various protective mechanisms have developed in the skin. The p53 protein (see tumor suppressor genes below) plays a key role in this process.
  • P53 checks the integrity of the DNA and is therefore also called the "guardian of the genome". In case of irreparable DNA damage, P53 triggers apoptosis, probably by inducing the synthesis of the apoptosis-promoting Bax protein. It therefore ensures the stability of the genome by switching off genetically modified cells and thus suppressing the formation of tumours.
  • UV-specific mutations in p53, Ras and INK4a/ARF as well as UV-inducible NF-kappaB and cyclooxygenase 2 (see below cyclooxygenases) are significantly involved in photocarcinogenesis.
  • Elevated COX-2 and PGE2 concentrations are detected in actinic keratoses and spinocellular carcinomas. COX inhibitors such as diclofenac have been shown to improve actinic keratoses.
  • In contrast to UVB, UVA (see below UV rays) is not directly absorbed by DNA, but by other photosensitizers. This leads indirectly to DNA damage via photooxidation and formation of oxygen radicals (ROS = reactive oxygen species).
  • A second mechanism for photocarcinogenesis is UV-induced immunosuppression. UV radiation inhibits the presentation of antigens and stimulates the release of immunosuppressive cytokines.

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Photocarcinogenesis plays a special role in various diseases. genodermatoses, such as the autosomal-recessive inherited Xeroderma pigmentosum.

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  1. Berking C (2007) Photocarcinogenesis. dermatologist 58: 398-405
  2. Diffey BL et al (1977) The anatomical distribution of sunlight. Br J Dermatol 97: 407-410
  3. Franceschi S et al (1996) Site distribution of different types of skin cancer: new aetiological clues. Int J Cancer 67: 24-28


Last updated on: 29.10.2020