The effect of solar ultraviolet radiation (UVR) on induction of skin cancers
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Uniwersytet Medyczny w Łodzi / Medical University of Lodz, Łódź, Poland (Katedra Nauk Podstawowych, Zakład Biologii i Genetyki Medycznej / Chair of Basic Sciences, Department of Biology and Medical Genetics)
Wyższa Szkoła Informatyki i Umiejętności w Łodzi / University of Computer Science and Skills in Lodz, Łódź, Poland (Wydział Pedagogiki i Promocji Zdrowia, Fizjoterapia / Faculty of Pedagogy and Health Promotion, Physiotherapy)
Marta Pacholczyk   

Uniwersytet Medyczny w Łodzi, Katedra Nauk Podstawowych, Zakład Biologii i Genetyki Medycznej, pl. Hallera 1, 90-647 Łódź
Med Pr 2016;67(2):255–266
Ultraviolet radiation is a physical mutagenic and cancerogenic factor. About 95% of ultraviolet A (UVA) (320–400 nm) and 5% of UVB (280–320 nm) reach the Earth’s surface. Melanin is a natural skin protective factor against UV radiation. Skin cancers associated with long-term exposure to UV radiation are: basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and cutaneous malignant melanoma (CMM). The high risk of BCC development is related to acute and repeated exposure to UV causing sunburn. Molecular studies of BBC demonstrated disorders in sonic hedgehog (SHH) cell signaling regulation pathway, associated with the suppressor protein patched homolog 1 gene (PTCH1) mutations. The risk of the BCC development is related to the polymorphism of melanokortin-1 receptor gene (MC1R). Tumor P53 gene mutations observed in BCC cells has been classified as secondary genetic changes. In SCC cells UV-induced mutations were mostly related to P53 gene. Increased expression of cyclooxigenase- 2 gene (COX-2) plays a significant role in the development of SCC. Other pathogenetic factors include intensification of the synthesis of pro-inflammatory cytokines (tumor necrosis factor α (TNF-α), interleukin-1 α (IL-1α), IL-1β and IL-6). Currently, the role of UVB has been recognized in the pathogenesis of CMM. In CMM cells the following gene mutations were noted: cyclindependent kinase inhibitor 2A INK4A (p16INK4A), cyclin-dependent kinase 4 (CDK4), Ras, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and proto-oncogene B-Raf (BRAF). The BRAF gene mutations were observed in ~50% of CMM cases. Mutations of P53 gene are not characteristic of CMM cells. Med Pr 2016;67(2):255–266