Skin cancer

Malignant melanoma 466 Non-melanoma skin cancer 468 • Malignant melanomas arise from melanocytes, mainly found in the basal layer of skin. These cells produce melanin and are responsible for the tanning response after exposure to ultraviolet (UV) radiation. • A few melanocytes exist elsewhere in the body—this explains the rare melanomas that can occur elsewhere, e.g. intracocular, oesophageal....

2003 ◽  
Vol 148 (5) ◽  
pp. 913-922 ◽  
Author(s):  
C.S. Sander ◽  
F. Hamm ◽  
P. Elsner ◽  
J.J. Thiele

2015 ◽  
Vol 135 (3) ◽  
pp. 901-904 ◽  
Author(s):  
Camilla Præstegaard ◽  
Susanne K. Kjær ◽  
Jane Christensen ◽  
Anne Tjønneland ◽  
Jytte Halkjær ◽  
...  

2018 ◽  
Vol 73 (5) ◽  
pp. 306-313
Author(s):  
Marianna B. Zhilova ◽  
Maria M. Butareva

The review presents modern data on the role of ultraviolet (UV) radiation in the pathogenesis of non-melanoma skin cancer (NMSC), the problem of THE risk of developing NMSC, in particular, squamous cell and basal cell skin cancer both in the population and in long-term repeated irradiation of phototherapy (PUVA therapy, UVB therapy, UVB-311 therapy) in patients with psoriasis. The paper considers the mechanisms of UV-induced cell damage by different spectral ranges (UVA, UVB) including the formation of photoproducts, damage to genomic DNA and other cellular structures, violation of the regulation of signaling pathways, the development of chronic inflammation, secondary immunosuppression. The review summarizes the results of large epidemiological studies discussing the role of gene polymorphisms in the homologous DNA repair XRCC3, gene telomerase TERT-CLPTMI, cytokine IL10 gene, MTHFR gene, encoding the folate synthesis, genes involved in pigmentirovanie MC1R, EXOC2, UBAC2 in the modulation of risk of carcinogenic effect of UV radiation. According to the authors’ opinion, the most vital and significant is data on the role of vitamin D receptor (VDR) gene polymorphisms as possible predictors of the risk of NMSC development. The further prospects of academic research on the cumulative role of the genome and environmental factors in the risk assessment of NMSC are revealed.


Author(s):  
Heidi Allen

This chapter focuses on the management of skin cancer, exploring both malignant melanoma and non-melanoma skin cancer. The epidemiology of melanoma is covered, and risk factors are described. Management looks at both early-stage and widespread disease, including surgery, adjuvant drug therapy, and radiotherapy. There is further emphasis on recent developments in biological and immunotherapy treatments such as ipilimumab and nivolumab. Non-melanoma skin cancer is discussed, covering risk factors and presentation of these diseases and a summary of their management.


2016 ◽  
Vol 17 (3) ◽  
pp. 389-403 ◽  
Author(s):  
K. Karimi ◽  
T. H. Lindgren ◽  
C. A. Koch ◽  
Robert T. Brodell

2007 ◽  
Vol 23 (4) ◽  
pp. 247-259 ◽  
Author(s):  
Ingo Nindl ◽  
Marc Gottschling ◽  
Eggert Stockfleth

Human papillomaviruses (HPV) infect cutaneous and mucosal epithelia and induce benign and malignant lesions. Non-melanoma skin cancer (NMSC), encompassing basal cell carcinoma and squamous cell carcinoma (SCC), is the most frequent cancer in the Caucasian population, and the incidence has increased dramatically worldwide. Ultraviolet (UV) radiation is a major risk factor for NMSC, and cutaneous HPV is also considered to play an active role during the pathogenesis of these cancers. The first evidence for the involvement of HPV in NMSC was reported in patients with Epidermodysplasia verruciformis (EV). HPV types detected in skin tumours of these patients are referred to as EV/cutaneous HPV types belonging to the beta- and gamma-papillomaviruses (PV). Epidemiological studies have shown a higher risk of several EV/cutaneous HPV types for NMSC. Furthermore,in vitroand animal models show transforming properties of some PV types. The anti-apoptotic activities, and the delay of DNA repair mechanism caused by some EV/cutaneous HPV E6 proteins in response to UV-induced mutations, may lead to the persistence of DNA-damaged keratinocytes. Thus, specific EV/cutaneous HPV types as co-factors in association with UV-radiation and the immune system seem to be involved in the early pathogenesis of cutaneous SCC.


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