Guest Editors
Dr. Emmanouil Karampinis
Email: ekarampinis@uth.gr
Affiliation: 1. Second Dermatology Department, School of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, 54124, Greece
2. Department of Dermatology, Faculty of Medicine, School of Health Sciences, University General Hospital of Larissa, University of Thessaly, Larissa, 41110, Greece
Homepage:
Research Interests: Skin Cancer, Dermoscopy, Artificial Intelligence, Psoriasis, skin of colour, Pediatric dermatology, Oxidative stress
Prof. Dr. Dimitrios Sgouros
Email: disgo79@gmail.com
Affiliation: Department of Dermatology and Venereology, "Attikon" General University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, 12462, Greece
Homepage:
Research Interests: Dermoscopy, Adnexal tumors, NMSC, Melanoma, pediatric dermatology, Nail and Hair diseases
Summary
This special issue provides a comprehensive overview of the multiple pathways that lead to skin cancer development besides cumulative photo-exposure. It highlights that skin carcinogenesis is a multifactorial process involving both ultraviolet (UV)induced mechanisms and nonUVrelated pathways.
UV radiations and especially UVB, undoubtedly is the most common skin cancer carcinogen that directly damages DNA by generating photoproducts. If unrepaired, these lesions cause characteristic mutations in critical genes that initiate tumorigenesis. The genetic mutations combined with cutaneous oxidative stress, inflammation and cutaneous immunosuppression create cutaneous tumor-promoting conditions that would finally lead to tumor formation, promotion, and progression.
The issue also discusses nonUV pathways. Systemic immunosuppression is an important risk of skin carcinogenesis as Individuals with compromised immune systems as organ transplant recipients receiving immunosuppressive therapy, show dramatically increased rates of skin cancer. Environmental and occupational chemical exposure such as polycyclic aromatic hydrocarbons have also been categorized as skin cancer risk factors and they act synergically with UV. Genetic predispositions as well as chronic inflammatory states (chronic wounds etc.), and infections (HPV etc.) can trigger similar mutagenic processes and complete further the puzzle of skin carcinogenesis.
We encourage submissions that integrate molecular, epidemiological, and clinical findings to provide a holistic view of UV and nonUVmediated skin carcinogenesis. Your contributions will help broaden our understanding of skin cancer etiology and pave the way for new strategies in prevention and treatment.
Keywords
skin carcinogenesis, UV-induced DNA damage, non-UV pathways, photocarcinogenesis, oxidative stress, cutaneous immunosuppression, systemic immunosuppression, genetic predisposition, environmental carcinogens, chronic inflammation, HPV infection, tumor promotion and progression, skin cancer risk factors
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