Abstract
According to the WHO classification of skin tumours from 2006 actinic keratoses are very common intraepidermal neoplasm of sun-damaged skin with variable atypia of the epidermal keratinocytes. Main cause of these changes is chronical exposition to UVB light, but Aks are also observed following long term PUVA-treatments as well as exposure to arsenic.1 The actinic keratoses can be considered to represent early squamous cell carcinomas in situ,2,3 respectively possess a striking potential to progress to fully developed neoplasms.4 But only small portions of actinic keratoses will develop into an invasive squamous cell carcinoma. Regression of some cases of actinic keratoses have been reported, most likely as a result of immune mechanisms.5 Metastases after transformation of actinic keratoses into invasive squamous cell carcinomas are very rare except for those tumours that arise on the ear, lip, anus and vulva, which have been reported to be often associated with a more aggressive behaviour.6 It has been widely accepted, that actinic keratoses are a clinical manifestation of UV-induced neoplastic transformation of keratinocytes representing a continuum with progress to a fully developed squamous cell carcinomas.7 Cockerell observed the same cytological features of keratinocytic atypia in actinic keratoses than in epidermal or metastatic SCCs.8 Like current nomenclature of cervical intraepidermal neoplasia (CIN) Cockerell therefore recommends the use of the term “keratinocytic intraepidermal neoplasia” to illustrate the biological nature of these lesions.7
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Mueller, C.S.L., Reichrath, J. (2008). Histology of Melanoma and Nonmelanoma Skin Cancer. In: Reichrath, J. (eds) Sunlight, Vitamin D and Skin Cancer. Advances in Experimental Medicine and Biology, vol 624. Springer, New York, NY. https://doi.org/10.1007/978-0-387-77574-6_17
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DOI: https://doi.org/10.1007/978-0-387-77574-6_17
Publisher Name: Springer, New York, NY
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