Actinic Keratosis: The Key Event in the Evolution from Photoaged Skin to Squamous Cell Carcinoma

Oppel, Tilmann; Körting, Hans Christian

doi:10.1159/000076016

Cited by 42 publications

(33 citation statements)

References 158 publications

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“…The onset of such benign papillomas in mice is analogous to the appearance of actinic keratosis (AK) in human skin. AKs are thought to be the key event in the evolution from photo-aged skin to SCC (33). Similar to skin papilloma formation in mice, the causative factor of AKs is believed to be chronic/long-term UVR exposure.…”

Section: Introductionmentioning

confidence: 99%

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

Dixon

Norman

Sequeira

et al. 2011

Cancer Prevention Research

106

153

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Exposure to ultraviolet radiation (UVR) can lead to a range of deleterious responses in the skin. An important form of damage is the DNA photolesion cyclobutane pyrimidine dimer (CPD). CPDs can be highly mutagenic if not repaired prior to cell division and can lead to UV-induced immunosuppression, making them potentially carcinogenic. UVR exposure also produces vitamin D, a prehormone. Different shapes of the steroid hormone 1a,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] can produce biological responses through binding either to its cognate nuclear receptor (VDR) to regulate gene transcription or to the VDR associated with plasma membrane caveolae to produce, via signal transduction, nongenomic physiologic responses. Here, we show that both 1,25(OH) 2 D 3 and 1a,25(OH) 2 -lumisterol (JN), a conformationally restricted analogue that can generate only nongenomic responses, are effective inhibitors of UV damage in an immunocompetent mouse (Skh:hr1) model susceptible to UV-induced tumors. Both 1,25(OH) 2 D 3 and JN significantly reduced UVR-induced CPD, apoptotic sunburn cells, and immunosuppression. Furthermore, these compounds inhibited skin tumor development, both papillomas and squamous cell carcinomas, in these mice. The observed reduction of these UV-induced effects by 1,25 (OH) 2 D 3 and JN suggests a role for these compounds in prevention against skin carcinogenesis. To the best of our knowledge, this is the first comprehensive report of an in vivo long-term biological response generated by chronic dosing with a nongenomic-selective vitamin D steroid.

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Section: Introductionmentioning

confidence: 99%

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

Dixon

Norman

Sequeira

et al. 2011

Cancer Prevention Research

106

153

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“…No questionnaire exists to compare our results. In the literature, there is no evidence on the strength of the characteristics; it is limited to observations and descriptions of AK [11,12,13,14]. Additional characteristics were provided by (only) four physicians (dermatologists or residents) of the dermato-oncology unit, and there might be more.…”

Section: Discussionmentioning

confidence: 99%

“…20 patient- and clinical lesion-related characteristics were obtained from the literature (table 1) [11,12,13,14]. In addition, one dermatologist and three residents of dermatology were interviewed at the dermato-oncology unit of the Catharina Hospital Eindhoven.…”

Section: Methodsmentioning

confidence: 99%

Development of a Non-Melanoma Skin Cancer Detection Model

et al. 2015

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Background: The incidence and prevalence of skin cancer is rising. A detection model could support the (screening) process of diagnosing non-melanoma skin cancer. Methods: A questionnaire was developed containing potential actinic keratosis (AK) and basal cell carcinoma (BCC) characteristics. Three nurses diagnosed 204 patients with a lesion suspicious of skin (pre)malignancy and filled in the questionnaire. Logistic regression analyses generated prediction models for AK and BCC. Results: A prediction model containing nine characteristics correctly predicted the presence or absence of AK in 83.2% of the cases. BCC was predicted correctly in 91.4% of the cases by a model containing eight characteristics. The nurses correctly diagnosed AK in 88.3% and BCC in 90.9% of the cases. Conclusions: Detection or screening models for AK and BCC could be made with a limited number of variables. Nurses also diagnosed skin lesions correctly in a high percentage of cases. Further research is necessary to investigate the robustness of these findings, whether the percentage of correct diagnoses can be improved and how best to implement model-based prediction in the diagnostic process.

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“…Actinically damaged skin has an accumulation of oncogenic mutations leading to a proliferation of atypical keratinocytes that may manifest as AK or SCC [8]. Underlying molecular changes in normal-appearing skin, detectable by histology or immunohistochemistry, are present before any clinical changes can be observed.…”

Section: Molecular Events In Ak Initiation and Ak-to-scc Progressionmentioning

confidence: 99%

New Strategies in the Prevention of Actinic Keratosis: A Critical Review

Krutmann

Berking

Berneburg

et al. 2015

Skin Pharmacol Physiol

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Actinic keratosis (AK) or lesions of epidermal dysplasia occurring in skin chronically exposed to solar radiation is very prevalent in lighter skin persons, with chronic long-term sun exposure being the major risk factor. With an aging population it is expected that the prevalence of AK will further increase. AK can progress to nonmelanoma skin cancer (NMSC) and is a public health concern. Six leading dermatologists with expertise in AK and NMSC from Germany met to discuss the nature of the disease and the prevention and treatment strategies available to dermatologists today. While cosmetic sunscreen products form an essential element of sun protection strategies, they are not adequate when damage has already been inflicted. Newly developed products of the medical device category offer DNA repair function paired with high sun protection factor (SPF) UV protection. An adjuvant treatment algorithm for various risk levels of AK was developed. For patients with low and moderate risk, sunscreen only is recommended. For patient groups with high and very high risk, a very high photoprotection and photorepair action (DNA repair enzymes) in medical device products all year round is recommended.

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Actinic Keratosis: The Key Event in the Evolution from Photoaged Skin to Squamous Cell Carcinoma

Cited by 42 publications

References 158 publications

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

1α,25(OH)2-Vitamin D and a Nongenomic Vitamin D Analogue Inhibit Ultraviolet Radiation–Induced Skin Carcinogenesis

Development of a Non-Melanoma Skin Cancer Detection Model

New Strategies in the Prevention of Actinic Keratosis: A Critical Review

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