Pathobiology of actinic keratosis: Ultraviolet-dependent keratinocyte proliferation

Berman, Brian; Cockerell, Clay J.

doi:10.1016/j.jaad.2012.09.053

Cited by 124 publications

(144 citation statements)

References 62 publications

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“…[19][20] Therefore, the main mechanisms in the development of AK are inflammation, oxidative stress, immunosuppression, impaired apoptosis, mutagenesis, cell growth dis-regulation and proliferation, and tissue remodeling. 21 This knowledge is the basis of AK medical management. The AK's ability to regress or progress to SCC, it has been considered as premalignant, however many publications suggested as more appropriate its reclassification as "cancerous".…”

Section: Genetics and Histologymentioning

confidence: 99%

“…15 These ROSs affect the cellular transduction pathways and cell-cell signaling, causing altered proliferation. 16 Thymine (T) -guanine (G) is the signature mutation of UV-A, due to the formation of 8-hydroxyguanine adducts. UV-B (290-320 nm) radiation directly leads to the formation of cyclobutane pyrimidine dimers and 6-4 photoproducts, which in turn give rise to the characteristic cytosine (C) -T and CC -TT mutations.…”

Section: Genetics and Histologymentioning

confidence: 99%

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How to treat actinic keratosis? An update

Costa

Scalvenzi

Ayala

et al. 2015

J Dermatol Case Rep

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Actinic keratosis (AKs) is one of the most common skin lesions leading to an increased risk of developing squamous cell carcinoma and other skin malignancies. The lesions principally arise as a result of excessive ultraviolet (UV) exposure. AKs may regress spontaneously, remain stable or evolve to invasive squamous cell carcinoma. The risk of squamous cell carcinoma is significantly increased patients with more than 5 AKs. The main mechanisms involved in the formation of AK are inflammation, mutagenesis, oxidative stress, impaired apoptosis, immunosuppression, disregulation of cell growth and proliferation, and tissue remodeling. Human papilloma virus has also been correlated with the formation of some AKs. As an individual ages, his skin is exposed to increasing cumulative amounts of UV light and other environmental insults. This is especially true for the head, neck and forearms. These insults do not target only the skin where individual lesions develop, but also the surrounding area. In this area undetectable preclinical AK lesions or dysplastic cells may be present. The whole affected area is known as the 'field'. Therefore, management is divided into lesion-directed and field-directed therapies. Currently, the therapies in use are lesion-directed cryotherapy and/or excision, and field-directed topical agents: 5-fluorouracil, diclofenac, photodynamic therapy, imiquimod, and ingenol mebutate. Combining lesion-and field-directed therapies showed good results and several novel therapies are under investigation. Treatment is variable and personalized, what makes a gold standard management algorithm difficult to design. This review aims to describe the rationale behind the available treatment options for AKs based on current understanding of pathophysiology and epidemiology. (J Dermatol Case Rep. 2015; 9(2): 29-35)

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Section: Genetics and Histologymentioning

confidence: 99%

Section: Genetics and Histologymentioning

confidence: 99%

How to treat actinic keratosis? An update

Costa

Scalvenzi

Ayala

et al. 2015

J Dermatol Case Rep

View full text Add to dashboard Cite

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“…The main etiological factor for SCC development remains cumulative UVB radiation exposure, which induces mutagenic DNA photoproducts (4). Long-term immunosuppression impairs repair of mutagenic photoproducts and accelerates UV-induced carcinogenesis, which typically progress from premalignant actinic keratosis to SCC (5).…”

Section: Introductionmentioning

confidence: 99%

Primary Prevention of Skin Dysplasia in Renal Transplant Recipients With Photodynamic Therapy: A Randomized Controlled Trial

Togsverd‐Bo

Omland

Wulf

et al. 2015

American Journal of Transplantation

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Organ transplant recipients (OTRs) are at high risk of developing cutaneous squamous cell carcinoma (SCC); prevention includes early treatment of premalignant actinic keratosis (AK). Photodynamic therapy (PDT) is a noninvasive field therapy that reduces new AKs in patients with existing AK and delays SCC development in mice. We investigated the effect of repeated PDT over 5 years for primary prophylaxis of skin dysplasia. These data represent an interim analysis of an on-going randomized controlled trial. During 2008-2011, 25 renal transplant recipients with clinically normal skin were randomized to split-side PDT of the face, forearm and hand, the contralateral side serving as untreated control. Patients received PDT on inclusion and at 6-monthly intervals for 5 years. Blinded evaluation was performed at each visit. We found that prophylactic PDT significantly delayed onset of AK compared with untreated skin, p ¼ 0.020. At 3-year follow-up, we observed AK in 63% of patients in untreated skin areas compared with 28% of patients in PDT-treated skin, with a total number of cumulated AKs in untreated skin (n ¼ 43) compared with PDT-treated skin (n ¼ 8), p ¼ 0.005. These preliminary data indicate a novel approach to early prevention of skin dysplasia that may reduce morbidity from multiple AKs and SCCs in OTR.

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“…In 2011, AK accounted for 8.3% of the 100 most frequently treated dermatological outpatient diagnoses in Germany, with the proportion of AK cases rising almost continuously over the last 10 years compared to other dermatological conditions [4]. Chronic long-term sun exposure is the major risk factor for AK [5]. In Germany, the medical consultation board of ‘occupational diseases' of the Ministry of Labor and Social affairs has investigated the association between occupational UV irradiation and skin cancer risk.…”

Section: Introductionmentioning

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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Pathobiology of actinic keratosis: Ultraviolet-dependent keratinocyte proliferation

Cited by 124 publications

References 62 publications

How to treat actinic keratosis? An update

How to treat actinic keratosis? An update

Primary Prevention of Skin Dysplasia in Renal Transplant Recipients With Photodynamic Therapy: A Randomized Controlled Trial

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

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