Summary Actinic keratoses (AKs) are common lesions in light‐skinned individuals that can potentially progress to cutaneous squamous cell carcinoma (cSCC). Both conditions may be associated with significant morbidity and constitute a major disease burden, especially among the elderly. To establish an evidence‐based framework for clinical decision making, the guidelines for actinic keratosis and cutaneous squamous cell carcinoma were developed using the highest level of methodology (S3) according to regulations issued by the Association of Scientific Medical Societies in Germany (AWMF). The guidelines are aimed at dermatologists, general practitioners, ENT specialists, surgeons, oncologists, radiologists and radiation oncologists in hospitals and office‐based settings as well as other medical specialties involved in the diagnosis and treatment of patients with AKs and cSCC. The guidelines are also aimed at affected patients, their relatives, policy makers and insurance funds. In the second part, we will address aspects relating to epidemiology, etiology, surgical and systemic treatment of cSCC, follow‐up and disease prevention, and discuss AKs and cSCC in the context of occupational disease regulations.

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UVA (320–400 nm) represents the main spectral component of solar UV radiation, induces pre-mutagenic DNA lesions and is classified as Class I carcinogen. Recently, discussion arose whether UVA induces DNA double-strand breaks (dsbs). Only few reports link the induction of dsbs to UVA exposure and the underlying mechanisms are poorly understood. Using the Comet-assay and γH2AX as markers for dsb formation, we demonstrate the dose-dependent dsb induction by UVA in G1-synchronized human keratinocytes (HaCaT) and primary human skin fibroblasts. The number of γH2AX foci increases when a UVA dose is applied in fractions (split dose), with a 2-h recovery period between fractions. The presence of the anti-oxidant Naringin reduces dsb formation significantly. Using an FPG-modified Comet-assay as well as warm and cold repair incubation, we show that dsbs arise partially during repair of bi-stranded, oxidative, clustered DNA lesions. We also demonstrate that on stretched chromatin fibres, 8-oxo-G and abasic sites occur in clusters. This suggests a replication-independent formation of UVA-induced dsbs through clustered single-strand breaks via locally generated reactive oxygen species. Since UVA is the main component of solar UV exposure and is used for artificial UV exposure, our results shine new light on the aetiology of skin cancer.

In Europe, little is known about the prevalence of indoor tanning. The aims of this study were therefore to estimate the prevalence of sunbed use and to identify risk groups and motives in a population-based survey. The cross-sectional "SUN-Study 2008" ("Sunbed-Use: Needs for Action-Study 2008") was conducted in 2008. A total of 500 adults, aged 18-45 years, were randomly selected and asked about their indoor tanning practices, their motivation and risk perception, and the compliance of staff with international sunbed use recommendations. Forty-seven percent of subjects reported having visited an indoor tanning facility at least once in their lives. Prevalence of use was not reduced in risk groups for skin cancer. Risk awareness of users equalled that of non-users. The poor quality of services and advice provided by many solariums was alarming. It can be concluded that appropriate measures to change tanning habits need to be identified. Legal regulations could be one option.

Background: Ultrasonography with 20 MHz frequency can be used to estimate tumour thickness preoperatively in malignant melanoma (MM) of the skin. The vertical invasion depth is the single most important prognostic factor for localised MM, and its preoperative knowledge would be very useful for the planning of surgical procedures. Since ultrasonographic distance measurements directly depend upon the tissue specific ultrasound velocity, we determined the ultrasound velocity in primary melanoma.