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Summary Basal cell carcinoma is the most common tumor in Central Europe, the U.S. and Australia. The increasing incidence of basal cell carcinoma presents the health care system, especially dermatology, with great challenges. In recent years new options for treating basal cell carcinoma have become available, enriching our therapeutic options. We review the current status of each of these treatment approaches.

Focal epithelial hyperplasia (FEH) or Heck disease is a rare skin disease caused by human papilloma viruses (HPV). The case of a 9-year old boy is presented to demonstrate the successful treatment of massive FEH with 5% imiquimod cream. Initially, the patient had noticed several separate papules, which spread and developed into multiple peri- and intraoral papillomatous nodules. The lesions were treated with carbon dioxide laser destruction. However, multiple, skin-coloured papillomatous nodules were found on the tongue, buccal mucosa and lips 1.5 years later. Treatment with imiquimod was initiated, because the patient suffered tremendously from the disease. 5 % imiquimod cream was applied 3 times per week. Regression of lesions was obvious after 1 month of treatment. Complete clearance was achieved after 2 additional months of treatment and no recurrence was detected over a follow-up period of 5 months. Our case points out the clinical value of imiquimod for the non-traumatic and almost painless therapy of HPV-induced skin diseases in children.

Background: Mutations of the stem cell factor receptor C-KIT play a major pathogenetic role in the development of different malignant diseases like human mastocytosis, myeloproliferative disorders, gastrointestinal stromal tumors, acute myelogenous leukemia, and sinonasal lymphomas. Furthermore, the expression of C-KIT has been described in Hodgkin's disease and nodal CD30+ anaplastic large cell lymphomas (ALCLs). As it is possible to inhibit C-KIT by innovative kinase inhibitors like STI571, it may be an attractive target for new therapeutical approaches. Therefore, we screened more than 50 different types of cutaneous T-cell lymphomas (TCLs) for the presence of C-KIT. Immunohistochemical stainings were performed on paraffin-embedded tissue sections using a polyclonal rabbit anti-human C-KIT antibody. Naphtol-ASD-chloroacetate esterase (NASDCE)-control stainings were performed on every positive sample to distinguish C-KIT-positive lymphoma cells from C-KIT-positive mast cells. Results: We found weak expression of C-KIT in seven of 18 patients with primary cutaneous CD30+ ALCL, two of eight patients with primary cutaneous pleomorphic TCL, six of 18 patients suffering from mycosis fungoides, and three of five patients with Sezary's syndrome. Generally, only a very small population of the lymphoma cells expressed C-KIT. This finding indicates a difference to the systemic variant of CD30+ ALCL. The potential use of C-KIT targeting new therapeutical approaches is therefore discussed critically, because C-KIT expression is very rare in all investigated types of primary cutaneous lymphoma.