Merkel cell carcinoma (MCC), an aggressive neuroendocrine carcinoma of the skin, is to date the only human cancer known to be frequently caused by a polyomavirus. However, it is a matter of debate which cells are targeted by the Merkel cell polyomavirus (MCPyV) to give rise to the phenotypically multifaceted MCC cells. To assess the lineage of origin of MCPyV-positive MCC, genetic analysis of a very rare tumor combining benign trichoblastoma and MCPyV-positive MCC was conducted by massive parallel sequencing. Although MCPyV was found to be integrated only in the MCC part, six somatic mutations were shared by both tumor components. The mutational overlap between the trichoblastoma and MCPyV-positive MCC parts of the combined tumor implies that MCPyV integration occurred in an epithelial tumor cell before MCC development. Therefore, our report demonstrates that MCPyV-positive MCC can derive from the epithelial lineage.

Background Mycetoma is a chronic granulomatous subcutaneous infection caused by anaerobic pseudofilamentous bacteria or fungi. It is commonly prevalent in tropical and subtropical countries. Men are more susceptible to the disease due to greater participation in agricultural works. Mycetoma commonly involves lower extremities, wherein untreated cases lead to aggressive therapeutic choices, such as amputation of the affected body organs and consequently lifelong disability. Case presentation In this report, we present the rare case of a 58-year-old man, originally from Algeria with a left foot chronic tumefaction of 5 years. In the initial clinical examination, mycetoma was diagnosed based on tumefaction and the presence of multiple sinuses with the emission of white grains. The latter was observed via direct examination. The histopathological analysis demonstrated an actinomycetoma caused by bacteria, as the etiological agent. Imaging showed a bone involvement with osteolysis at the levels of 2nd to 4th metatarsal diaphysis. The mycological and bacterial cultures were both negative. For an accurate diagnosis, the obtained grains were subjected to molecular analysis, targeting the 16S-rDNA gene. Molecular identification yielded Actinomadura madurae as the causal agent, and 800/160 mg of trimethoprim/sulfamethoxazole was prescribed twice a day for 1 year, as a treatment. Conclusion Considering low information about this disease, especially in non-endemic areas, it is of high importance to enhance the knowledge and awareness of clinicians and healthcare providers, in particular in the countries with immigration issues.

Medicopsis romeroi phaeohyphomycosis is increasingly reported in immunocompromised patients living in or originating from tropical and subtropical areas. We report a case of subcutaneous phaeohyphomycosis caused by M. romeroi in a 56-year-old Malian woman residing in France for 20 years. She developed a small nodule on her dominant hand’s ring finger 15 months after starting immunosuppressive medications for paraneoplastic dermatomyositis. A first surgical debridement was followed by a local recurrence. Despite a second surgical excision combined with posaconazole treatment, the infection recurred one year after antifungal therapy discontinuation. A wide excision was performed again, and antifungal therapy was resumed and maintained for six months, resulting in the absence of relapse during the 18 months following the surgery. This case highlighted the high risk of relapse in immunocompromised patients, suggesting the need for long-term follow-up and prolonged antifungal treatment following surgical excision in cases with sustained immunosuppression. The literature review was performed according to PRISMA guidelines and included 51 scientific publications. A noteworthy predominance of the subcutaneous phaeohyphomycosis presentation was found in immunocompromised patients, whereas eumycetoma had been reported in apparently healthy individuals. A combination of complete excision with antifungal treatment seemed to confer the best outcome.

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Nierenzellkarzinom Multimodale Therapie im 21. JahrhundertDie Behandlung des Nierenzellkarzinoms ist in den letzten Jahren deutlich facettenreicher geworden. Neben der radikalen Nephrektomie stellen organerhaltende und laparoskopische Operationen Standardverfahren dar. In der Systemtherapie stehen seit 2006 neben der Immuntherapie zwei potente Breitspektrum-KinaseInhibitoren ("multi-target tyrosine kinase inhibitors", MTKI) zur Verfügung. Weitere molekulare Substanzen drängen in die Klinik. In fortgeschrittenen Stadien profitieren Patienten darüber hinaus von lokaltherapeutischen und palliativ-chirurgischen Maßnahmen. Der Stellenwert einzelner Modalitäten untereinander als auch deren Kombination in multimodalen Therapieansätzen bleibt noch zu klären. Unter Beachtung der gegenwärtigen Datenlage geben wir im Folgenden einen Überblick über die therapeutischen Möglichkeiten.