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Aims: Spindle cell differentiation is not an uncommon finding in common acquired naevi, and may represent a form of neurotisation with Schwannian differentiation of melanocytes. Perineurial differentiation in this context appears to be very rare, and is only poorly documented in the literature. We therefore aimed to study this rare form of neurotisation in melanocytic naevi more comprehensively. Methods and results: We have identified six melanocytic tumours showing spindle cell morphology and perineurial differentiation from routine and referral material. Clinical data and follow‐up were obtained, and the histological and immunohistochemical features were analysed. The tumours affected middle‐aged adults (median, 48 years; range, 26–74 years), with a wide anatomical distribution and benign follow‐up (median, 13 months; range, 6–48 months). All tumours were nodular and circumscribed but asymmetrical, with extension into the deep dermis and superficial subcutis. A characteristic finding was a biphasic growth pattern with a lentiginous compound naevus in the superficial aspect and abrupt transition to a prominent nodular spindle cell proliferation in the deeper reaches. Spindle cells were bland and uniform, and arranged singly and in short fascicles in a loose fibromyxoid stroma. In areas, a whorled arrangement of slender spindle cells with wavy nuclei was seen. Distinctive intratumoral hypocellular nodules and peripheral lymphoid aggregates were additional features. By immunohistochemistry, the spindle cells were mainly S100‐positive melanocytes. In areas, S100‐negative/epithelial membrane antigen‐positive spindle cells showing coexpression of Glut‐1 and claudin‐1 were closely admixed. Conclusion: This perineurial differentiation probably represents a rare and unusual form of neurotisation. The tumours are benign but may be mistaken for desmoplastic melanoma. Awareness of and careful attention to the clinicopathological and immunohistochemical features allow reliable separation. [ABSTRACT FROM AUTHOR]

Background Studies of Merkel cell polyomavirus ( MCPyV) in nonmelanoma skin cancers ( NMSC) other than Merkel cell carcinoma ( MCC) produced controversial results. Therefore, we studied the prevalence of MCPyV in basal cell carcinoma ( BCC) and in squamous cell carcinoma ( SCC). Methods Tissue specimens were analyzed for the presence of MCPyV DNA by conventional polymerase chain reaction ( PCR). Expression of MCPyV large T protein was determined by immunohistochemistry. Results MCPyV DNA was frequently detected in skin cancers by PCR, in 36 of 88 BCCs, in 21 of 75 SCCs and in 10 of 47 normal skin samples. In BCC, a significant difference in the detection rate compared to normal skin was observed. In contrast, weak reactivity for MCPyV large T antigen was detected only sporadically in immunosuppressed patients (2 of 88 BCCs, 1 of 75 SCCs). Mutations of the large T antigen of MCPyV were more frequently observed in MCC than in BCC/ SCC. Conclusions Our results suggest that the frequent detection of the MCPyV genome in NMSC by PCR reflects ubiquitous spread of the virus. However, the low immunohistochemical detection rate of MCPyV and the lack of MCC-specific MCPyV mutations argue against an essential role of MCPyV in the development of skin cancers other than MCC. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses the case of a 60-year old male patient with metastatic colorectal cancer (CRC) that shows two different Kirsten ras (KRAS) gene mutations (G12D and G12V).

Peritoneal injury is often associated with alterations of the mesothelium, resulting in peritoneal healing and adhesion formation. We analyzed the effects of pro-inflammatory cytokines on cell morphology and proliferation of human peritoneal mesothelial cells (HPMC). After 48 hours, HPMC formed a confluent layer with cell volumes of 2,662±111 fL. Treatment of HPMC with interleukin-1β and tumor necrosis factor-α (TNF-α) induced mesothelial disintegration and alterations in mesothelial cell morphology, which were associated with an interleukin-1β–triggered increase in cell volume (3,028±118 fL; p<0.05) and exfoliation of cells into the supernatants of cell cultures ( p<0.05). Whereas TNF-α arrested HPMC in the G0/G1 phase ( p<0.05), interleukin-1β caused an increase of cells into the S phase of the cell cycle. In addition, interleukin-1β and interferon-γ exerted a proliferative effect on HPMC. These changes were independent from mesothelial Na+/H+ antiporter-1 expression. Our data indicate that the response of HPMC to inflammatory injury is regulated by interleukin-1β and TNF-α reflecting their putative role in peritoneal wound healing and adhesion formation. [ABSTRACT FROM AUTHOR]

The fulminant form of post-transplant lymphoproliferative disorder (PTLD) is very uncommon and occurs in approximately 1% of PTLD patients. Approximately 85% of these lesions are of B-cell origin, and most of them are associated with Epstein–Barr virus infection. Fulminant PTLD is frequently associated with a systemic inflammatory response syndrome, and may be difficult to differentiate from septicemia. We describe the case of a 59-yr-old man who suffered from prolonged septicemia in the immediate post-transplant period, and presented again four months after cardiac transplantation with fever, painful liver edge and gastrointestinal bleeding. The diagnosis of fulminant PTLD with advanced multiorgan infiltration by a diffuse large-cell lymphoma of B-cell phenotype was made. During treatment with rituximab, the patient died from Enterococcus faecium septicemia. The sequence of septicemia, PTLD and, finally again, septicemia is an unusual challenge and urges for an aggressive diagnostic approach, where markers like procalcitonin may aid in the discrimination of fulminant PTLD from septicemia. [ABSTRACT FROM AUTHOR]