Tumors can develop a blood supply not only by promoting angiogenesis but also by forming vessel-like structures directly from tumor cells, known as vasculogenic mimicry (VM). Understanding mechanisms that regulate VM is important, as these might be exploitable to inhibit tumor progression. Here, we reveal the adhesion molecule desmoglein 2 (DSG2) as a novel mediator of VM in melanoma. Analysis of patient-derived melanoma cell lines and tumor tissues, and interrogation of The Cancer Genome Atlas (TCGA) data, revealed that DSG2 is frequently overexpressed in primary and metastatic melanomas compared to normal melanocytes. Notably, this overexpression was associated with poor clinical outcome. DSG2+ melanoma cells self-organized into tube-like structures on Matrigel, indicative of VM activity, which was inhibited by DSG2 knockdown or treatment with a DSG2-blocking peptide. Mechanistic studies revealed that DSG2 regulates adhesion and cell-cell interactions during tube formation, but does not control melanoma cell viability, proliferation or motility. Finally, analysis of patient tumors revealed a correlation between DSG2 expression, VM network density and expression of VM-associated genes. These studies identify DSG2 as a key regulator of VM activity in human melanoma and suggest this molecule might be therapeutically targeted to reduce tumor blood supply and metastatic spread.

Plasmablastic lymphoma (PBL) is a recently described rare variant of diffuse large B-cell lymphoma characterised by its aggressive nature and plasmacytic differentiation. It most frequently arises in the oral cavity of human immunodeficiency virus (HIV)-infected patients. However extra-oral involvement is becoming increasingly recognised, particularly in HIV-negative patients. We report a case of PBL presenting as multiple violaceous nodules and plaques on the leg of a HIV-negative patient, 13-years post-renal transplant. To date, 20 cases of PBL presenting in the skin have been reported. We review and compare the clinico-pathological features of these cases.

Approximately half the survival increase was not explained by changes in thickness, level, lesion site, and age and sex. Other possible contributors warranting further study include changes in ulceration, nodal or more distant site involvement, treatment gains and changes in tumour biology. The trend for deeper Clark levels within Breslow thickness categories requires independent confirmation.

Neurological involvement is a rare extracutanenous manifestation of Sweet's syndrome. We present a novel case of radiation therapy-induced neuro-Sweet disease in a patient receiving treatment for an oral squamous cell carcinoma.

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