Primary melanoma of the esophagus (PME) is an uncommon malignancy with less than 250 cases reported in the literature. Amelanotic PME is exceedingly rare and accounts for 10-25% of melanomas of the esophagus. A 59-year-old male with a history of mild dysphagia, heartburn, moderate anorexia and weight loss for 1 month is described. Barium swallow examination and videogastroscopy showed a polypoid, ulcerated mass located 30-38 cm from the incisors. No skin or eye melanoma lesions were found. Five biopsy samples were obtained. Histological examinations revealed proliferation of large, loosely cohesive cells of variable shapes and prominent central nucleoli in the deep mucosa. Immunohistochemical findings included positive vimentin, protein S-100, Melan A, and HMB-45, and negative AE1/AE3, CD 17, and desmin. A total transhiatal esophagectomy with high cervical esophagogastric anastomosis was performed. Peritumoral lymph nodes revealed malignant invasion. A diagnosis of primary amelanotic melanoma of the esophagus was made. Fourteen months after diagnosis the patient developed disseminated PME.

Although tamoxifen (TAM) is routinely used in advanced melanoma, it is still uncertain whether evidence exists to support this practice. This review assesses the benefits and harms of systemic therapy with TAM vs. without TAM on response and mortality in patients with advanced melanoma. MEDLINE, The Cochrane Database of Systemic Reviews, The Cochrane Central Register of Controlled Trials, EMBASE and LILACS were searched for randomized controlled trials comparing chemotherapy using and not using TAM in any dose, in patients of any age with advanced melanoma. References lists, databases of ongoing trials and conference proceedings were hand-searched. All included trials were evaluated for quality assessment. Primary outcomes were response and mortality. Secondary outcomes were hematologic and non hematologic toxicity, treatment-related mortality and quality of life. A meta-analysis was performed and results were presented as relative risk with 95% confidence interval. Nine randomized controlled trials met the inclusion criteria. Patients treated with TAM were more likely to respond, with a relative risk 1.36 (95% CI: 1.04-1.77, P = 0.02). However, there was no improvement in 1-year mortality. The incidence of hematologic toxicity was higher in the TAM group. Subgroup analyses showed that female patients were more likely to respond. Chemotherapies with TAM improve overall and partial response, but do not improve mortality in 1 year in advanced melanoma. Further use of TAM in melanoma should be done only in the context of clinical trials.

Induction of Th1 cytokines, those associated with cell-mediated immunity, is critical for host defense against infection by intracellular pathogens, including mycobacteria. Signaling lymphocytic activation molecule (SLAM, CD150) is a transmembrane protein expressed on lymphocytes that promotes T cell proliferation and IFN-γ production. The expression and role of SLAM in human infectious disease were investigated using leprosy as a model. We found that SLAM mRNA and protein were more strongly expressed in skin lesions of tuberculoid patients, those with measurable CMI to the pathogen, Mycobacterium leprae, compared with lepromatous patients, who have weak CMI against M. leprae. Peripheral blood T cells from tuberculoid patients showed a striking increase in the level of SLAM expression after stimulation with M. leprae, whereas the expression of SLAM on T cells from lepromatous patients show little change by M. leprae stimulation. Engagement of SLAM by an agonistic mAb up-regulated IFN-γ production from tuberculoid patients and slightly increased the levels of IFN-γ in lepromatous patients. In addition, IFN-γ augmented SLAM expression on M. leprae-stimulated peripheral blood T cells from leprosy patients. Signaling through SLAM after IFN-γ treatment of Ag-stimulated cells enhanced IFN-γ production in lepromatous patients to the levels of tuberculoid patients. Our data suggest that the local release of IFN-γ by M. leprae-activated T cells in tuberculoid leprosy lesions leads to up-regulation of SLAM expression. Ligation of SLAM augments IFN-γ production in the local microenvironment, creating a positive feedback loop. Failure of T cells from lepromatous leprosy patients to produce IFN-γ in response to M. leprae contributes to reduced expression of SLAM. Therefore, the activation of SLAM may promote the cell-mediated immune response to intracellular bacterial pathogens.