101/3479. Clinical and immunocytochemical findings in a case of melanoma-associated retinopathy. OBJECTIVE: To describe an unusual case of melanoma-associated retinopathy (MAR). DESIGN: Retrospective, observational case report and experimental study. PARTICIPANTS: A 61-year-old man with a history of cutaneous melanoma, acquired bilateral central scotomas, and night blindness. INTERVENTION: Serial full-field electroretinography (ERG) and Goldmann perimetry were performed. serum was screened for cancer-associated retinopathy (CAR) antibodies by Western blotting. Sections of human and rat retina were examined by immunofluorescence microscopy to determine whether retinal cells were reactive with this patient's serum. A metastatic workup was performed. MAIN OUTCOME MEASURES: electroretinography, Goldmann visual field testing, and immunocytochemistry were performed. RESULTS: The results were as follows: (1) The ERG showed a profound loss of the b-wave amplitude and a "negative" b-wave characteristic of congenital stationary night blindness; (2) a central scotoma and peripheral constriction were identified on Goldmann visual field tests; (3) as in other patients with MAR, bipolar cells in human and rat retinas were immunolabeled with this patient's serum; and (4) a previously unsuspected focus of metastatic melanoma was discovered. CONCLUSIONS: Recognition of this condition may help to identify an occult focus of metastatic melanoma. ( info) |
102/3479. Acquired streptococcal necrotizing fasciitis following excision of malignant melanoma. Necrotizing fasciitis is an uncommon condition which may complicate any surgical procedure, including 'minor' dermatological procedures. However, it may arise de novo in the absence of any discernible trauma. We report a patient who acquired a fulminant form of this condition following excision of a malignant melanoma. The development of necrotizing fasciitis in association with melanoma has not previously been reported. ( info) |
103/3479. Common blue naevus with satellite lesions: possible perivascular dissemination resulting in a clinical resemblance to malignant melanoma. We report a case of common blue naevus with polymorphous guttate and linear satellite lesions, thereby mimicking peripherally spreading malignant melanoma. Histopathologic examination showed that the naevus cells are clustered around blood vessels in the primary as well as satellite lesions, suggestive of spreading of the naevus cells along the perivascular space. Such biological behaviour resulting in a clinical manifestation of a malignant melanoma-like lesion is a rarity in common blue naevus, a benign cutaneous disorder that is devoid of a malignant potential, and has not been described before. ( info) |
104/3479. In vivo selective expansion of a tumour-specific cytotoxic T-cell clone derived from peripheral blood of a melanoma patient after vaccination with gene-modified autologous tumour cells. melanoma-specific cytotoxic T lymphocytes (CTL) can be generated from peripheral blood lymphocytes (PBL) by mixed lymphocyte-tumour cell cultures. Analysis of CTL precursor frequencies in peripheral blood of melanoma patients is generally used for immunomonitoring purposes to evaluate vaccination efficacy. At present, it is unclear whether PBL-derived CTL generated in vitro are indicative of an anti-tumour immune response in vivo. Three tumour-specific human leucocyte antigen (HLA)-B/C-restricted CTL clones were derived from peripheral blood of a melanoma patient immunized with interleukin-7 (IL-7) gene-modified tumour cells. CTL clones differing in their T-cell receptor-gamma (TCRgamma) rearrangement produced interferon-gamma, IL-4 and/or IL-10. On the basis of their unique TCRgamma gene rearrangements clone-specific primers were generated for detection of clone-specific dna by polymerase chain reaction. One CTL clone (E5) of the three was found to be selectively expanded in one of seven metastases obtained at autopsy, as determined by Southern blot hybridization. However, the presence of E5 in only one of seven metastases at death indicates that the in vivo accumulation of the specific CTL clone was not sufficient to contain tumour progression. Nevertheless, our data support the proposition that analysis of anti-tumour activity of PBL-derived CTLs may reflect an anti-tumour immune response in vivo. ( info) |
105/3479. Primary invasive signet-ring cell melanoma. The histopathological variants of malignant melanoma include the common type (lentigo maligna, superficial spreading melanoma, nodular melanoma, acrolentiginous melanoma), spindle cell, desmoplastic, balloon cell, pleomorphic (fibrohistiocytic), myxoid, small cell melanoma and malignant blue nevus. Recently, signet-ring cell melanoma was introduced as an additional cytologic variant. We describe a 72-year-old patient with a primary signet-ring cell melanoma of the skin located on the upper arm. Histopathologic examination disclosed a melanocytic tumor extending from the epidermis to the deep reticular dermis. Numerous pleomorphic tumor cells showed large, intracellular vacuoles and oval to spindle-shaped nuclei at their periphery. Mitotic figures and multinucleated melanocytes were also observed. Some of the signet-ring cells exhibited cytoplasmatic periodic acid-Schiff (PAS)-positivity. immunohistochemistry showed positive reaction of the tumor cells for S-100, HMB-45 protein and vimentin, confirming their melanocytic differentiation. Tumor cells were negative for cytokeratins, epithelial membrane antigen (EMA), and carcinoembryonic antigen (CEA). The signet-ring cell melanoma disclosed an invasion to Clark Level IV and tumor thickness of 2.2 mm. Signet-ring cell melanoma is a rare morphologic variant of melanoma. Its recognition is important for differentiation from other tumors featuring signet ring cells. ( info) |
| OBJECTIVE: This article focuses on the clinical, diagnostic, and therapeutic aspects of malignant melanoma metastases to the gastrointestinal (GI) tract. The subject of primary malignant melanoma arising from the GI tract is also discussed. Malignant melanoma is the most common tumor metastatic to the GI tract, and can present with fairly non-specific symptoms. methods: Up to 60% of patients with melanoma are found to have metastases at autopsy. Frequent GI sites of invasion include the small bowel (50%), colon (31.3%), and anorectum (25%), seen in our institution over the past 9 yr. Malignant melanoma is a frequent source of metastases to the gastrointestinal (GI) tract. RESULTS: Herein we report the case of a melanoma masquerading as a rectal polyp. We have also discovered 16 cases of melanoma metastases to the GI tract, at our institution, over the past 9 yr. The most frequent sites included small bowel (50%), colon (31.3%), and anorectum (25%). CONCLUSION: Despite innocuous gastrointestinal symptoms, metastatic melanoma should be a diagnostic consideration in any patient with a history of melanoma. ( info) |
107/3479. Actin-rich desmoplastic malignant melanoma: report of three cases. We report three cases of desmoplastic malignant melanoma (DMM) rich in smooth muscle actin. They occurred in two men (Cases 1 and 3) and in one woman (Case 2). Cases 1 and 2 were recurrent lesions from common melanomas excised, respectively, 3 and 1 years previously. In Case 3, DMM was associated with lentigo maligna at the time of presentation. Morphologically, DMMs were composed of spindle neoplastic cells organized in haphazardly orientated long fascicles separated by collagen bundles. Perineural invasion was present and mitotic activity was prominent in all cases. The neoplastic spindle cells were intensely positive with S100 protein and smooth muscle actin antisera and negative with HMB45 and Melan-A (Mart-1) antibodies. Double staining for smooth muscle actin and S100 protein revealed no definite coexpression of the two antigens. Follow-up was available for patients 1 and 2 who had local recurrences and are still alive. It is possible that actin rich elements differentiate toward mesenchymal elements, paralleling the phenotypic changes seen in sarcomatoid carcinomas. Therefore, multidirectional differentiation may explain the mesenchymal (sarcomatoid) differentiation of neoplastic melanocytes and may be responsible for the different biologic behavior of DMMs, which is closer to mesenchymal tumors than to conventional melanomas. ( info) |
108/3479. Metastatic melanoma of the maxilla presenting as a gingival swelling. Malignant melanoma metastatic to the gingiva has been reported only once. We present a case in which the occurrence of melanoma in the gingiva followed extraction of a periapically "abscessed" tooth. Since the initial periapical mass may well have been a metastatic tumor, particularly in a patient undergoing therapy for disseminated malignant disease, the need for biopsy of such lesions is emphasized. ( info) |
109/3479. The umbilicus: a rare site for melanoma. Clinical considerations in two cases. case reports. The umbilicus is a rare site for malignant melanoma. We report two cases of umbilical melanoma and analyse the mechanisms of diffusion of the neoplasm in relationship to the arterial, venous, and lymphatic anatomy of the region. Because of the peculiarity of these connections, we propose a revision of the concept of melanoma stage for the umbilical region. ( info) |
110/3479. Analysis of tumor cell evolution in a melanoma: evidence of mutational and selective pressure for loss of p16ink4 and for microsatellite instability. Tumorigenesis and tumor progression can be considered an evolutionary process. In order to deduce information on the mutational and selective pressures during melanoma progression we performed microsatellite analysis at 42 autosomal and two X-linked loci in a microdissected primary melanoma and its nine metastases. Loss of heterozygosity at locus D9S259 was the only genetic change observed in all metastases. The pattern of loss of heterozygosity at loci D9S162 and D9S171 within the region of common loss on chromosome 9p21 which encompasses the tumor suppressor gene p16ink4 enabled the distinction of four genetically different tumor cell populations. Three cell lineages showed homozygous loss of the p16ink4 gene, which evolved independently in each tumor cell population within the primary tumor. Additional allele losses could be demonstrated at markers D14S53 and DXS998. The fourth lineage did not demonstrate loss of heterozygosity at loci D9S162 and D9S171 and contained the wild type p16ink4 gene but was characterized by abundant microsatellite instability. The evolutionary approach towards tumorigenesis and tumor progression used in this study thus confirms the role of p16ink4 inactivation for melanoma progression but not for melanoma initiation; it suggests the existence of additional putative tumor suppressor genes located on 9p as well as on the long arm of chromosome 14 and shows that microsatellite instability may represent an alternative pathway of tumor cell evolution in malignant melanoma. ( info) |