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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant transformation of melanocytes and further neoplastic progression may be associated with qualitative and/or quantitative changes in expression of HLA class I and class II antigens. Since previous immunohistochemical studies of surgically removed melanoma lesions have suggested a relationship in the expression of HLA class I and class II antigens, we have investigated the expression of these antigens at the single cell level. Double immunofluorescence staining of frozen sections of melanoma metastases and immunoelectron microscopic double labelling of melanoma cell suspensions prepared from three of these lesions has detected three HLA phenotypes on the large majority of melanoma cells: either both HLA class I and class II antigens, neither HLA antigen or only HLA class I antigens. In four out of the 11 lesions a few melanoma cells were found to express HLA class II antigens and to lack HLA class I antigens. A relationship was also found in the level of expression of HLA class I and class II antigens, as estimated by the intensity of staining with monoclonal antibodies. The level of expression of HLA class II antigens appeared to be similar to or lower than that of HLA class I antigens on the large majority of melanoma cells. This coordinated heterogeneity in the expression of HLA class I and class II antigens by melanoma cells may have implications in the interactions of tumour cells with the host's immune system.
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PMID:Associated expression of HLA class I and class II antigens on melanoma cells in surgically removed metastases. 353 48

A case of recurrent Hodgkin's disease of the "sarcomatoid" or "syncytial variant" type was seen that occurred as an extension from the mediastinum to a previously uninvolved extranodal site (breast) and pericardium after treatment of classical nodular sclerosing Hodgkin's disease based in the lymph nodes. This histologic variant was composed of sheets of large, undifferentiated neoplastic cells with few, if any, diagnostic features of nodular sclerosing Hodgkin's disease. For this reason, the differential diagnosis of this variant was difficult and included non-Hodgkin's lymphoma (peripheral T-cell lymphoma), Ki-1-positive lymphoma, medullary carcinoma, metastatic carcinoma, melanoma, and granulocytic sarcoma. Immunologic analysis by immunoperoxidase technique showed a phenotype consistent with "syncytial variant" Hodgkin's disease: Leu-M1+, Ki-1+, IL-2+, HLA-DR+, T11-, pan B-, K-, lambda-, cytokeratin-, S-100-, muramidase-.
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PMID:Recurrent "syncytial variant" of Hodgkin's disease: an immunohistologic diagnosis. 359 90

A family with four cases of melanoma, seven cases of basal cell carcinoma, and two cases of gastric adenocarcinoma, is described. The proband, who had three different primary tumors, died of gastric cancer, as did his father. Four of the proband's six siblings were affected with melanoma or basal cell cancer, as were two of his three children. Both daughters of one melanoma patient developed basal cell cancers. No spouses were affected, the cases were widely separated in time and place, and no unusual exposures were reported. HLA analysis of affected and unaffected first-degree relatives showed no association with antigens previously described in familial melanoma or segregation with a specific HLA haplotype. Although there was no association with HLA phenotype, these results suggest that melanoma, basal cell carcinoma, and gastric adenocarcinoma can be inherited in an autosomally dominant pattern similar to other familial tumor syndromes.
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PMID:Familial aggregation of melanoma, basal cell carcinoma, and gastric adenocarcinoma. 369 21

In a family displaying the familial atypical multiple-mole melanoma syndrome, linkage analyses were performed between HLA and an assumed dominant gene respectively determining each of the following affected phenotypes: precursor lesions; cutaneous malignant melanoma (CMM); and precursor lesions or CMM or both. The results suggest that there is a complex mechanism involving several factors, genetic and environmental interacting with the gene determining precursor lesions to cause the neoplastic transformation.
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PMID:HLA in familial malignant melanoma. 377 Feb 56

The parameters of a sandwich assay to analyze syngeneic polyclonal and monoclonal anti-idiotypic antibodies to murine anti-HLA and anti-human melanoma associated antigen monoclonal antibodies have been characterized. Furthermore, the sensitivity of the sandwich assay has been compared with that of assays widely used to characterize anti-idiotypic antibodies, i.e., the binding assay to F(ab')2 fragments of monoclonal antibodies and the radioimmunoassay. The latter is more sensitive than the sandwich assay when monoclonal anti-idiotypic antibodies are tested, but less sensitive when anti-idiotypic antisera are analyzed. Both assays are less sensitive than the binding assay to F(ab')2 fragments of monoclonal antibodies.
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PMID:A sandwich assay to detect and characterize syngeneic anti-idiotypic antibodies to murine anti-HLA and tumor associated antigen monoclonal antibodies. 378 25

The dysplastic nevus (DN) was first described by Clark in 1976. It was subsequently recognized to be a precursor of melanoma. Dysplastic nevi present with typical clinical and histological criteria. The dysplastic nevus syndrome (DNS) can be considered when at least two other family members have been shown to have multiple dysplastic nevi. From our own experience of over 2000 non-selected patients with melanoma only 60 (3%) were shown to have the DNS. In these 60 we could prove direct genetic penetration even though no HLA phenotype preference could be seen. Evaluation of the biological activity of the DN in cell cultures, as well as T-lymphocyte analysis in the neighborhood of the DN have shown signs of incipient malignant transformation of the DN. The practical implications of these findings and observations are discussed.
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PMID:[Dysplastic nevus syndrome]. 378 85

The phenotypic changes in human melanoma cells during the course of tumor progression were studied with monoclonal antibodies (MAbs) against the melanoma-associated antigens (MAA) M.2.2.4, H.2.8.10, K.1.2, A.1.43, and A.10.33, and HLA-(A,B,C and D). Cryostat sections of 172 primary melanomas of the skin, 157 melanoma metastases and 56 nevi were investigated with an indirect immunoperoxidase method. Phenotypic heterogeneity was observed within lesions at all stages, and also within different tumors of the same patients. Despite this heterogeneity, principles of antigen expression were found. From the reaction pattern of MAbs, the following classifications of antigens were derived: "constitutive" markers of nevomelanocytic cells (M.2.2.4 and H.2.8.10) were found expressed over a wide range of local and systemic tumors. One MAA, K.1.2 (Suter et al., 1985), that declines with progression of melanoma, was classified as an "early" antigen, whereas MAA that appear in primary melanoma in proportion to invasiveness, and which are expressed in metastases of lymph nodes and visceral organs (A.1.43, and A.10.33), were classified as "late" markers of tumor progression. HLA-antigens were classified as "intermediate" markers, HLA-A,B,C, as an "early-intermediate", and HLA-DR as a "late-intermediate" marker. The occurrence of class II HLA, A.1.43-, and A.10.33-positive tumor cells in primary melanoma indicates a high metastatic potential of tumors, independent of tumor thickness. The data show that local and systemic progression of melanoma is associated with qualitative changes in tumor cells which can be recognized by MAbs.
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PMID:Phenotypic dynamics of tumor progression in human malignant melanoma. 386 Apr 79

We have reported previously that pulmonary alveolar macrophages (PAMs) from individuals with lung cancer and active chronic pulmonary diseases were cytotoxic to tumor cells in vitro, whereas PAMs from normal individuals or patients with acute pulmonary disorders were noncytotoxic. In the present study, we evaluated 20 PAM preparations for both suppressor and cytotoxic functions to determine if PAMs could function as suppressor cells and, if so, whether a correlation between the two functions exists. Cytotoxicity was assessed in a 60-hr cytotoxicity assay against [3H]proline-prelabeled human melanoma target cells. More than 20% cytotoxicity was considered to be significant. Suppressor activity was measured by determining whether admixing PAMs at various ratios with autologous or allogeneic mononuclear cells could suppress concanavalin A-induced blastogenesis by T-lymphocytes. At least 50% suppression was considered to be significant. Of the 20 specimens evaluated, 13 were cytotoxic and 5 of these exhibited suppressor activity. None of the 7 noncytotoxic PAM preparations had suppressor activity. Suppression was nonspecific and not HLA restricted, since autologous and allogeneic mononuclear cells were inhibited to a similar extent. Suppression was probably not due to prostaglandin production by the PAMs since assays were performed under optimal conditions and required extremely high concentrations of prostaglandins. A significant correlation between suppressor and cytotoxic activity was found. Suppression was observed only with PAM specimens that were also highly cytotoxic to tumors, but not all cytotoxic PAM specimens were suppressive. Whether these actions reflect different levels of activation of PAMs or are the properties of different macrophage subsets remains to be clarified.
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PMID:Correlation between cytotoxic and suppressor activities of human pulmonary alveolar macrophages. 387 Nov 73

The frequency of HLA-DR5 was significantly increased in a large group of malignant melanoma patients (33.7% vs 20.5% for controls). The subgroup of patients with poor prognosis showed both a DR5 increase and a relative decrease in DR1. Although none of these differences was significant after correction for the number of antigens tested, similar findings have been made for other malignancies and further studies should be encouraged.
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PMID:HLA and DR antigen frequencies in melanoma patients: possible relation to disease prognosis. 387 14

Recombinant interferon-gamma (IFN-gamma) induced the expression of HLA-DR when added to the culture medium of HLA-DR- melanoma cell lines. In addition, IFN-gamma induced the expression of another class II antigen, HLA-DC, on a HLA-DR+ and -DC-melanoma cell line and to a lower level on a -DR- and -DC-melanoma line. IFN-gamma also enhanced the expression of HLA-ABC and beta 2-microglobulin, as well as HLA-DR on DR+ melanoma cells. In contrast, IFN-alpha gave no induction of expression of HLA-DR and DC on two DR- melanoma lines, while it did enhance the expression of HLA-ABC and of beta 2-microglobulin. The expression of 3 out of 6 melanoma-associated differentiation antigens was enhanced by IFN-gamma treatment. The modulation of antigens by IFN-gamma was both dose and time dependent. A minimum incubation time of 48 h was necessary for the appearance of HLA-DR on the two HLA-DR- melanoma lines, whereas HLA-ABC and beta 2-microglobulin were already increased after 24 h. A dose of 20 U/ml IFN-gamma started to induce the expression of HLA-DR and DC on melanoma cells GLL-19 and Me-43 and a plateau of maximum antigen expression was reached with 100 U/ml. Analyses of IFN-gamma-treated cells by flow microfluorometry showed a homogeneous distribution of increased staining intensity rather than the appearance of two cell populations. Immunoprecipitation experiments using detergent-solubilized 125I-labeled membrane proteins of IFN-gamma-treated melanoma cells and a monoclonal anti-HLA-DR antibody confirmed the presence of HLA-DR antigens. When IFN-gamma-treated cells were cultured without IFN the induced or enhanced expression of HLA antigens was reversible. Eight days after removal of IFN, the HLA-DR level was reduced by more than 90% and the level of HLA-ABC and beta 2-microglobulin by more than 50%. The demonstration of the ability of HLA-DR- melanoma cells to express HLA-DR after IFN-gamma treatment was extended to cells from other types of tumor such as gliomas, colon carcinomas and one cervical carcinoma cell line.
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PMID:Recombinant interferon-gamma can induce the expression of HLA-DR and -DC on DR-negative melanoma cells and enhance the expression of HLA-ABC and tumor-associated antigens. 391 69


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