Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell lines Raji and K 562, lacking tyrosinase, and two melanotic human melanoma cell lines (IRE 1 and IRE 2), were exposed to concentrations from 5 X 10(-3) M to 10(-5) M of different phenols which are substrates of tyrosinase, i.e. l-dopa, dopamine, hydroquinone, terbutylcatechol, and of phenols which are not substrates of the tyrosinase, i.e. resorcinol, butylated hydroxyanisole and hydroquinone dimethyl ether. Cultures were carried out in the presence or in the absence of oxygen radical scavenger enzymes superoxide dismutase, catalase and peroxidase. The stability of each substance in culture medium was assayed by high performance liquid chromatography (HPLC). Results showed that: catechols which are substrates of tyrosinase decompose fully after 24 hr in medium; they are equally toxic for melanoma and non-melanoma cell lines; their toxicity increases when they are preincubated in medium for 24 hr and 48 hr before addition of cells; their toxicity is significantly reduced by addition of scavenger enzymes; on the contrary, phenols not substrates of tyrosinase are stable in medium and their toxicity is not reduced by scavenger enzymes. It is concluded that tyrosinase does not play a major role in catechol toxicity in vitro, which is probably due to some products of catechol decomposition, especially oxygen radicals, acting outside the cells.
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PMID:Mechanism of antitumoral activity of catechols in culture. 310 24

The substitution of glucose-antiglucose oxidase complex (GAG) for peroxidase antiperoxidase (PAP) in the Sternberger three-layer unlabeled antibody method avoids the problems associated with the use of the chromogen 3,3,diaminobenzidine (DAB). The blue final reaction product obtained using the GAG complex is not obscured by melanin granules, which is often the case when using the PAP-DAB combination. The replacement of PAP with GAG complexes facilitates the detection of melanocytes in melanoma and blue nevi. The absence of endogenous glucose oxidase in mammals provides for greater image contrast, which is not possible using alternative chromogens and immunoperoxidase.
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PMID:The substitution of glucose-antiglucose oxidase complex (GAG) for peroxidase-antiperoxidase (PAP) in immunohistochemical studies of skin. 330 93

With the increasing use of immunoperoxidase technics, it may be difficult to differentiate between the dark staining of 3,3'-diaminobenzidine (DAB) compound reaction product and melanin pigment. The latter may be particularly observed in skin. Samples of both normal skin and melanotic malignant melanoma were treated for the removal of melanin by standard technics both before and after a peroxidase-antiperoxidase (PAP) immunohistologic sequence. Many methods for the removal of melanin pigment resulted in diminished DAB staining intensity. Some also caused cellular disruption. However, the method of choice was found to be treatment with 0.25 g/dL potassium permanganate and 1 g/dL oxalic acid before the immunoperoxidase sequence.
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PMID:The effect of melanin pigment removal on the peroxidase-antiperoxidase immunoperoxidase technic. 331 Jun 9

The lectin-binding patterns of primary malignant melanoma, nevocellular nevus, and Spitz nevus were studied on formalin-fixed, paraffin-embedded sections using a series of biotinylated lectins--concanavalin A (ConA), Ricinus communis agglutinin-1 (RCA1), dolichos biflorus agglutinin (DBA), soybean agglutinin (SBA), maclura pomifera agglutinin (MPA), peanut agglutinin (PNA), wheat germ agglutinin (WGA), and Ulex europeus agglutinin-1(UEA1)--and employing the avidin-biotin-peroxidase complex method. In nevocellular and Spitz nevi, all of the nevus cells were positively stained with ConA and RCA1. No positive staining was observed, however, with the other lectins and no change in binding patterns occurred following neuraminidase pretreatment. In malignant melanoma, all of the melanoma cells were positively stained with ConA and RCA1, and some were also stained with MPA, PNA, and WGA. In addition, DBA, SBA, MPA, PNA, and WGA labeled all of the melanoma cells after neuraminidase pretreatment. No positive staining was observed with UEA1 despite neuraminidase pretreatment. The present results showed that malignant melanoma and nevocellular and Spitz nevi have different lectin-binding patterns and different responses to neuraminidase pretreatment. We, therefore, believe that the lectin staining on paraffin-embedded sections can be a useful probe for the differentiation of these diseases.
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PMID:Differing lectin-binding patterns of malignant melanoma and nevocellular and Spitz nevi. 331 32

The immunohistochemical localization of melanoma-associated antigen p94 kd200 was investigated in frozen sections of 3 congenital nevi, 4 benign intradermal nevi, 1 regressing nevus, 1 blue nevus, 1 dysplastic nevus, 1 lentigo maligna, 1 superficial spreading melanoma and 2 metastatic melanomas. The original avidin-biotin complex lectin method (Hsu SM, Raine L, Fanger H: Am. J. Clin. Pathol., 75: 734-738, 1981) was modified to detect the antigen. The sections were exposed to the monoclonal antibody to p94 kd200 (Hybritech Inc.), the linking biotin-labelled anti-mouse IgG, the avidin-biotin peroxidase complex and the 3-amino-9-ethylcarbazole solution in an incubator at 37 degrees C and 100% humidity. We found that the percentage of cells expressing p94 kd200 varied between 0 and 100% in congenital nevi, between 80 and 100% in benign intradermal nevi, between 0 and 20% in the regressing, blue and dysplastic nevi, and in the lentigo maligna, 80 to 100% in the superficial spreading melanoma, and between 0 and 40% in the metastatic melanomas. Positive cells were found to be hypomelanotic (did not have heavy melanin content). The intensity of labelling or the degree of antigen expression on benign and malignant hypomelanotic cells was also found to vary. These findings 1) reinforce the concept of quantitative rather than qualitative antigenic differences in benign and malignant cells 2) suggest that kd200 is lost with increasing pigment production 3) offer a potentially significant tool to investigate the antigenic changes during cell differentiation.
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PMID:Immunohistochemical localization of melanoma-associated antigen p94 kd200 with the use of a modified avidin-biotin-complex lectin method. 331 50

Cultured human melanoma, lung carcinoma, and colon carcinoma cells were isotope labeled and incubated with a combination of effector cells and mouse monoclonal antibodies to tumor-associated cell surface antigens. The former were derived from the peritoneal cavity of mice or from peripheral blood of healthy human subjects. Monoclonal antibodies MG-21, 96.5, and L6, which are IgG3, IgG2a, and IgG2a, respectively, were all cytolytic when added in the presence of mouse effector cells to target cells expressing the relevant antigens. MG-21 and L6 were cytolytic also with human effector cells, while monoclonal antibody 96.5 was not. The effector cells attached to plastic surfaces, stained with neutral red, were peroxidase positive and mediated their effect over a 24- to 72-h time period as compared to the 4 h generally sufficient for antibody-dependent cellular cytotoxicity by natural killer cells. In tests on human effector cells with a fluorescence-activated cell sorter, they stained with antibody LCM-3C10 to the CD14 antigen, as well as with antimonocyte antibody 61D3. The cytolytic effect of human effector cells and antitumor antibody was not abolished by incubation with antibodies FC2 or 60.3 to CD16 and CD18, respectively, known to interfere with the antibody-dependent cellular cytotoxicity activity and natural killing of natural killer cells. This suggests, together with the other findings, that the effector cells were macrophages.
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PMID:Antibody-mediated killing of human tumor cells by attached effector cells. 333 25

Repeated selection of an adherent subpopulation from B16-F1 melanoma cells growing in suspension culture on poly(hydroxyethylmethacrylate) [poly(HEMA)] coated plates resulted in the isolation of an adherent variant designated B16-A10. B16-A10 cells are more adherent to poly(hydroxyethylmethacrylate) coated plates than are B16-F1 cells and express an organized actin structure characteristic of highly adherent low metastatic cells as opposed to the poor cytoskeletal organization of B16-F1 cells. Upon growth in suspension, B16-A10 cells do not acquire the enhanced metastatic capability characteristic of B16-F1 cells and they express similar lung colonizing ability irrespective of the culture conditions. The increased metastatic ability of B16-F1 cells in suspension culture has previously been associated with the decreased accessibility of surface proteins to lactoperoxidase catalyzed iodination and with the increased expression of sialylated peanut agglutinin-binding oligosaccharides on these proteins. B16-A10 cells which show no cell shape induced increase in metastatic ability do not undergo alteration in either of these two properties in suspension culture. The absence of these two phenomena on B16-A10 cells grown in suspension indicates that they are interrelated and involved in the increased metastatic ability of B16-F1 cells grown in suspension.
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PMID:Loss of metastatic responsiveness to cell shape modulation in a newly characterized B16 melanoma adhesive cell variant. 334 5

Tertiary amine local anesthetics, such as dibucaine and tetracaine, have been found to reversibly modify the blood-borne implantation and experimental metastatic properties of B16 melanoma cells in syngeneic C57BL/6 mice. Local anesthetic treatment in vitro of low (B16-F1) and high (B16-F10) lung-colonizing melanoma variants reduced significantly their abilities to form lung tumor colonies, but the cells recovered their original in vivo colonizing properties within several hours after drug removal. Low drug concentrations (0.5 mM tetracaine) that altered the metastatic properties of these cells did not modify cell plating efficiencies or tumor growth rates at subcutaneous sites. With the use of [125]-5-iodo-2'-deoxyuridine-labeled B16 cells, the kinetic distributions of viable tumor cells in mice were also shown to be altered. Fewer cells were initially localized and retained in the lungs, and more cells reached extrapulmonary sites. Local anesthetics modified B16 cell morphology, inducing cell rounding and loss of microvilli. These effects occurred concomitant with alterations in microfilament organization. Anesthetic-treated cells also exhibited decreased cell-adhesion characteristics in both homotypic and heterotypic (endothelial and subendothelial matrix) cell-adhesion assays. Despite these changes, cell surface lactoperoxidase-catalyzed iodination of external proteins and labeling of cellular glycoproteins on polyacrylamide gels with 125I-labeled lectins did not reveal differences in the displays or quantities of cell surface glycoproteins after drug treatment. The data are consistent with the idea that reversible disruptions in transmembrane cytoskeletal control induced by local anesthetics result in alterations in cell shape, loss of stable adhesive interactions, and a decrease in blood-borne arrest and metastatic properties.
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PMID:Effects of tertiary amine local anesthetics on the blood-borne implantation and cell surface properties of metastatic mouse melanoma cells. 345 65

S-100 protein has been demonstrated on histologic sections in a number of neural and nonneural tissues, including a variety of neoplasms. Since pleural or peritoneal effusions are frequently the initial presentation of cancer, a study was undertaken to determine if S-100 protein in exfoliated cancer cells could be used as a marker for melanoma. Cells in 36 serous fluids obtained from 32 patients were retrospectively examined for S-100 protein by the peroxidase-antiperoxidase technique. All samples had been previously studied as Papanicolaou-stained cytology specimens, and 25 samples had been studied by transmission electron microscopy. All benign effusions were negative for S-100 protein. Malignant effusions were negative except for some that contained malignant melanoma cells: two of five pigmented melanomas and both cases of amelanotic melanoma. This study indicates that S-100 protein in malignant cells is a useful marker for malignant melanomas, especially the amelanotic type.
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PMID:An immunoperoxidase study of S-100 protein in neoplastic cells in serous effusions. Use as a marker for melanoma. 352 Nov 74

Sera of patients with breast cancer (as well as control normal sera and sera of patients with ovarian cancer or melanoma) were screened for the presence of antibodies against antigens expressed by the MDA breast cancer cell line. The techniques employed were radioimmunoassay with radioiodinated protein A and immunodotting with peroxidase-conjugated anti-human immunoglobulin antibodies. Sera reacting strongly by immunodotting were subsequently tested against antigens of the MDA and T47D cell lines in immunoblotting experiments. Both the breast cancer and the control sera yielded highly complex band patterns, which varied from serum to serum. The cancer sera differed from the normal sera, however, as they produced in most cases one or several bands that were distinctly stronger than the others. One of the strong bands, in fact a doublet of approximately 50 kilodaltons (kd), was produced preferentially (although not exclusively) when breast cancer sera were reacted with T47D cell membrane antigens. Absorption of selected sera with normal tissue or MDA antigens abolished or greatly reduced the intensity of some of the bands. It is concluded that, with the possible exception of the 50-kd band, most (probably all) of the bands seen in immunoblots resulted from the binding of autoantibodies to normal antigens expressed by the breast cancer cell lines. The main difference between cancer and normal sera would seem to be an increased content of autoantibodies in cancer, the specificity of these autoantibodies varying, however, from serum to serum.
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PMID:(Auto)antibodies in human breast cancer sera against antigens associated with breast cancer cells, detected by immunoblotting. 354 Apr 17


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