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

Melanoma B-16 grew slowly in mice with hyperglycemia induced by alloxan, glucagon, or glucose. The mechanism of retarded tumor growth is different and depends on the origin of hyperglycemia. The concentration of immunoreactive insulin in blood of mice with melanoma and in the tumor tissue is increased in nondiabetic as well as in diabetic mice. The chemotherapy of melanoma in diabetic mice is as effective as in nondiabetic mice whereas immunotherapy in diabetic mice is not effective. Combined chemoimmunotherapy of melanoma in diabetic mice is more effective than either therapy alone only when mice are given a daily dose of insulin.
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PMID:Growth and treatment of B 16 melanoma in hyperglycemic mice. 740 88

The aim of this work was to study the in vitro effect of ozone on the 70 kDa family of inducible heat shock proteins (HSPs70). We also performed tests to investigate possible toxic effects of ozone at the different doses employed. In human haematic mononucleated cells ozone at doses up to 20 micrograms/ml had no toxic effects and induced biosynthesis of the HSPs70. Biosynthesis of these proteins was greater at 40 micrograms/ml. In murine macrophages testing with tetrazolium salt (MTT), neutral red, and 2-deoxy-D-[1-3H]glucose uptake and study of the cell morphology showed a remarkable resistance or no toxic effects at a dose of 100 micrograms/ml also. Melanoma B16 murine cells assayed with the MTT test demonstrated less resistance to the toxic effects of ozone than normal cells. These results provide indications relevant to the problems of ozone therapy.
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PMID:Effects of ozone on some biological activities of cells in vitro. 760 Feb 55

1H-nuclear magnetic resonance spectroscopy was used to study malignant melanoma extract. The aim of this work was to study low molecular weight metabolites soluble in water, which can be helpful for a more detailed understanding of tumor metabolism with a view to using this knowledge for diagnosis. The authors found in a well distinguished spectrum the presence of numerous low molecular weight metabolites such as glutamate, glutamine, choline, inositol, creatine, phosphocreatine, phosphocholine, glucose, acetate, alanine, lactate. It is necessary to correlate these in-vitro findings with a study of the above mentioned metabolites in-vivo. Malignant melanoma is appropriate for this investigative and diagnostic technique because of its superficial localization. (Fig. 1, Ref. 18.)
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PMID:[Study of malignant melanoma using 1H-nuclear magnetic resonance spectroscopy]. 763 25

While the primary targets for granulocyte-macrophage colony-stimulating factor (GM-CSF) are hematopoietic precursors and mature myeloid cells, GM-CSF receptors (GMR) are also found on normal tissues including placenta, endothelium, and oligodendrocytes as well as certain malignant cells. The function of GMR in these nonhematopoietic cells is unknown. We studied the function of GMR in human melanoma cell lines. Six of seven cell lines tested (clones 1-5 and 3.44 of SK-MEL-131, SK-MEL-188, SK-MEL-23, SK-MEL-22, and SK-MEL-22A) expressed mRNA encoding the membrane-bound and soluble isoforms of the alpha subunit of the GMR. Melanoma cell lines in early stages of differentiation expressed the largest quantities of alpha-subunit mRNA. Although five of these lines expressed trace levels of mRNA encoding the beta subunit of the GMR, Scatchard analysis of equilibrium binding data derived from three of the cell lines showed that they expressed only low-affinity GMR. Clones 3.44 and 1-5 of SK-MEL-131, and SK-MEL-188 cells expressed receptors with a dissociation constant (kd) for GM-CSF in the following ranges: 0.7 to 0.8, 1.2 to 1.8, and 0.4 to 0.8 nmol/L, respectively. GM-CSF stimulated glucose uptake in four of the melanoma cell lines expressing the alpha subunit, presumably through facilitative glucose transporters, as uptake was blocked by cytochalasin B but not cytochalasin E. Stimulation of glucose uptake was transient, with maximum stimulation occurring at approximately 30 minutes in the presence of 1 nmol/L GM-CSF. GM-CSF stimulated glucose uptake 1.4- to 2.0-fold but did not stimulate cell proliferation. These results suggest a metabolic role for the low-affinity GMR in melanoma cell lines and indicate that the alpha subunit of the GMR can signal for increased glucose uptake in nonhematopoietic tumor cells.
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PMID:Granulocyte-macrophage colony-stimulating factor signals for increased glucose uptake in human melanoma cells. 784 18

Chemotactic activity of granulocytes attracted by tumor cells loaded either with anti-ganglioside monoclonal antibodies (mAb) or with antibody-glucose oxidase conjugates (mAb-GO) was investigated. The melanoma cell line SK-Mel-28 which expresses the ganglioside GD3 at high density as well as the neuroectodermal cell line SK-N-LO which expresses GD2 were used for the experiments. In the presence of 50% human AB-serum, antibody-loaded tumor cells induced chemotactic activity on granulocytes, probably due to the generation of C3a/C5a which could be detected in serum incubated with anti-GD3 loaded SK-Mel-28 cells. Both compounds could also be detected in vivo in the plasma of patients suffering from neuroblastoma during therapy with anti-GD2 antibodies. In another set of experiments mAb-GO conjugates generating high amounts of H2O2 in the presence of glucose were bound to these tumor cells. A significant lipid peroxidation could be observed in the simultaneous presence of iron and ascorbate. The lipid peroxidation products were measured as thiobarbituric acid-reactive substances (TBARS) and were also shown to induce chemotactic effects on granulocytes.
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PMID:Chemotactic activity of substances derived from antibody-loaded tumor cells on granulocytes. 795 5

An IgM human monoclonal antibody (human MAb) was generated by fusing lymph node cells isolated from a surgical specimen of malignant melanoma with the heteromyeloma cell line SHMD-33. The antibody, designated 7c11.e8, reacted with surface antigens on human melanoma cells as shown by live cell immunofluorescence and absorption assays. The MAb 7c11.e8 reacted with DSI, SPG, GM4, GM3 and GD3 in enzyme-linked immunosorbent assays (ELISA), and did not react with GD2, GM1, GM2, GD1a, GD1b, GT1b and a number of neutral glycosphingolipids. The main binding epitope for the MAb was, therefore, the terminal N-acetylneuraminic acid 2-3 Gal linked by a beta 1-1 bond to the ceramide, or a beta 1-4 bond to glucose or glucosamine. As shown by immunohistochemical assays, 7c11.e8 antigen was expressed on all melanoma tumour tissues, and on a few samples of colon carcinoma, normal colon, skin, spinal cord, kidney and liver. However, other normal organs such as breast, lung, small intestine, stomach and lymph nodes did not react with the MAb. In the presence of human serum the antibody initiated a strong lysis of melanoma tumour cells in complement-dependent cellular cytotoxicity (CDCC) assays. This study demonstrates that it is possible to isolate human monoclonal antibodies directed to cell surface antigens using viable cell assays in the screening protocol. The preferential binding of 7c11.e8 to melanoma tissues and the reactivity with two of the major melanoma gangliosides (GM3 and GD3) suggest that 7c11.e8 may provide a useful reagent for diagnosis and therapy of malignant melanoma.
Melanoma Res 1993 Dec
PMID:Cell surface reactive human monoclonal antibody directed to human melanoma-associated gangliosides. 816 81

Bovine corneal endothelial cells showed a strong migratory response to specific simple sugars (D-glucose and sucrose, but not L-glucose, sorbitol, lactose, or D-galactose) at concentrations above 10 mM. Checkerboard analysis of the migratory responses in modified Boyden chambers indicated both chemotactic and chemokinetic effects. Serum starvation of the cultures increased the chemotaxis towards D-glucose and 2-deoxy-D-glucose, but not towards sucrose. Migration to sucrose and glucose was inhibited by chelation of extracellular calcium or by inhibition of Na+, K+ ATPase with ouabain. To date, this migratory response has been found only in corneal endothelial cells. Neither human melanoma cells, human breast carcinoma cells, bovine aortic endothelial cells, nor bovine microvascular endothelial cells migrated towards simple sugars, although all cell types migrated toward fibronectin in chemotaxis assays. After 16-19 passages in culture, bovine corneal endothelial cells retained their ability to migrate towards fibronectin, but lost their ability to migrate towards sugars. This loss of migratory response was accompanied by a sevenfold decrease in Na+, K+ ATPase activity. Although loss of Na+, K+ ATPase activity accompanied the loss of migratory response, pretreatment of cell cultures with 25 mM glucose did not stimulate, but rather lowered Na+, K+ ATPase activity in low or high passage cultures.
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PMID:Specific simple sugars promote chemotaxis and chemokinesis of corneal endothelial cells. 822 67

The effects of systems generating active oxygen species (superoxide anion, hydrogen peroxide, hydroxyl radical) on tyrosinase have been studied in cultured human melanoma cells. Tyrosinase activity was determined by measuring the quantity of 5-S-L-cysteinyl-L-dopa (5-S-CD) formed in the presence of D,L-dopa and L-cysteine. In some experiments, the enzyme protein was determined by radio immunoassay [RIA]. Exposure of cells to xanthine/xanthine oxidase or glucose/glucose oxidase resulted in a dose-related elevation of tyrosinase. Catalase, but not superoxide dismutase, prevented this increase indicating that hydrogen peroxide may be the agent responsible for the action, whereas superoxide anion is not involved. Hydroxyl radicals formed by the Haber-Weiss or Fenton type reactions were not found to produce elevation of tyrosinase. Catalase determinations showed no enzyme in the medium but a high concentration in the cells. Inhibition of intracellular catalase by 3-amino-1,2,4-triazole caused an increase in the tyrosinase level. The effects of dopac, xanthine/xanthine oxidase, and glucose/glucose oxidase all producing hydrogen peroxide, and increasing tyrosinase, were enhanced by the inhibition of catalase. It is concluded that hydrogen peroxide, formed by the systems, accounts for the elevation of tyrosinase level. When tyrosinase activities determined by 5-S-CD formation were compared to enzyme amounts found by RIA, the ratios of these values were always constant. This fact indicates that the increase in the tyrosinase activities was not due to an activation of the enzyme, but mirrored the quantities of enzyme protein present in the samples. On the basis of our findings, it is assumed that hydrogen peroxide is a regulator of tyrosinase in normal melanocytes and melanoma cells.
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PMID:Hydrogen peroxide as an inducer of elevated tyrosinase level in melanoma cells. 843 9

Radionuclides are applied in oncology for diagnosis and therapy. The former demands gamma--emitting radionuclides for labeling specific substrates for localizing malignant tissue and for analyzing tumor metabolism in vivo. Here, positron emission tomography (PET) may register in vivo the metabolism, for example, of glucose, amino acids, and receptors and of potentially useful cytotoxic agents. The advantage of the positron emitting radionuclides of carbon, nitrogen and fluorine is the labeling of substrates without changing substrate specificity within the metabolic reaction chain; also, substrate concentration in situ may be quantified. With regard to therapy radionuclides that emit beta- and alpha-particles or decay by electron capture with the Auger effect, are administered in ionic form or with tumor seeking substrates. Examples are radioiodine for treating thyroid malignancy and radiophosphorus for myeloproliferative diseases. Organically bound radionuclides are given as labeled ligands for specific receptors, such as meta-iodo-benzylguanidine (MIBG) for treating the catecholamine producing tumors phaeochromocytoma and neuroblastoma and labeled monoclonal antibodies for tumors specific receptors. Highly localized energy depositions come from Auger emitters such as 125I and by the neutron capture therapy, where boron-10 in the tumor cell is exposed to thermal neutrons for initiating the B10 (n; alpha) Li7 reaction, especially for treating neuro- and glioblastoma and melanoma. Endogenous radiotherapy with radionuclides rely on the success of delivering a proper amount of energy into individual tumor cells with optimal protection of normal tissue. The inevitable heterogeneity of energy deposition events from such approaches demands careful dosimetric assessment for which the classical methods of dosimetry for percutaneous radiotherapy are not applicable.
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PMID:Contributions of nuclear medicine to the therapy of malignant tumors. 844 68

Hepsulfam (sulfamic acid 1,7-heptanediyl ester, NSC 329680) is an alkylating agent currently in Phase I clinical trials. Hepsulfam was developed as an analog of busulfan, an alkylating agent that is used to treat patients with chronic myelogenous leukemia and for marrow ablation prior to bone marrow transplantation. The objective of this study was to identify the spectrum of human tumor cells that were sensitive to hepsulfam. The following three cytotoxicity assays were employed to evaluate the in vitro cytotoxic potential of hepsulfam: 1) primary human tumors were exposed to three levels of hepsulfam for a one hour or continuous exposure, and growth in soft agar was determined; 2) human non-tumor cells and tumor cell lines were compared in an assay that measured the conversion of 14C-glucose to 14CO2 as an index of viability; and 3) the toxicity of hepsulfam to hematopoietic progenitor cells was determined in a progenitor cell colony forming assay. Cytotoxicity was not observed for human tumor cells following one hour hepsulfam exposures; in contrast, marked dose-dependent cytotoxicity was observed with continuous exposures. In human tumor cell lines, the cytotoxicity of hepsulfam was compared directly with busulfan at equimolar concentrations. Hepsulfam was more cytotoxic than busulfan in all cell lines tested. Cytotoxic activity was seen in lung, melanoma, kidney, breast, colon, ovary and brain tumor cells. These results, along with the information obtained from Phase I trials, will facilitate selection of patients who could receive this agent in Phase II efficacy trials.
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PMID:In vitro cytotoxicity of hepsulfam against human tumor cell lines and primary human tumor colony forming units. 845 83


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