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

Antibody reactivity to melanocyte-derived cells was investigated in patients with alopecia areata or totalis by use of Western blot analysis of detergent-solubilized membrane antigens of a human melanoma cell line, M14. Reactivity was detected in the sera of 9 of 27 alopecia areata or totalis patients, 8 of 13 vitiligo patients, and 6 of 24 normal control subjects. Significant differences between patient and control sera were found in the number and distribution of antibody specificities detected. In vitiligo sera, there was an increased prevalence of reactivity to a melanoma antigen of 52,000 mol wt. In contrast, the predominant specificities in alopecia areata sera were for antigens of 74,500 and 70,800 mol wt, and the majority of positive sera were from patients with total hair loss. These findings suggest that autoreactivity to pigmented cells occurs in certain patients with alopecia areata or totalis.
 ...
PMID:Western blot analysis of serum antibody reactivity with human melanoma cell antigens in alopecia areata and vitiligo. 304 12

The cell membranes of human melanoma express a tumor-associated ganglioside, GD2. We previously established a human melanoma cell line, M14-A, that metastasizes to the lung, liver, skin, lymph nodes, and abdominal organs of nude mice in addition to forming ascites and pleural effusions. We also reported the successful in vitro production of human IgM monoclonal antibody to GD2. In the present study, we evaluated the GD2 expression of human melanoma cells at the primary and metastatic sites and their reactivity to human monoclonal anti-GD2 antibody in vivo. GD2 was expressed strongly on the melanoma cells from both primary and metastatic sites, except for cells from pleural effusions and ascites. When M14-A-bearing nude mice received systemic injections of the human monoclonal antibody, the anti-GD2 titer in the sera was reduced markedly at 2 hours, whereas the reduction was minimal in sera from tumor-free mice and mice bearing GD2-negative human M24 cells. The immune adherence test confirmed that antibody was fixed on cells of primary subcutaneous M14-A tumors and on their metastases to liver, lung, abdominal organs and skin. These results suggest that this large molecule protein can penetrate the blood-tumor barrier and bind immunologically to antigen-positive melanoma cells in vivo.
 ...
PMID:Human IgM monoclonal anti-GD2 antibody: reactivity to a human melanoma xenograft. 308 93

We have isolated and characterized a melanoma tumor-associated antigen (TAA) from the spent culture medium of a melanoma cell line. Its presence has been detected in 72% of different melanoma specimens but not in normal tissues. Because tumor antigens may stimulate or perhaps block immune reactions to cancer cells, their presence on the cell surface may be a critical factor influencing tumor growth. Therefore, to define further the immunobiological characteristics of melanoma TAA, this antigen was investigated by membrane immunofluorescence. Serum from a melanoma patient known to have a high anti-TAA antibody titer was absorbed quantitatively with lymphoblastoid cells autologous to the target melanoma cells to remove non-anti-TAA antibodies. The absorbed serum was reacted with three cultured melanoma cell lines, UCLA-SO-10 (M10), UCLA-SO-14(M), and UCLA-SO-24 (M24). Of these cell lines, M10 and M14 are known to express the antigen as assessed by radioimmunoassay. Reaction of the antibody(s) to the antigen(s) on the melanoma cell surface was detected by fluorescein-conjugated goat anti-human IgG. The reactivity of the absorbed serum was inhibited by preincubation with purified melanoma TAA. These results clearly demonstrate that melanoma TAA is expressed on the cell surface of cultured melanoma cells.
 ...
PMID:Demonstration of a well-characterized tumor-associated antigen on melanoma cell surface. 329 43

N10-Propargyl-5,8-dideazafolic acid (CB 3717), a new antifolate which directly inhibits thymidylate synthase and which is now under early clinical investigation, was compared with methotrexate (MTX) for its antiproliferative activity and mode of action on M14 human melanoma cell line and NIH/3T3 murine fibroblasts transfected with human c-Ha-ras oncogene (NIH/3T3R). CB 3717 was as active as MTX on both cell lines in inhibiting colony formation, but 20-100 times less potent. After 24 h of exposure both drugs caused an accumulation of cells in the G1 phase of the cell cycle, probably because of inhibition of DNA synthesis and blockage at the G1-S boundary. In NIH/3T3R treated for 16 h with 2 microM MTX or 200 microM CB 3717, we found DNA single-strand breaks amounting to approximately 130 and 140 rad equivalents, respectively, and a considerable number of DNA double-strand breaks, far more than expected if they had been the result of the proximity of single-strand breaks on the two complementary DNA strands. No DNA-protein cross-links were detected. When cells were incubated in drug-free medium for 8 h, there was a further accumulation of single-strand breaks, possibly due to the effects of the drug retained intracellularly as polyglutamyl derivative. Simultaneous treatment with 1.77 microM cycloheximide prevented DNA damage produced by both drugs. Thymidine (10 microM), renewed in the culture medium every 24 h, also prevented DNA damage and cytotoxicity. Since after 16 h treatment with MTX or CB 3717 cells were completely viable, as assessed by [3H]thymidine release, trypan blue exclusion test, and 51Cr release, DNA damage appears to be an early event preceding cell death and may be a feature of the killing ability of the drugs. The involvement of a protein in the formation of DNA breaks is suggested by the fact that when protein synthesis was inhibited with cycloheximide DNA damage was no longer seen.
 ...
PMID:Accumulation of DNA strand breaks in cells exposed to methotrexate or N10-propargyl-5,8-dideazafolic acid. 334 74

A human melanoma cell line, M14, was first exposed to a nontoxic dose of Rhodamine-123 (1 microgram/ml) for one hour, then subjected to a treatment with a single mode argon laser at 514.5 nm. The temperature and energy levels delivered to the target cells were determined by a reproducible method of dosimetry. Cell viability was assessed by the Trypan Blue exclusion test. Cell duplication and DNA synthesis were measured by the incorporation of 3H-thymidine at 6 and 24 hours post-treatment. At energy levels and temperatures higher or equal to 950 J/cm2 (40 degrees C), an immediate suppression of DNA synthesis was accompanied by nonviability of the M14 carcinoma cells. At energy levels between 130-900J/cm2 corresponding to temperatures between 28 to 39 degrees C, both an immediate and delayed inhibition of DNA synthesis was noted but the cells remained viable. The results indicate that Rhodamine-123 at nontoxic doses of 1 microgram/ml enhances the tumoricidal effects of the argon laser at reduced temperatures as low as 40 degrees C. Furthermore, at physiological temperature ranges as low as 28 to 30 degrees C, an immediate inhibition of cell duplication was demonstrated while cell viability was not affected. These observations suggest that Rhodamine-123 can be used effectively as a chemosensitizing agent in the treatment of human tumor cells with the argon laser at 514.5 nm.
 ...
PMID:The effects of argon lasers on human melanoma cells sensitized with rhodamine-123 in vitro. 335 83

The inhibition of DNA synthesis in a human malignant melanoma cell line as measured by tritiated thymidine (3H-TdR) incorporation was both time- and temperature dependent. Two components of cell damage were identified: a cytostatic, temporary component from which cells recovered within 2-6 days, and a cytotoxic, permanent component from which no recovery was observed. Thermotolerance was induced in M14 cells by sublethal heat treatment at 41 degrees C for 1 hr. However, induction of thermotolerance was blocked by indomethacin, a prostaglandin synthetase inhibitor. Exogenous PGE2 at concentrations up to 10 micrograms/ml also protected cells from heat damage. These data suggest that prostaglandin synthesis increases during heat stress and may play a role in protecting cells from thermal damage.
 ...
PMID:Thermal resistance of human malignant melanoma modulated by prostaglandin E2. 342 97

The human melanoma cell line M14 has been proven in previous experiments to be much less sensitive to the action of heat (42 degrees C, 60 min) than other melanoma lines. In the present study, we have investigated the possibility of increasing the effect of heat by means of drug treatment. Thermochemotherapy was applied to exponentially growing cells according to different schedulings, and was analyzed in its efficacy by measuring the impairment of the cellular colony-forming ability. Findings of the present study point out that: (a) appropriate sequencing between hyperthermia and cis-diamminedichloroplatinum II(DDP), melphalan (L-Pam), 1,2,4-dichlorobenzyl-1H-indazol-3-carboxylic acid (LNA) or 5-3,3-dimethyl-1-triazeno-imidazole-4-carboxamide (DTIC) strongly influences the cytotoxic effect of the two agents; and (b) the optimal combination appears to be the simultaneous application of heat and drugs. However, as far as thermochemotherapy with DDP is concerned, a synergistic effect may also be achieved when hyperthermia precedes DDP.
 ...
PMID:Effect of sequential application of hyperthermia and chemotherapy on the survival of a thermoresistant human melanoma cell line. 343 95

A murine monoclonal antibody (mAb), designated mAb 202, was generated using a human melanoma cell line, UCLASO-M14 as the immunogen. mAb 202 reacted with two (GM2 and GM3) of the four (GM2, GM3, GD2, and GD3) gangliosides expressed by M14. Several authentic monosialogangliosides, including GM4, GM3, GM2, GM1, GM1b, and sialylparagloboside were then tested for their binding to 202 mAb by the immune adherence inhibition assay, TLC-enzyme immunostaining, and enzyme-linked immunosorbent assay. All showed positive binding but in varying degrees. GM4 showed the strongest affinity. No significant differences of reactivity were observed between the sialic acid derivatives, N-acetyl and N-glycolyl, in these gangliosides. Disialogangliosides such as GD3, GD2, GD1a, and GD1b, trisialoganglioside GT1b, and neutral glycolipids including GlcCer, GalCer, LacCer, GbOs3Cer, GbOs4Cer, GgOs3Cer, GgOs4Cer, and nLcOs4Cer were all negative. These results indicate that the 202 mAb detects sialyl alpha 2----3Gal residue in the monosialoganglioside, irrespective of the internal structure. Since GM4 is not expressed by M14 cells, the terminal disaccharide (sialyl alpha 2----3Gal) in GM3 and/or GM2 must have been the epitope responsible for the generation of the antibody.
 ...
PMID:Monoclonal antibody detects monosialogangliosides having a sialic acid alpha 2----3-galactosyl residue. 357 Dec 88

Lonidamine (LND), an indazole-carboxylic acid derivative, was delivered alone and together with adriamycin (ADM) or hyperthermia to the human melanoma cell line M14, and cell survival was assessed. Cell cycle-specific effects were investigated by analyzing sequences of DNA content histograms by means of a suitable mathematical procedure. LND delivered for 1 h at a dose of 50 micrograms/ml did not affect proliferation and survival of the cells. Exposure of the cells for 1 h to ADM (1.0 microgram/ml) followed by LND for 1 h (50 micrograms/ml) produced the highest effect on the survival. Kinetic parameters were affected by the combined treatment slightly more than by ADM exposure alone. Simultaneous delivery of LND (50 micrograms/ml) with hyperthermia (42 degrees C, 1 h) reduced the survival and enhanced the block of cells in the G2M phase, as compared with the heat treatment alone. The effect of the treatments on cell survival appeared to be related to the perturbation of the G2M phase of the cycle.
 ...
PMID:Kinetic and survival response of the M14 cell line to lonidamine associated with adriamycin or hyperthermia. 362 1

Challenge of human A375 melanoma cells with sodium arsenite induced the synthesis of stress proteins and stimulated [3H]mannose incorporation into a novel component migrating on sodium dodecyl sulfate-polyacrylamide gel electrophoresis with an apparent molecular mass of 14 kDa (designated M14). Enhanced M14 expression was elicited by heavy metals (zinc, copper, cadmium, and nickel), thiol-reactive agents (iodoacetamide and auranofin), and hyperthermia. The kinetics of M14 induction and recovery from stress were similar to those of the stress proteins, but M14 half-life was only 15 min. Incorporation of [3H]mannose into M14 was inhibited by tunicamycin but not by cycloheximide or actinomycin D. M14 was metabolically labeled with [32P]orthophosphate but not by [35S] methionine or [3H]asparagine. Further studies revealed that M14 was selectively soluble in chloroform/methanol/water (10:10:3) and sensitive to both endo-beta-N-acetylglucosaminidase H digestion and mild acid hydrolysis. The latter released a water-soluble mannose-labeled moiety which eluted from Bio-Gel P-6 in a manner similar to Glc3Man9GlcNAc2. Together, these data suggest that M14 is a lipid-oligosaccharide intermediate of N-linked protein glycosylation and that enhanced expression of this class of molecule in response to chemical insults and hyperthermia is a newly described cellular reaction to stress.
 ...
PMID:Alterations in lipid-linked oligosaccharide metabolism in human melanoma cells concomitant with induction of stress proteins. 366 5


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>