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)

Previous 31P-magnetic resonance spectroscopy (31P-MRS) studies have suggested that the spin-lattice relaxation time (T1) of the inorganic phosphate (Pi) resonance is shorter in well-oxygenated than in poorly oxygenated tumors. Amelanotic human melanoma xenografts were therefore subjected to 31P-MRS to investigate whether the T1 of the Pi resonance might be a useful parameter for assessment of tumor oxygenation status. It was searched for possible correlations between the T1 of the Pi resonance and oxygen tension or parameters closely related to oxygen tension, including 31P-MRS tumor energy status and blood supply per viable tumor cell. Oxygen tension, tumor energy status, and blood supply per viable tumor cell decreased with increasing tumor volume. In contrast to previous suggestions, the T1 of the Pi resonance decreased with increasing tumor volume and decreasing oxygen tension, tumor energy status, and blood supply per viable tumor cell, possibly because the tumors developed necrotic regions concomitantly with the decrease in oxygenation status, resulting in increased concentrations of freely dissolved para-magnetic ions in the tissue. Consequently, the T1 of the Pi resonance can probably not be utilized to estimate the oxygenation status of tumors, at least not in tumors with necrotic regions.
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PMID:Spin-lattice relaxation time of inorganic phosphate in human tumor xenografts measured in vivo by 31P-magnetic resonance spectroscopy. Influence of oxygen tension. 777 20

In the present experiments we planned to ascertain whether an abnormal production of nitric oxide (NO) by human CHP100 neuroblastoma cells in culture following stimulation of N-methyl-D-aspartate (NMDA) receptors, produced lethal effects in co-cultured human BMEL melanoma cells. Human BMEL melanoma cells in culture were found to be positive to the nicotinamide adenine dinucleotide phosphate diaphorase (NADPH diaphorase) histochemical reaction and produced NO as revealed by measurements of nitrite under basal culture conditions. Exposure for 50 min to aspartate (1-2 mM) or to NMDA (0.5-1.5 mM) did not evoke significant melanoma cell death. The dose of 1.0 mM NMDA applied for 1 min to BMEL cell cultures did not increase significantly nitrite concentrations in comparison to controls. Incubation for 50 min of human CHP100 neuroblastoma cells with NMDA (0.5-1.5 mM) elicited dose-dependent death of BMEL melanoma cells co-cultured in trans-wells. Under these experimental conditions, nitrite levels in cell culture-inserts containing melanoma cells increased by 120% 1 min after application of the excitotoxin (1 mM) to CHP100 neuroblastoma cultures. The lethal effects produced in BMEL cell culture-inserts by application of NMDA (1.0 mM) to CHP100 cultures were prevented by pretreatment of neuroblastoma cultures with MK801 (200 nM). Similar protection was also afforded by N omega-nitro-L-arginine methyl ester (L-NAME; 0.2 mM) and N omega-monomethyl-L-arginine (L-NMMA; 0.2 mM), two inhibitors of nitric oxide synthase, and by haemoglobin (10 microM), a nitric oxide trapping agent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:N-methyl-D-aspartate-induced excessive formation of nitric oxide in CHP100 neuroblastoma cells produces death of BMEL melanoma cells in co-culture. 783 19

Phosphorus spin-lattice relaxation times (T1s) were measured in vivo by 31P-nuclear magnetic resonance spectroscopy in tumors from four amelanotic human melanoma xenograft lines grown subcutaneously in BALB/c-nu/nu mice. The T1s were analyzed in relation to tumor volume, fractional tumor water content, and fraction of necrotic tumor tissue. The following resonances were studied: phosphomonoesters (PME), inorganic phosphate (Pi), phosphodiesters (PDE), phosphocreatine (PCr), and nucleoside triphosphates gamma, alpha, and beta (NTP gamma, alpha, and beta). Two different techniques were used to measure the T1s: superfast inversion recovery (SUFIR) and conventional inversion recovery (IR). The SUFIR and IR methods gave similar results. Tumors in the volume range 100-3000 mm3 were studied. The PME, Pi, PDE, and PCr resonances showed significantly longer T1s than the NTP gamma, alpha, and beta resonances at small tumor volumes. The T1s at small tumor volumes also differed significantly between the tumor lines. The T1s either decreased or remained unchanged with increasing tumor volume; the volume-dependence of the T1s differed significantly between the tumor lines but not between the resonances. Calculations based on the T1s measured here indicated that the errors in PCr/Pi and NTP beta/Pi resonance ratios due to partial saturation can vary with tumor volume but are usually < 20% at a repetition time of 2.0 s and < 15% at a repetition time of 3.0 s. There was no correlation between the T1s and fractional tumor water content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:31P-nuclear magnetic resonance spectroscopy in vivo of four human melanoma xenograft lines: spin-lattice relaxation times. 793 79

Microwave oven (mwo) is used to stimulate tissue fixation and to retrieve antigens damaged by fixation. Heavy metal salt solutions, water, and citric acid buffer (cab) have been suggested for this purpose. A serie of tumors treated with cab and phosphate-buffered saline (pbs) with mwo were studied immunohistochemically with 24 antibodies. Controls were treated in the same way, except for microwaving. The antibodies were directed against antigens of the following tumors: breast and prostate carcinoma, carcinoid, lymphoma and melanoma. The results showed that cab enhanced the immunoreactivity of the following antigens: estrogen receptors (AMAC), progesterone receptors (Novocastra), HMB45, vimentin, leukocyte common antigen, PCNA, p53, MIB-1 (Ki-67) and prostatic specific antigen. The antigens that did not improve their immunoreactivity, when compared with the control series were: factor VIII, keratin, Leu 22, L26, neuron-specific enolase, CEA, chromogranin, HBME-1, smooth muscle actin and EMA. Microwaving equally improved protein S100 and desmin either with cab or pbs. The only antigen that improved with pbs was actin. The results with B72.3 and NKI/C3 were poor and not reliable. In conclusion microwaving with cab enhances the immunoreactivity of the antibodies mentioned above leading to an increase in sensibility without loosing specificity.
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PMID:[Antigen retrieval by microwave oven with buffer of citric acid]. 799 28

Neoplastic meningitis due to the dissemination of systemic cancer or primary central nervous system tumors through the cerebrospinal fluid carries a very poor prognosis. Current treatments for this disease are ineffective, and new therapeutic modalities such as immunotoxins may be beneficial. We created an animal model of human carcinomatous meningitis with LOX melanoma-derived tissue-culture cells in athymic rats for testing the efficacy of intrathecal therapy with transferrin-Pseudomonas exotoxin A (Tfn-PE) immunotoxin. An injection of 5 x 10(5) LOX cells into the intrathecal space through an indwelling catheter resulted in the reproducible development of lower-extremity paraplegia at 9.24 +/- 1.77 days because of focal deposits of tumor growth adjacent to the thoracic and lumbar spinal cord. A dose of 2.5 or 5 micrograms of intrathecal Tfn-PE immunotoxin was neurotoxic and resulted in the deaths of 8 of 10 animals within 24 hours. Histological evidence of central nervous system damage was seen as hemorrhagic degeneration around the central canal or a pathological cleft at the level of the cervical spinal cord. Because no neurotoxicity was seen with 1 microgram of intrathecal Tfn-PE immunotoxin, this dose was administered in treatment experiments. Twenty-four hours after the intrathecal instillation of LOX cells, 10 animals received intrathecally either 1 microgram of Tfn-PE or phosphate-buffered saline with 0.1% human serum albumin (control group).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo efficacy of intrathecal transferrin-Pseudomonas exotoxin A immunotoxin against LOX melanoma. 800 62

Liposomes consisting of dicetyl-phosphate, cholesterol, lecithin and stearic or myristic or oleic acid, exert a protective effect for mice against experimental infection by Salmonella typhimurium, and delay both the onset and mortality B16 melanoma in these animals. Liposomes labelled with 3H-myristic acid were used as probes in the spleen and liver. We found that the treatment schedule rather than route of administration of liposomes, is important. The results show that in order to induce protection, preventive treatment must start at least three days before. Longer treatments do not increase the degree of protection, and treatments started at the same time as, or following experimental infection or tumor transplantation, have no effect.
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PMID:Beneficial effects of myristic, stearic or oleic acid as part of liposomes on experimental infection and antitumor effect in a murine model. 804 Dec 29

Antimelanoma effects of 4-S-cysteaminylphenol (4-S-CAP), which is a newly synthesized melanin precursor, as a chemotherapeutic agent specific to malignant melanoma were determined in an in vivo system using mouse B16 melanoma. The intraperitoneal injection of 4-S-CAP induced a slight delay in the growth period of subcutaneous melanoma of C57BL/6 mice. Survival times of mice after treatment with 4-S-CAP were a little longer than those of control mice (P < 0.05), although all mice died from the local growth of tumours. The viable cell ratio of in vivo subcutaneous tumour cells reduced to 52.8% within 24 h after treatment with 4-S-CAP, but the ratio had recovered to the control level 72 h after treatment (> 90%). Similarly, the proliferating-cell-nuclear-antigen-positive cell ratio of melanotic melanoma had reduced 24 h after treatment and recovered within 72 h after treatment, while 4-S-CAP had no effect on amelanotic tumours. The formation of lung colonies by intravenous inoculation of malignant melanoma cells was compared between mice with intraperitoneal injection of 4-S-CAP and phosphate-buffered saline only. The 4-S-CAP-treated mice had significantly fewer lung colonies compared with the control mice (P < 0.01). The results indicate that the agent, 4-S-CAP, would have a therapeutic effect on malignant melanoma for a short time in vivo and therefore the agent can be effective against a small number of tumour cells, such as lung colonies, although it had little effect on the local tumours.
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PMID:In vivo antimelanoma effects of 4-S-cysteaminylphenol, a newly synthesized therapeutic agent specific to melanoma. 809 88

Sphingosine-1-phosphate (Sph-1-P), the initial product of Sph catabolism, inhibited chemotactic motility of a few lines of tumor cells [(1992) Proc. Natl. Acad. Sci. USA 89, 9686]. We now report that Sph-1-P even at very low concentration (10-100 nM) inhibits integrin-dependent motility of melanoma cells induced by extracellular matrix (ECM), although it did not affect integrin-dependent adhesion to ECM. Other Sph-related compounds tested (including sphinganine-1-P) were much less effective than Sph-1-P at inhibiting motility, and also had no effect on integrin-dependent adhesion of tumor cells to ECM. Our findings suggest that Sph-1-P inhibits actin filament reorganization by affecting cytoplasmic connection integrin in ECM-stimulated motility of melanoma cells.
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PMID:Sphingosine-1-phosphate inhibits extracellular matrix protein-induced haptotactic motility but not adhesion of B16 mouse melanoma cells. 811 17

On addition of [4,5-3H]sphinganine 1-phosphate to human fibroblast monolayers, the label was efficiently removed from the culture medium. In contrast with the reported stability of phosphorylated sphingenine in 3T3 cells [Desai, Zhang, Olivera, Mattie and Spiegel (1992). J. Biol. Chem. 267, 23122-23128] and B16 melanoma cells [Sadahira, Ruan, Hakomuri and Igarashi (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 9686-9690], sphinganine 1-phosphate appeared to be subjected to a fast and extensive metabolism in fibroblasts, the major pathways being cleavage and dephosphorylation. The first of these pathways, catalysed by sphingosine-phosphate lyase, resulted in the formation of labelled palmitaldehyde, which was recovered, mainly after oxidation, in glycerophospholipids in an ester bond. A smaller part of the palmitaldehyde was reduced and incorporated in alk(en)ylphospholipids. Dephosphorylation of spinganine 1-phosphate, a hitherto overlooked pathway catalysed by an unknown phosphatase(s), gave rise to sphinganine, which was converted by N-acylation into ceramide and then incorporated in spingomyelin and glycosphingolipids.
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PMID:Sphinganine 1-phosphate metabolism in cultured skin fibroblasts: evidence for the existence of a sphingosine phosphatase. 819 48

In this study, we examined the effect of triflavin, an Arg-Gly-Asp (RGD)-containing snake venom peptide, on human cervical carcinoma (HeLa) cell- and B16-F10 mouse melanoma cell-induced platelet aggregation (TCIPA) in heparinized platelet-rich plasma. TCIPA appears to play an important role in the development of certain experimental tumor metastases. Two ADP-scavenging agents, apyrase (10 U/ml) and creatine phosphate (CP) (5 mM)/creatine phosphokinase (CPK) (5 U/ml) completely inhibited B16-F10 TCIPA, but hirudin (5 U/ml) had no effect. In contrast, apyrase and CP/CPK did not inhibit HeLa TCIPA while hirudin completely inhibited it. Furthermore, HeLa cells initially induced platelet aggregation and then blood coagulation at a later stage. In addition, HeLa cells shortened, in a concentration-dependent manner, the recalcification time of normal as well as factor VIII- and IX-deficient human plasma, but did not affect the recalcification time of factor VII-deficient plasma. This suggests that HeLa TCIPA occurs via activation of the extrinsic pathway, probably owing to tumor cell expression of tissue factor-like activity. HeLa cell-induced thrombin generation was confirmed by detection of amidolytic activity towards a chromogenic substrate, S-2238 (H-D-Phe-Pip-Arg-p-NA). Triflavin and GRGDS inhibited, in a dose-dependent manner, TCIPA caused by either cell line. On a molar basis, triflavin was 10,000-30,000 times more potent than GRGDS in this regard. Moreover, monoclonal antibodies raised against glycoprotein (GP) IIb/IIIa complex (i.e., 7E3 and AP2) and against GP Ib (i.e., AP1) completely inhibited HeLa TCIPA. 7E3 and AP2 inhibited B16-F10 TCIPA by up to 80% whereas AP1 showed only 30% inhibition of B16-F10 TCIPA. In conclusion, the inhibitory effect of triflavin on HeLa and B16-F10 TCIPA may be mediated principally by the binding of triflavin to the fibrinogen receptor associated with GP IIb/IIIa complex on the platelet surface. However, GP Ib is also involved in HeLa TCIPA as thrombin formation is the key factor in triggering platelet aggregation caused by HeLa cells.
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PMID:Triflavin, an Arg-Gly-Asp-containing peptide, inhibits tumor cell-induced platelet aggregation. 822 81


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