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

New 5'-nucleotidase inhibitors named melanocidins A and B were produced by Nocardioides sp. 1681 J. They were isolated from fermentation broth by trichloracetic acid extraction, ethanol precipitation and CM-cellulose and DEAE-cellulose column chromatography. They inhibited 5'-nucleotidase activity from snake venom but not from rat liver membrane at 200 micrograms/ml. They also show antitumor activity against melanoma B16.
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PMID:New 5'-nucleotidase inhibitors, melanocidin A and melanocidin B. I. Taxonomy, fermentation, isolation and biological properties. 299 Nov 79

The influence of ethinylestradiol and the three natural estrogens, i.e. estrone, 17-beta-estradiol and estriol, was studied in a melanoma cell line producing a tissue-type plasminogen activator (t-PA). The cell cultures were exposed to the four estrogens by addition of the steroids dissolved in a weak alcoholic solution to the culture media, in which the released t-PA was assayed by an immunoradiometric method. Ethanol (0.76% w/v) stimulated the t-PA production, while no significant effect of the estrogens in the concentration of 1.7 X 10(-7) M was seen. By tenfold increase in estrogen concentration a highly significant reduction of t-PA levels was recorded in the cultures exposed to ethinylestradiol and 17-beta-estradiol. Estriol differed from these two estrogens in having rather weak inhibitory effect; whereas estrone in this concentration had toxic effect on melanoma cells. It was concluded that the present estrogens, in particular ethinylestradiol and 17-beta-estradiol, had a dose-dependent inhibitory effect on the production of t-PA in melanoma cell culture.
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PMID:Estrogen regulation of tissue plasminogen activator in a human melanoma cell line. 308 11

The influence of progestogens, i.e. medroxyprogesterone, levonorgestrel and norethisterone, was studied in a melanoma cell line producing tissue-type plasminogen activator (t-PA). The cell cultures were exposed to the three progestogens by addition of the steroids dissolved in a weak alcoholic solution to the culture media, in which the released t-PA was assayed by an immunoradiometric method. Ethanol (0.76% w/v) stimulated the t-PA production, while significant inhibitory effect of the present progestogens in the concentration of 1.7 x 10(-6) M was recorded. By tenfold decrease in progestogen concentration significant reduction of t-PA levels was still seen in the cultures exposed to levonorgestrel, while medroxyprogesterone and norethisterone in this dose had no effect on t-PA release. Norethisterone differed from the other two progestogens in having weak toxic effect on melanoma cells. It was concluded that the progestogens studied, in particular norethisterone and levonorgestrel, had an inhibitory effect on the production of t-PA in melanoma cell culture.
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PMID:Progestogen regulation of tissue plasminogen activator in a human melanoma cell line. 312 18

This report describes a method by which mitotic cells were isolated from nonsynchronized Cloudman melanoma cells that had been pulse labeled with 5-bromo-2'-deoxyuridine (BrdUrd) and double-stained with a fluoresceinated monoclonal antibody to BrdUrd and with propidium iodide (PI). In initial experiments, melanoma cells were first pulse labeled with BrdUrd, treated with prostaglandin E1 (PGE1 10 micrograms/m1) or vehicle (0.1% ethanol) for up to 24 hours, then stained with anti-BrdUrd and PI. PGE1-treated cells monitored at 3-hour intervals were observed to migrate from S phase to G2 phase, then, enigmatically, back into the late S phase region of the distribution. In other experiments, cells treated with PGE1 were pulse labeled with BrdUrd at the end of the treatment period and harvested. In these experiments, there was a small, discrete subpopulation of cells within the late S phase region of the DNA distribution that was negative for anti-BrdUrd. This subpopulation of cells was sorted and examined by light microscopy. We observed that 95% of these BrdUrd-negative "S phase" cells were mitotic cells. Since mitotic cells and G2 cells have equivalent amounts of DNA, the reduced red fluorescence exhibited by these cells may be due to a greater sensitivity to denaturation, which has been described for DNA of mitotic cells, and would account for the phenomenon of cells appearing to move "backwards" in the cell cycle. This report indicates that although the BrdUrd/PI method can further define the cell cycle into four compartments, it can also lead to over-estimation of S phase cells in kinetic studies because of contaminating mitotic cells.
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PMID:Differentiation of mitotic melanoma cells from G2 cells and their isolation by use of 5-bromo-2'-deoxyuridine and propidium iodide. 318 Sep 43

Melanoma growth stimulatory activity (MGSA) is an acid and heat stable, auto-stimulatory growth factor which was first isolated from culture medium conditioned by the Hs294T human melanoma cell line. In this report, we describe the purification of MGSA from acid ethanol extracts of Hs294T tumors grown in nude mice using a series of Bio-Gel P30, reverse phase-high performance liquid chromatography and heparin-sepharose steps. This modified procedure provides a 10-fold improved yield of MGSA over previously published procedures. Purified MGSA-stimulated melanoma cell growth in both 3H-thymidine and cell number assays over a concentration range of 0.06 to 6 ng/ml. The MGSA bioactivity was primarily associated with fractions which exhibited molecular weights of 16 and 13-14 Kd based upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Purified platelet-derived growth factor (PDGF), insulin-like growth factor (IGF-1), transforming growth factor-beta (TGF beta), and epidermal growth factor (EGF) in combination with TGF beta did not stimulate 3H-thymidine incorporation in Hs294T cells under the conditions used for MGSA bioassay. Monoclonal antibody to MGSA was used to screen melanoma and benign nevus cultures as well as fixed sectioned tissue for MGSA. The majority of the melanoma cultures were MGSA positive, while most nevus cultures were MGSA negative. However, when fixed sectioned tissue was screened for MGSA immunoreactivity, melanoma tissue was MGSA positive and three-fourths of the benign nevi were MGSA positive. In addition, epidermal keratinocytes and several tissues exhibiting proliferative disorders contained immunoreactive MGSA. These data suggest that MGSA may be a normal regulator of growth and that the microenvironment of the cell may regulate both production of MGSA and response to MGSA.
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PMID:Melanoma growth stimulatory activity: isolation from human melanoma tumors and characterization of tissue distribution. 335 54

The induction of stress proteins was studied in two human and two murine melanoma cell lines. Exposure for 1 h to heat (42 degrees C), to ethanol (6%), to arsenate (100 microM) and to disulfiram (50 microM) induced the expression of SPs with apparent molecular weights of 100, 86, 70-72 and 24-26 Kd. Quantitation of the single SPs indicated that the basal level as well as the enhanced synthesis following the various stressors were different in each cell line. The induction of the 100 Kd species occurred in only one murine melanoma and not in the others. The 86 and in particular the 70-72 Kd species were the most prominent groups, whereas the 24-26 SPs were induced only following arsenate and disulfiram exposure in the three melanoma cell lines. In one of the murine melanomas, the expression of SPs was markedly reduced compared to the other cell lines. No definite specific patterns of SP expression could be identified in tumors of the same histologic type.
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PMID:Induction of stress proteins in murine and human melanoma cell cultures. 370 84

Verapamil had previously been shown to increase cellular melphalan uptake and cytotoxicity in fibrosarcomas, and increased the area under the blood concentration versus time curve (AUC) for melphalan in CBA mice. Verapamil (10 mg kg-1 i.p.) had no effect on the fractional distribution of cardiac output (FDCO), measured with 86Rb-rubidium chloride, to subcutaneous fibrosarcomas. 14C-Melphalan uptake by FS13 fibrosarcomas was increased 60 min after verapamil (10 mg kg-1 i.p.), but not after lower doses which did not affect the AUC. Flunarizine (5 mg kg-1 i.p.) also had no effect on FDCO to FS13 fibrosarcomas, and tended to increase 14C-melphalan content of blood and the fibrosarcomas and to promote growth delay by melphalan. Alcohol increased FDCO to FS13 fibrosarcomas, maximally at a 1:20 dilution in saline, but had no effect on 14C-melphalan uptake or growth delay. Thus, melphalan cytotoxicity correlated with tumour melphalan uptake, and both followed changes in the AUC for melphalan but not changes in FDCO. In these murine fibrosarcomas melphalan uptake and cytotoxicity were not limited by blood flow. In subcutaneous human melanoma HX46 xenografts, verapamil had no effect on the FDCO, nor on 14C-melphalan uptake, and did not affect blood 14C-melphalan levels, suggesting absence of effects on the AUC and on cellular uptake. Alcohol did not increase the FDCO to HX46 xenografts, providing evidence for a different vascular supply.
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PMID:Effects of verapamil and alcohol on blood flow, melphalan uptake and cytotoxicity, in murine fibrosarcomas and human melanoma xenografts. 371 18

Primary malignant melanoma of the esophagus is exceedingly rare. We identified six patients seen at Memorial Hospital for Cancer and Allied Diseases over a period of 35 years. All patients were Caucasian, with an age range of 30 to 74 years (mean: 60 years). There were three men and three women. No association was noted with tobacco or ethanol use, nor was there a personal or family history of malignant melanoma. Symptoms were related to obstruction or hemorrhage. All tumors were polypoid and had attained large size at the time of initial diagnosis. Histologically, the melanomas had epithelioid, spindle-cell, and pleomorphic areas with focal melanin production. An intraepithelial "in situ" component was present in five cases and melanosis of the non-neoplastic esophagus in five. All six neoplasms were immunoreactive for S-100 protein, and none reacted with anticytokeratins. Two cases examined ultrastructurally showed premelanosomes. All patients were treated by esophagogastrectomy. The mean survival for four patients was only 2.1 months. The two remaining patients are alive at 5.5 and 11 months.
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PMID:Primary malignant melanoma of the esophagus. 378 58

A number of nucleoside and nucleotide derivatives of 4-hydroxy-3-beta-D-ribofuranosylpyrazole-5-carboxamide (pyrazofurin, 1) were prepared and tested for their antiviral and cytostatic activity in cell culture. Treatment of 1 with benzyl bromide gave 4-O-benzylpyrazofurin (4). Methylation of 4 with CH2N2 and subsequent removal of the benzyl group by catalytic hydrogenation provided 1-methylpyrazofurin (8). Direct methylation of 1 with CH3I furnished 4-O-methylpyrazofurin (6). Dehydration of the pentaacetylpyrazofurin (9) with phosgene furnished 4-acetoxy-3-(2,3,5-tri-O-acetyl-beta-D-ribofuranosyl)-1-acetylpyrazol e-5-carbonitrile (10). A similar dehydration of the precursor tetraacetyl derivative of 4 gave the corresponding carbonitrile, which on deprotection and subsequent treatment with hydroxylamine furnished 4- (benzyloxy)-3-beta-D-ribofuranosylpyrazole-5-carboxamidoxime (13). Treatment of the tetraacetyl derivative of 4 with Lawesson's reagent and subsequent deacetylation furnished a mixture of 4- (benzyloxy)-3-beta-D-ribofuranosylpyrazole-5-thiocarboxamide (15) and the corresponding nitrile derivative (16). Phosphorylation of unprotected 4 with POCl3 and subsequent debenzylation of the intermediate 17 gave pyrazofurin 5'-phosphate (18), which provided the first chemical synthesis of 18. Similar phosphorylation of 4 with POCl3 and quenching the reaction mixture with either EtOH or MeOH, followed by debenzylation, furnished the 5'-O-(ethyl phosphate) (19b) and 5'-O-(dimethyl phosphate) (20b) derivatives of pyrazofurin. DCC-mediated cyclization of 17, followed by debenzylation, gave pyrazofurin 3',5'-(cyclic)phosphate (21b). The NAD analogue 23b was also prepared by the treatment of 17 with an activated form of AMP in the presence of AgNO3. The structural assignment of 7,8, and 20a were made by single-crystal X-ray analysis, and along with pyrazofurin, their intramolecular hydrogen bond characteristics have been studied. All of these compounds were tested in Vero cell cultures against a spectrum of viruses. Compounds 18 and 23b were active at concentrations very similar to pyrazofurin but are less toxic to the cells than pyrazofurin. Compounds 19b, 20b, and the 3',5'-(cyclic)phosphate 21b are less active than 1. Compounds 18, 19b, 20b, and 23b also exhibited significant inhibitory effects on the growth of L1210 and P388 leukemias and Lewis lung carcinoma cells in vitro, whereas B16 melanoma cells were less sensitive to growth inhibition by these compounds. Pyrazofurin derivatives modified at the 1-, 4-, or 5-position showed neither antiviral nor cytostatic activity in cell culture.
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PMID:Synthesis and biological activity of certain nucleoside and nucleotide derivatives of pyrazofurin. 395 Sep 8

The effect of melatonin on the growth of B16 mice melanoma was examined. Male and female BALB/c athymic mice, inoculated with 7 X 10(4) melanoma cells, were given drinking water containing melatonin (5 micrograms/g body weight/day) and 0.5% ethanol. Compared to control animals the melatonin treated male and female athymic mice had significantly smaller tumors on Day 40. The weights of the testes, the ovaries, and the adrenal glands of melatonin treated mice were significantly reduced compared to control animals. These data indicate that melatonin p.o. significantly inhibited the growth of B16 mouse melanoma and that the antitumor effect of melatonin was associated with a significant decrease in gonadal and adrenal weights.
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PMID:Effect of melatonin on B16 melanoma growth in athymic mice. 402 9


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