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

Ethanol precipitate (70-95%) of the water extract of mouse melanoma (ME) contains suppressors for melanocyte cell division. A fraction which had preferential melanocyte cell line suppressor activity (ME IV2) was shown to inhibit protein synthesis by cell-free systems and RNA synthesis by isolated nuclei of rat liver. The separation and some characterization of the inhibitory factors in ME IV2 were carried out. Upon being boiled, the factor in ME IV2 inhibiting cell-free protein synthesis became inactive, whereas that inhibiting cell-free RNA synthesis remained active. Bio-Gel p-2 column chromatography of ME IV2 gave three distinct fractions (ME IV2-A, -B and -C). ME IV2-A was inhibitory to cell-free protein synthesis but non-inhibitory to cell-free RNA synthesis. On the contrary, ME IV2-B was non-inhibitory to cell-free protein synthesis but inhibitory to cell-free RNA synthesis. ME IV2-C was non-inhibitory to cell-free protein synthesis and seemed to be somewhat inhibitory to cell-free RNA synthesis. Preliminary analyses of the components in these subfractions are also reported.
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PMID:Inhibition of cell-free protein and RNA syntheses by partially purified fractions of mouse melanoma extract. 617 8

The substance fraction precipitated in 81% ethanol from blood or tumour tissue of mice with Lewis (3LL) carcinoma on the 13th, 20th and 32nd day after the tumour transplantation is established to inhibit the processes of proliferation in the cell culture of the same tumour. The fraction isolated on the 7th day after transplantation stimulated the proliferation. No inhibition of proliferation was observed when studying the effect of the same fraction isolated on the 13th and 20th day from blood of mice with B-16 melanoma on the 3LL carcinoma. This fact suggests a tissue-specific action of proliferation inhibitors isolated from blood of mice with Lewis 3LL carcinoma and permits considering them as chalones. An assumption is advanced that the primary tumour synthesizing chalones and secreting them into blood can regulate not only its own growth but also the growth of remoted metastases.
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PMID:[Detection of chalones produced by a primary tumor in the blood of mice with Lewis carcinoma]. 623 16

The effects of various forms of tocopherol (vitamin E) on the growth and differentiation of mouse melanoma (B-16) and mouse fibroblast (L-cells) cells in culture were studied. D-alpha-tocopherol acid succinate induced morphological alterations and growth inhibition in melanoma cells. When vitamin E acid succinate was removed 4 days after treatment, the above changes remained irreversible for a period of 24 hr, after which resistant cells and partially affected cells renewed cell division and eventually reached confluency. The relative efficacy of D and DL forms of vitamin E acid succinate remains to be evaluated. However, other forms of vitamin E such as DL-alpha-tocopherol free alcohol, Aquasol DL-alpha-tocopherol acetate, DL-alpha-tocopherol nicotinate, or sodium succinate with an equivalent volume of ethanol, at similar concentrations, were ineffective. Vitamin E acid succinate at similar concentrations did not induce morphological changes in fibroblasts. Melanoma cells were about 2-fold more sensitive to vitamin E acid succinate than were fibroblasts for the criterion of growth inhibition. Vitamin E acid succinate-induced morphological changes and growth inhibition in melanoma cells were expressed in hormone-supplemented serum-free medium, but the concentration requirement was about 5 times less than that needed in serum-supplemented medium. Although cyclic adenosine 3': 5'-monophosphate-stimulating agents are known to cause growth inhibition and morphological changes in melanoma cells in culture, vitamin E acid succinate-induced morphological alterations in melanoma cells are no mediated by a rise in cellular cyclic adenosine 3':5'-monophosphate. Ethanol was sufficient to increase the melanin content in melanoma cells. These data show that vitamin E acid succinate may be a potentially useful tumor therapeutic agent.
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PMID:Effects of tocopherol (vitamin E) acid succinate on morphological alterations and growth inhibition in melanoma cells in culture. 627 80

Two partially purified fractions of the ethanol precipitate (70-95%) of the water extract of Harding-Passey mouse melanoma, which inhibit protein and DNA syntheses of B-16 melanoma cells in culture, also inhibit protein synthesis in various cell-free systems. By examining their inhibitory effects on limited reactions of protein synthesis, it was found that one of them (ME II) inhibits protein synthesis by blocking aminoacyl-tRNA formation, while the other (ME IV) does not. This inhibition of aminoacyl-tRNA formation was not limited to specific amino acids. Since the amino acid-dependent pyrophosphate (PPi)-ATP exchange reaction catalyzed by aminoacyl-tRNA synthetases was not inhibited, it was concluded that some factor(s) in ME II inhibits amino acid transfer from aminoacyl-AMP to tRNA. ME II contains more than 20 proteins from 10,000 to 90,000 daltons. EDTA treatment of this fraction caused the release of low-molecular substances with inhibitory activity from the proteins. The molecular weights of the active substances are less than 5,000 daltons. The active low-molecular substances are apparently not peptides or nucleotides.
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PMID:Inhibition of aminoacyl-transfer RNA formation by low-molecular substances from melanoma extract. 632 50

The objectives of this study are to demonstrate the specificity of sera from melanoma patients undergoing autologous immunization and to localize melanoma antigens on a cellular level. Five melanoma patients were immunized with autologous melanoma cells and Bacillus Calmette-Guerin. This immunization program was conducted at Tulane University. Indirect immunofluorescence using both viable and fixed melanoma cells was employed. Four of five postimmune sera were reactive to five of seven melanoma cell lines. Two of the four reactive antisera showed positive binding with two additional melanoma lines obtained from other laboratories. All these sera were negative against seven nonmelanoma lines. Negative controls consisted of sera from 65 nonimmunized melanoma patients and 140 nonmelanoma patients. Membrane immunofluorescence (MIF) demonstrated sequential full MIF, capping, polarization, and extrusion of antigen-antibody complexes on the cell surface. MIF inhibition showed shedding of melanoma antigens in the culture medium. Ethanol, methanol, formalin, trichloroacetic acid, and acetone yielded sharp MIF. Isopentane and isooctane gave bright cytoplasmic fluorescence. In conclusion, this study provides suggestive evidence for the existence of common melanoma antigens as defined by the postimmune antimelanoma sera. These antigens may be localized in the membrane or within the cytoplasm.
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PMID:Detection of human malignant melanoma antigens by immunofluorescence and autologous postimmune antimelanoma sera. 637 92

Ethanol-fixed cells stored at 4 degrees C exhibit fixation time-dependent hyperchromatism in comparison with freshly fixed cells when stained with mithramycin and examined by flow cytometry. This hyperchromatism has been found to be temperature-dependent, developing fully within 72 hr at room temperature, and within 2 hr at 37 degrees C. Cells from normal donors that are stained with mithramycin exhibit spurious aneuploid peaks. These spurious aneuploid peaks can be eliminated by incubating ethanol-fixed cells at 37 degrees C for 2 hr prior to staining; true aneuploidy is not affected by this procedure. In rare instances, cytoplasmic fluorescence can be observed in mithramycin-stained cells. In addition, unexplained hypochromatism and hyperchromatism can be observed in some clinical samples, particularly in human melanoma. The effects of these unexplained staining artifacts can be minimized or eliminated by adopting strict criteria for the clinical detection of aneuploidy by flow cytometry.
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PMID:Artifacts associated with mithramycin fluorescence in the clinical detection and quantitation of aneuploidy by flow cytometry. 646 Aug 1

The influence of ethinylestradiol (EE2) and d-norgestrel (d-Ng) was studied in a melanoma cell line producing a tissue-type plasminogen activator (t-PA) very similar to or identical with the t-PA isolated in extracts from human uterus. The cell cultures were exposed to the two contraceptive steroids by addition of EE2 or d-Ng dissolved in a week alcoholic solution to the culture media, in which the released t-PA was assayed by an immunoradiometric method. A strongly stimulating effect of ethanol (0.76% w/v) on the t-PA production was demonstrated. Whereas, EE2 in the concentration of 1.7 X 10(-7)M and d-Ng in the concentration of 8.6 X 10(-7)M both caused a significantly reduced secretion of t-PA, and this effect was independent of whether the cell cultures were grown to confluency in the presence of the two synthetic steroids or not. It was concluded, that the two contraceptive steroids had an inhibitory effect on the production of t-PA in melanoma cell culture.
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PMID:Ethinylestradiol and d-norgestrel regulation of plasminogen activator in a human melanoma cell line. 654 56

SW-13 cells, derived from a human adenocarcinoma of the adrenal cortex, formed only a few small colonies when suspended in soft agar at low cell densities. The number and size of colonies increased dramatically following stimulation with serum-free medium conditioned by SW-13 cells, indicating the possibility of autostimulation in these malignant cells. Evidence is presented suggesting that SW-13 cells form progressively growing soft agar colonies upon stimulation by epithelial tissue-derived growth factor-like polypeptides. Both acid-ethanol extracts and conditioned media from three human carcinoma cell lines (A431, D562, and A549) caused similar increases in colony number and size of SW-13 cells. Extracts from 26 of 32 freshly excised human carcinomas and five freshly excised nonneoplastic human kidneys and one human lung stimulated soft agar growth of SW-13 cells as well. None of the nine extracts from nonepithelial human solid malignant tumors stimulated SW-13 cells. However, a benign nonepithelial tumor (uterine leiomyoma) caused a low level of soft agar growth of SW-13 cells. Cell extract from A204 human sarcoma cells and both conditioned medium and acid-ethanol cell extract from A375 human melanoma cells lacked SW-13 activity, whereas medium conditioned by A204 cells stimulated soft agar growth of SW-13 cells. Chemical and physical treatment data indicated that the epithelial tissue-derived growth factor-like substances are acid- and heat-stable polypeptides with disulfide bonds. The major peak of this activity had an apparent molecular weight of 20,000 to 22,000 and was clearly separable from transforming growth factors reported previously which stimulate colony formation by nontransformed mouse AKR-2B and rat NRK cells. The major peaks of SW-13, NRK, and AKR-2B activity could be separated by high-performance liquid chromatography. This SW-13 activity induced irreversible anchorage-independent growth of SW-13 cells and an increase in DNA synthesis as measured by [3H]thymidine incorporation.
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PMID:Epithelial tissue-derived growth factor-like polypeptides. 657 59

Bioassay-directed fractionation of an EtOH extract of the moss Polytrichum pallidisetum (Polytrichaceae) led to the isolation of three novel benzonaphthoxanthenones, 1-O-methylohioensin B [6], 1-O-methyldihydroohioensin B [7] and 1,14-di-O-methyldihydroohioensin B [8], and two novel cinnamoyl bibenzyls, pallidisetin A [9] and pallidisetin B [10]. Their structures and relative stereochemistry were established by spectral analyses and chemical correlation. Compounds 6-10 exhibited cytotoxic activity against the human tumor cell lines RPMI-7951 melanoma and U-251 glioblastoma multiforme. These two types of compounds could hypothetically be derived from cinnamic acid and bibenzyls through different biogenetic pathways.
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PMID:Ohioensins and pallidisetins: novel cytotoxic agents from the moss Polytrichum pallidisetum. 751 23

Ethanol (20% w/v) given to female C57BL/6 mice in their drinking water reduces splenic natural killer (NK) cell cytolytic activity after 2, 4, and 10 weeks of consumption. This reduction is transient because the levels of NK cell cytotoxicity from ethanol-consuming mice are nearly equal to those of water-drinking mice after splenocytes were incubated in 1000 IU/ml of recombinant interleukin-2 (rIL2) for 16-18 hr. In this study, mice were given 20% w/v ethanol in the drinking water for 2 weeks. Splenic NK cells were enriched up to 88% by negative selection based on surface expression of NK1.1. Enriched NK cells were expanded in rIL2 for 6 days. Lymphokine-activated killer (LAK) cells from both ethanol-consuming and water-drinking mice were > 95% NK1.1+. LAK cell cytolytic activity was significantly lower against NK-insensitive P815 mastocytoma [6.67 +/- 2.18 vs. 17.21 +/- 1.8 lytic units (LUs), p < 0.01], moderately NK-sensitive B16 melanoma (25.3 +/- 6.6 vs. 66.2 +/- 14.2 LU, p < 0.05), and NK-sensitive YAC-1 lymphoma targets (80.5 +/- 34.7 vs. 177.0 +/- 43.6 LU, p < 0.005) in cells from ethanol-consuming mice compared with water-drinking controls. Ethanol consumption did not affect the morphology or phenotype of LAK cells with respect to surface expression of NK1.1, B220, CD3, CD25, CD11a, CD54, CD45RB, or class I major histocompatibility complex.
Alcohol Clin Exp Res 1995 Apr
PMID:Ethanol consumption reduces the cytolytic activity of lymphokine-activated killer cells. 762 74


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