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1. Ferrer P, Asensi M, Segarra R, Ortega A, Benlloch M, Obrador E, Varea MT, Asensio G, Jordá L, Estrela JM: Association between pterostilbene and quercetin inhibits metastatic activity of B16 melanoma. Neoplasia; 2005 Jan;7(1):37-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between pterostilbene and quercetin inhibits metastatic activity of B16 melanoma.
  • In vitro growth of highly malignant B16 melanoma F10 cells (B16M-F10) is inhibited (56%) by short-time exposure (60 min/day) to PTER (40 microm) and QUER (20 microm) (approximate mean values of plasma concentrations measured within the first hour after intravenous administration of 20 mg/kg each polyphenol).
  • Our findings demonstrate that the association of PTER and QUER inhibits metastatic melanoma growth and extends host survival.
  • [MeSH-major] Liver Neoplasms / drug therapy. Melanoma, Experimental / drug therapy. Phenols / therapeutic use. Quercetin / therapeutic use. Stilbenes / therapeutic use

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  • (PMID = 15736313.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alpha4beta1; 0 / Nitrates; 0 / Nitrites; 0 / Phenols; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Stilbenes; 0 / Vascular Cell Adhesion Molecule-1; 537-42-8 / pterostilbene; 9IKM0I5T1E / Quercetin; BBX060AN9V / Hydrogen Peroxide
  • [Other-IDs] NLM/ PMC1490314
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2. Miyano-Kurosaki N, Kurosaki K, Hayashi M, Takaku H, Hayafune M, Shirato K, Kasuga T, Endo T, Tomoda A: 2-aminophenoxazine-3-one suppresses the growth of mouse malignant melanoma B16 cells transplanted into C57BL/6Cr Slc mice. Biol Pharm Bull; 2006 Nov;29(11):2197-201
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  • [Title] 2-aminophenoxazine-3-one suppresses the growth of mouse malignant melanoma B16 cells transplanted into C57BL/6Cr Slc mice.
  • Since phenoxazine is an essential structure of actinomycin D, which exerts a strong anticancer effect, we examined the anticancer effect of 2-aminophenoxazine-3-one (Phx-3) on mouse malignant melanoma B16 cells in vitro and in vivo.
  • Phx-3 inhibited proliferation of the B16 cells in a dose-dependent manner in vitro.
  • We furthermore studied the in vivo effects of Phx-3 on mouse malignant melanoma B16 cells transplanted in female C57BL/6Cr Slc mice.
  • Treatment with Phx-3 (0.5 mg/kg) completely suppressed the growth of mouse malignant melanoma B16 cells transplanted in mice as compared with the control group.
  • These results suggest that Phx-3 may be used to treat patients affected by malignant melanoma in future.
  • [MeSH-major] Cell Proliferation / drug effects. Melanoma, Experimental / prevention & control. Oxazines / pharmacology

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  • (PMID = 17077514.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Oxazines; 1916-59-2 / 3-aminophenoxazone; AYI8EX34EU / Creatinine; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
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3. Ferrer P, Asensi M, Priego S, Benlloch M, Mena S, Ortega A, Obrador E, Esteve JM, Estrela JM: Nitric oxide mediates natural polyphenol-induced Bcl-2 down-regulation and activation of cell death in metastatic B16 melanoma. J Biol Chem; 2007 Feb 2;282(5):2880-90
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  • [Title] Nitric oxide mediates natural polyphenol-induced Bcl-2 down-regulation and activation of cell death in metastatic B16 melanoma.
  • Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity.
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Line, Tumor. Endothelium, Vascular / physiology. Endothelium, Vascular / physiopathology. Hydrogen Peroxide / metabolism. Male. Melanoma. Mice. Mice, Inbred C57BL. Mitochondrial Membranes / physiology. Neoplasm Metastasis. Nitrates / metabolism. Nitrites / metabolism. Polyphenols. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17135264.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Nitrates; 0 / Nitrites; 0 / Phenols; 0 / Polyphenols; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 31C4KY9ESH / Nitric Oxide; BBX060AN9V / Hydrogen Peroxide
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4. Murozuka Y, Kasuya MC, Kobayashi M, Watanabe Y, Sato T, Hatanaka K: Efficient sialylation on azidododecyl lactosides by using B16 melanoma cells. Chem Biodivers; 2005 Aug;2(8):1063-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficient sialylation on azidododecyl lactosides by using B16 melanoma cells.
  • To establish the optimal condition for the bioproduction of a large amount of valuable materials containing GM3-type oligosaccharides, two kinds of lactoside primers having the azido group in different positions were synthesized and introduced into B16 melanoma cells.
  • These results represent the optimal conditions that are necessary for the mass production of GM3-type oligosaccharide using azidododecyl lactoside primers and B16 cells.
  • [MeSH-major] Glycosphingolipids / chemistry. Glycosphingolipids / metabolism. Melanoma, Experimental / metabolism

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  • (PMID = 17193190.001).
  • [ISSN] 1612-1880
  • [Journal-full-title] Chemistry & biodiversity
  • [ISO-abbreviation] Chem. Biodivers.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Glycosphingolipids
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5. Gatouillat G, Balasse E, Joseph-Pietras D, Morjani H, Madoulet C: Resveratrol induces cell-cycle disruption and apoptosis in chemoresistant B16 melanoma. J Cell Biochem; 2010 Jul 1;110(4):893-902
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resveratrol induces cell-cycle disruption and apoptosis in chemoresistant B16 melanoma.
  • In this study, we show that resveratrol (0-500 microM) inhibits the growth of a doxorubicin-resistant B16 melanoma cell subline (B16/DOX) (IC(50) = 25 microM after 72 h, P < 0.05).
  • The G(1)-phase arrest of cell cycle in resveratrol-treated (10-100 microM) B16/DOX cells was followed by the induction of apoptosis, which was revealed by pyknotic nuclei and fragmented DNA.
  • Resveratrol also potentiated at subtoxic dose (25 microM for 24 h) doxorubicin cytotoxicity in the chemoresistant B16 melanoma (P < 0.01).
  • When administered to mice, resveratrol (12.5 mg/kg) reduced the growth of an established B16/DOX melanoma and prolonged survival (32% compared to untreated mice).
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Melanoma, Experimental / pathology. Stilbenes / pharmacology

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  • [Copyright] J. Cell. Biochem. 110: 893-902, 2010. (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20564188.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Stilbenes; 80168379AG / Doxorubicin; Q369O8926L / resveratrol
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6. Sun B, Zhang S, Zhang D, Yin X, Wang S, Gu Y, Wang Y: Doxycycline influences microcirculation patterns in B16 melanoma. Exp Biol Med (Maywood); 2007 Nov;232(10):1300-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Doxycycline influences microcirculation patterns in B16 melanoma.
  • To examine the effects of doxycycline on invasion-related protein expression and proliferation of melanoma cells and to evaluate its effect on microcirculation patterns in melanoma, we injected murine melanoma B16 cell suspensions into the groin areas of C57BL/6 mice that were randomly divided into treatment and control groups.
  • Doxycycline treatment partly suppressed the growth of engrafted B16 melanoma, with an inhibition rate of 35.63%.
  • Doxycycline inhibits the growth of engrafted melanoma and results in reduced expression of MMP-2, MMP-9, and VM formations.
  • [MeSH-major] Doxycycline / pharmacology. Melanoma, Experimental / blood supply. Microcirculation / drug effects

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  • (PMID = 17959842.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.- / Matrix Metalloproteinases; N12000U13O / Doxycycline
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7. Lee YS, Kim DW, Kim S, Choi HI, Lee Y, Kim CD, Lee JH, Lee SD, Lee YH: Downregulation of NFAT2 promotes melanogenesis in B16 melanoma cells. Anat Cell Biol; 2010 Dec;43(4):303-9
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  • [Title] Downregulation of NFAT2 promotes melanogenesis in B16 melanoma cells.
  • Western blot analysis was performed to investigate the expression of NFAT2 protein in B16 melanoma cells.
  • Our data showed that NFAT2 expression was increased in the hypopigmented B16 cells, while tyrosinase and MITF expression was decreased.
  • To investigate the potential role of NFAT2, the recombinant adenovirus expressing microRNA specific for NFAT2 was transduced into the cultured B16 melanoma cells.

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  • (PMID = 21267404.001).
  • [ISSN] 2093-3673
  • [Journal-full-title] Anatomy & cell biology
  • [ISO-abbreviation] Anat Cell Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC3026182
  • [Keywords] NOTNLM ; B16 melanoma cells / Cyclosprorin A / Melanocyte / Melanogenesis / NFAT2
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8. Curran MA, Montalvo W, Yagita H, Allison JP: PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors. Proc Natl Acad Sci U S A; 2010 Mar 2;107(9):4275-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors.
  • Vaccination with irradiated B16 melanoma cells expressing either GM-CSF (Gvax) or Flt3-ligand (Fvax) combined with antibody blockade of the negative T-cell costimulatory receptor cytotoxic T-lymphocyte antigen-4 (CTLA-4) promotes rejection of preimplanted tumors.
  • Here, we show that the combination of CTLA-4 and PD-1 blockade is more than twice as effective as either alone in promoting the rejection of B16 melanomas in conjunction with Fvax.
  • Combination blockade also synergistically increases Teff-to-myeloid-derived suppressor cell ratios within B16 melanomas.

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  • (PMID = 20160101.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Cancer Vaccines; 0 / Pdcd1 protein, mouse; 0 / Programmed Cell Death 1 Receptor; 82115-62-6 / Interferon-gamma; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse
  • [Other-IDs] NLM/ PMC2840093
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9. Matsuda H, Nakashima S, Oda Y, Nakamura S, Yoshikawa M: Melanogenesis inhibitors from the rhizomes of Alpinia officinarum in B16 melanoma cells. Bioorg Med Chem; 2009 Aug 15;17(16):6048-53
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  • [Title] Melanogenesis inhibitors from the rhizomes of Alpinia officinarum in B16 melanoma cells.
  • The 80% aqueous acetone extract from the rhizomes of Alpinia officinarum, a Chinese medicinal herb, were found to inhibit melanogenesis in theophylline-stimulated murine B16 melanoma 4A5 cells.
  • [MeSH-major] Alpinia / chemistry. Antineoplastic Agents / chemistry. Enzyme Inhibitors / chemistry. Melanoma, Experimental / drug therapy. Monophenol Monooxygenase / antagonists & inhibitors

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  • (PMID = 19615910.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Kaempferols; 0 / kaempferide; 142FWE6ECS / galangin; EC 1.- / Oxidoreductases; EC 1.14.18.- / tyrosinase-related protein-1; EC 1.14.18.1 / Monophenol Monooxygenase
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10. Ohguchi K, Akao Y, Nozawa Y: Involvement of calpain in melanogenesis of mouse B16 melanoma cells. Mol Cell Biochem; 2005 Jul;275(1-2):103-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Involvement of calpain in melanogenesis of mouse B16 melanoma cells.
  • In the current study, the involvement of calpain, a cysteine proteinase in the regulation of melanogenesis was examined using mouse B16 melanoma cells.
  • In response to alpha-melanocyte-stimulating hormone (a-MSH), B16 melanoma cells underwent differentiation characterized by increased melanin biosynthesis.
  • Treatment of B16 cells with ALLN caused marked decrease in both tyrosinase protein and mRNA levels.
  • These results indicate that calpain would be involved in the melanogenic signaling by modulating the expression of tyrosinase in mouse B16 melanoma cells.
  • [MeSH-minor] Animals. Blotting, Western. Calcium-Binding Proteins / pharmacology. Cell Differentiation / drug effects. Cysteine Proteinase Inhibitors / pharmacology. Electrophoresis, Polyacrylamide Gel. Hormones / pharmacology. Indolequinones / analysis. Leupeptins / pharmacology. Melanins / biosynthesis. Melanoma, Experimental. Mice. Monophenol Monooxygenase / analysis. Monophenol Monooxygenase / metabolism. RNA, Messenger / metabolism. Tumor Cells, Cultured. alpha-MSH / pharmacology

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  • (PMID = 16335789.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Cysteine Proteinase Inhibitors; 0 / Hormones; 0 / Indolequinones; 0 / Leupeptins; 0 / Melanins; 0 / RNA, Messenger; 110044-82-1 / acetylleucyl-leucyl-norleucinal; 3571-34-4 / dopachrome; 581-05-5 / alpha-MSH; 79079-11-1 / calpastatin; EC 1.14.18.1 / Monophenol Monooxygenase; EC 3.4.22.- / Calpain
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11. Williams P, Rafei M, Bouchentouf M, Raven J, Yuan S, Cuerquis J, Forner KA, Birman E, Galipeau J: A Fusion of GMCSF and IL-21 Initiates Hypersignaling Through the IL-21Rα Chain With Immune Activating and Tumoricidal Effects In Vivo. Mol Ther; 2010 Jul;18(7):1293-1301

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • B16 melanoma cells gene-enhanced to produce GIFT-21 were immune rejected by syngeneic C57Bl/6 mice comparable to the effect of IL-21 alone.
  • However, a significant GIFT-21-driven survival advantage was seen when NOD-SCID mice were implanted with GIFT-21-secreting B16 cells, consistent with a meaningful role of macrophages in tumor rejection.

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  • [Copyright] Copyright © 2010 The American Society of Gene & Cell Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28178447.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Koo JH, Kim HT, Yoon HY, Kwon KB, Choi IW, Jung SH, Kim HU, Park BH, Park JW: Effect of xanthohumol on melanogenesis in B16 melanoma cells. Exp Mol Med; 2008 Jun 30;40(3):313-9
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  • [Title] Effect of xanthohumol on melanogenesis in B16 melanoma cells.
  • Xanthohumol (XH), the principal prenylflavonoid of the hop plant (Humulus lupulus L.), dose-dependently inhibited isobutylmethylxanthine (IBMX)-induced melanogenesis in B16 melanoma cells, with little cytotoxicity at the effective concentrations.
  • [MeSH-minor] 1-Methyl-3-isobutylxanthine / pharmacology. Animals. Cell Line. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation. Drug Antagonism. Flavonoids. Intramolecular Oxidoreductases / antagonists & inhibitors. Intramolecular Oxidoreductases / biosynthesis. Melanoma, Experimental. Membrane Glycoproteins / antagonists & inhibitors. Membrane Glycoproteins / biosynthesis. Mice. Microphthalmia-Associated Transcription Factor / antagonists & inhibitors. Microphthalmia-Associated Transcription Factor / biosynthesis. Monophenol Monooxygenase / antagonists & inhibitors. Monophenol Monooxygenase / biosynthesis. Monophenol Monooxygenase / genetics. Oxidoreductases / antagonists & inhibitors. Oxidoreductases / biosynthesis. Signal Transduction / drug effects. alpha-MSH / metabolism

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  • (PMID = 18587269.001).
  • [ISSN] 1226-3613
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Melanins; 0 / Membrane Glycoproteins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Mitf protein, mouse; 0 / Propiophenones; 1F7A44V6OU / Colforsin; 581-05-5 / alpha-MSH; EC 1.- / Oxidoreductases; EC 1.14.18.- / Tyrp1 protein, mouse; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase; T4467YT1NT / xanthohumol; TBT296U68M / 1-Methyl-3-isobutylxanthine
  • [Other-IDs] NLM/ PMC2679287
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13. Wei J, Xiong Y: Inhibitory effect of recombinant fibronectin polypeptide CH50 on invasion and metastasis of melanoma B16 cells. J Huazhong Univ Sci Technolog Med Sci; 2007 Feb;27(1):17-9
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  • [Title] Inhibitory effect of recombinant fibronectin polypeptide CH50 on invasion and metastasis of melanoma B16 cells.
  • In order to investigate the inhibitory effect and mechanism of recombinant polypeptide CH50 on invasion and metastasis of melanoma B16 cells, the recombinant polypeptide CH50 was separated and purified by ion exchange chromatographic technique.
  • The melanoma B16 cells treated with purified CH50 were cultured in vitro, the number was counted at 4, 24, 48 and 72 h and their morphological changes were observed in order to detect their adhesion and spreading abilities.
  • In in vivo study, the melanoma B16 cells were labeled with CFSE and treated with CH50 and then they were injected into mice via mouse-tail veins.
  • Accumulation and invasion abilities of B16 cells on lung tissues were observed under the fluorescent microscopy.
  • The results showed that the morphological character of B16 cells treated with CH50 changed greatly and the number of B16 cells treated with CH50 decreased significantly (P<0.05).
  • The adhesion and spreading abilities of B16 cells treated with CH50 were weakened obviously and the metastasis foci on lung tissues reduced.
  • It was concluded that the recombinant polypeptide CH50 inhibited invasion and metastasis of melanoma B16 cells on tissues and could be a prospective bio-product in tumor general therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Fibronectins / pharmacology. Melanoma, Experimental / pathology. Neoplasm Invasiveness / prevention & control. Neoplasm Metastasis / prevention & control. Recombinant Proteins / pharmacology

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  • (PMID = 17393099.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CH50 recombinant polypeptide; 0 / Fibronectins; 0 / Recombinant Proteins
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14. Triba MN, Starzec A, Bouchemal N, Guenin E, Perret GY, Le Moyec L: Metabolomic profiling with NMR discriminates between biphosphonate and doxorubicin effects on B16 melanoma cells. NMR Biomed; 2010 Nov;23(9):1009-16
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  • [Title] Metabolomic profiling with NMR discriminates between biphosphonate and doxorubicin effects on B16 melanoma cells.
  • The metabolomic profiles of B16 melanoma cells were investigated in vitro with high resolution-magic angle spinning proton magnetic resonance spectroscopy and OPLS multivariate statistical analyse.
  • We compared the profiles for untreated melanoma B16-F10 cells and Ca(2+) chelating EGTA, doxorubicin or BP7033 bisphosphonate treated cells.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Bone Density Conservation Agents / therapeutic use. Diphosphonates / therapeutic use. Doxorubicin / therapeutic use. Magnetic Resonance Spectroscopy / methods. Melanoma, Experimental. Metabolomics / methods

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  • (PMID = 20963798.001).
  • [ISSN] 1099-1492
  • [Journal-full-title] NMR in biomedicine
  • [ISO-abbreviation] NMR Biomed
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 80168379AG / Doxorubicin
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15. Ohguchi K, Koike M, Suwa Y, Koshimizu S, Mizutani Y, Nozawa Y, Akao Y: Inhibitory effects of whisky congeners on melanogenesis in mouse B16 melanoma cells. Biosci Biotechnol Biochem; 2008 Apr;72(4):1107-10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effects of whisky congeners on melanogenesis in mouse B16 melanoma cells.
  • We examined the effect of whisky congeners, substances other than ethanol in whisky, on melanogenesis in mouse B16 melanoma cells.
  • [MeSH-major] Alcoholic Beverages. Flavonoids / pharmacology. Melanins / biosynthesis. Melanoma, Experimental / metabolism. Phenols / pharmacology

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  • (PMID = 18391453.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Melanins; 0 / Phenols; 0 / Polyphenols; 581-05-5 / alpha-MSH; EC 1.14.18.1 / Monophenol Monooxygenase
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16. Koo JH, Lee I, Yun SK, Kim HU, Park BH, Park JW: Saponified sunflower and safflower oils inhibit melanogenesis in B16 melanoma cells. Mol Med Rep; 2010 Mar-Apr;3(2):281-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Saponified sunflower and safflower oils inhibit melanogenesis in B16 melanoma cells.
  • Saponified sunflower (sap-SU) and safflower (sap-SA) oils dose-dependently inhibited isobutylmethylxanthine-induced melanogenesis in B16 melanoma cells, with no cytotoxicity.

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  • (PMID = 21472234.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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17. Sitdikova SM, Amandzholov BS, Kiselevskii MV, Donenko FV: Specificity of relapses and metastases of experimental transplanted Ehrlich carcinoma and B16 melanoma. Bull Exp Biol Med; 2007 Jan;143(1):80-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specificity of relapses and metastases of experimental transplanted Ehrlich carcinoma and B16 melanoma.
  • Experiments on female (CBAxC57Bl/6)F1 mice with simultaneously transplanted Ehrlich carcinoma and B16 melanoma showed that removal of one of the primary nodes led to metastasizing of the removed tumor alone.
  • [MeSH-major] Carcinoma, Ehrlich Tumor / secondary. Melanoma, Experimental / secondary

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  • (PMID = 18019019.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Ohguchi K, Ito M, Yokoyama K, Iinuma M, Itoh T, Nozawa Y, Akao Y: Effects of sesquiterpene lactones on melanogenesis in mouse B16 melanoma cells. Biol Pharm Bull; 2009 Feb;32(2):308-10
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  • [Title] Effects of sesquiterpene lactones on melanogenesis in mouse B16 melanoma cells.
  • In this study, we examined the effect of sesquiterpene lactones isolated from Calea urticifolia and Tanacetum parthenium (feverfew) on melanogenesis in mouse B16 melanoma cells.
  • In response to 3-isobutyl-1-methylxanthin (IBMX), B16 melanoma cells underwent differentiation characterized by increased melanin biosynthesis.
  • Treatment of B16 cells with 2,3-epoxyjuanislamin elicited significant decreases in tyrosinase protein and mRNA levels.
  • [MeSH-major] Lactones / pharmacology. Melanins / biosynthesis. Melanoma, Experimental / metabolism. Sesquiterpenes / pharmacology

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  • (PMID = 19182396.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Lactones; 0 / Melanins; 0 / Phosphodiesterase Inhibitors; 0 / Plant Extracts; 0 / Sesquiterpenes; EC 1.14.18.1 / Monophenol Monooxygenase; TBT296U68M / 1-Methyl-3-isobutylxanthine
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19. Huang X, Yamada Y, Kidoya H, Naito H, Nagahama Y, Kong L, Katoh SY, Li WL, Ueno M, Takakura N: EphB4 overexpression in B16 melanoma cells affects arterial-venous patterning in tumor angiogenesis. Cancer Res; 2007 Oct 15;67(20):9800-8
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  • [Title] EphB4 overexpression in B16 melanoma cells affects arterial-venous patterning in tumor angiogenesis.
  • Here we found that overexpression of EphB4 in B16 melanoma cells suppressed tumor growth in a s.c. transplantation tumor model.
  • Histologic examination of these tumors revealed that EphB4 overexpression in B16 cells selectively suppressed arterial ephrinB2+ EC development.
  • By coculturing ephrinB2-expressing SV40-transformed mouse ECs (SVEC) with EphB4-overexpressing B16 cells, we found that EphB4 induced the apoptosis of SVECs.
  • However, ephrinB2 did not induce the apoptosis of EphB4-overexpressing B16 cells.
  • Based on results from these experiments, we concluded that EphB4 overexpression in B16 tumor cells suppresses the survival of arterial ECs in tumors by a reverse signaling via ephrinB2.
  • [MeSH-major] Melanoma, Experimental / blood supply. Receptor, EphB4 / biosynthesis

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  • (PMID = 17942910.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Ephrin-B2; EC 2.7.1.- / Ephb4 protein, mouse; EC 2.7.10.1 / Receptor, EphB4
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20. Seo WG, Hwang JC, Kang SK, Jin UH, Suh SJ, Moon SK, Kim CH: Suppressive effect of Zedoariae rhizoma on pulmonary metastasis of B16 melanoma cells. J Ethnopharmacol; 2005 Oct 3;101(1-3):249-57
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  • [Title] Suppressive effect of Zedoariae rhizoma on pulmonary metastasis of B16 melanoma cells.
  • The inhibitory effect of Curcuma zedoaria Roscoe (WE-CZ) on experimental pulmonary metastasis of B16 melanoma cells was investigated.
  • When the duration of WE-CZ intake was examined, survival time was not affected by pre-intake before B16 melanoma cell inoculation and was slightly extended by post-intake after B16 melanoma cell inoculation, although the life span was prolonged by intake throughout the experiment.
  • The elevated NO was found to serve as a cytotoxic mediator against B16 melanoma cells in co-culture with macrophages.
  • On the contrary, B16 melanoma-conditioned medium reduced NO production by macrophages.
  • These findings indicate that WE-CZ possesses anti-migratory effects on B16 melanoma cells and that the macrophage function-modulating activity by WE-CZ appears to underlie its anti-metastatic activity, which leads to a decrease in the number of lung metastatic surface nodules and the extension of life span.
  • [MeSH-major] Curcuma. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Melanoma, Experimental / drug therapy. Phytotherapy. Plant Extracts / therapeutic use

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  • (PMID = 16023317.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Plant Extracts; 31C4KY9ESH / Nitric Oxide
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21. Chang TS, Lin JJ: Inhibitory effect of danazol on melanogenesis in mouse B16 melanoma cells. Arch Pharm Res; 2010 Dec;33(12):1959-65
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  • [Title] Inhibitory effect of danazol on melanogenesis in mouse B16 melanoma cells.
  • In the present study, more than 200 generic drugs were screened to verify their applicability as a skin-lightening agent using mouse B16 melanoma cells.
  • Of the numerous agents, danazol was found to inhibit melanogenesis in B16 cells in a dose-dependent manner with an IC(50) value of 9.3 μM.
  • In addition, danazol reduced cellular tyrosinase activity in B16 cells but did not directly inhibit the murine tyrosinase activity in the cell-free system.
  • Western blotting analysis confirmed that danazol downregulated the levels of tyrosinase protein in B16 cells, and reverse-transcription polymerase chain reaction (RT-PCR) analysis revealed that danazol did not downregulate the levels of tyrosinase mRNA in the cells.
  • These results indicate that danazol inhibits melanogenesis in B16 cells via reducing the tyrosinase activity by post-transcriptional regulation.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell-Free System / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Drug Evaluation, Preclinical. High-Throughput Screening Assays. Melanoma, Experimental. Mice. Monophenol Monooxygenase / genetics. Monophenol Monooxygenase / metabolism. RNA, Messenger / metabolism. Transcription, Genetic

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  • (PMID = 21191761.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Melanins; 0 / RNA, Messenger; EC 1.14.18.1 / Monophenol Monooxygenase; N29QWW3BUO / Danazol
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22. Nakashima S, Matsuda H, Oda Y, Nakamura S, Xu F, Yoshikawa M: Melanogenesis inhibitors from the desert plant Anastatica hierochuntica in B16 melanoma cells. Bioorg Med Chem; 2010 Mar 15;18(6):2337-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Melanogenesis inhibitors from the desert plant Anastatica hierochuntica in B16 melanoma cells.
  • The methanolic extract from the whole plants of Anastatica hierochuntica, an Egyptian herbal medicine, was found to inhibit melanogenesis in theophylline-stimulated murine B16 melanoma 4A5 cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brassicaceae / chemistry. Enzyme Inhibitors / pharmacology. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology. Plant Extracts / pharmacology

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • [RepublishedFrom] Bioorg Med Chem. 2010 Jan 1;18(1):182-9 [19963390.001]
  • (PMID = 20189399.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Corrected and Republished Article; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Membrane Glycoproteins; 0 / Plant Extracts; 0 / RNA, Messenger; EC 1.- / Oxidoreductases; EC 1.14.18.- / Tyrp1 protein, mouse; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
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23. Lee YS, Kim HK, Lee KJ, Jeon HW, Cui S, Lee YM, Moon BJ, Kim YH, Lee YS: Inhibitory effect of glyceollin isolated from soybean against melanogenesis in B16 melanoma cells. BMB Rep; 2010 Jul;43(7):461-7
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  • [Title] Inhibitory effect of glyceollin isolated from soybean against melanogenesis in B16 melanoma cells.
  • We found that glyceollin inhibits melanin synthesis and tyrosinase activity in B16 melanoma cells without cytotoxicity.
  • Additionally, glyceollin effectively inhibited intracellular cAMP levels in B16 melanoma cells stimulated by alpha-melanocyte stimulating hormone (alpha-MSH).
  • These results suggest that the whitening activity of glyceollin may be due to the inhibition of cAMP involved in the signal pathway of alpha-MSH in B16 melanoma cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclic AMP / metabolism. Intramolecular Oxidoreductases / antagonists & inhibitors. Intramolecular Oxidoreductases / metabolism. Melanoma, Experimental / enzymology. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / antagonists & inhibitors. Monophenol Monooxygenase / metabolism. Oxidoreductases / antagonists & inhibitors. Oxidoreductases / metabolism. Signal Transduction. alpha-MSH / metabolism

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  • (PMID = 20663406.001).
  • [ISSN] 1976-670X
  • [Journal-full-title] BMB reports
  • [ISO-abbreviation] BMB Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Cosmetics; 0 / Melanins; 0 / Pterocarpans; 581-05-5 / alpha-MSH; 6461TV6UCH / glyceollin; E0399OZS9N / Cyclic AMP; EC 1.- / Oxidoreductases; EC 1.14.18.- / tyrosinase-related protein-1; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
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24. Yang Z, Cox JL: Cathepsin L increases invasion and migration of B16 melanoma. Cancer Cell Int; 2007;7:8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cathepsin L increases invasion and migration of B16 melanoma.
  • METHODS: We have examined the role of cathepsin L in highly metastatic B16F10 murine melanoma cells through genetic antisense constructs of cathepsin L.
  • The effects of cathepsin L antisense were examined for melanoma cell proliferation, invasion, migration and adhesion.
  • Cathepsin L contributed to melanoma cell invasion and also augmented melanoma cell migration.
  • Finally, the inhibition of melanoma cell migration via down-regulation of cathepsin L appears to be independent of cystatin C expression.
  • CONCLUSION: This study shows that cathepsin L facilitates high metastatic B16 melanoma cell invasion and migration.

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  • (PMID = 17488522.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1885792
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25. Yun CY, Kim D, Lee WH, Park YM, Lee SH, Na M, Jahng Y, Hwang BY, Lee MK, Han SB, Kim Y: Torilin from Torilis japonica inhibits melanin production in alpha-melanocyte stimulating hormone-activated B16 melanoma cells. Planta Med; 2009 Nov;75(14):1505-8
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  • [Title] Torilin from Torilis japonica inhibits melanin production in alpha-melanocyte stimulating hormone-activated B16 melanoma cells.
  • Torilin dose-dependently inhibited melanin production, with an IC(50) value of 25 microM, in alpha-melanocyte stimulating hormone (alpha-MSH)-activated B16 melanoma cells.
  • [MeSH-major] Apiaceae / chemistry. Dermatologic Agents / pharmacology. Melanins / biosynthesis. Melanoma, Experimental. Plant Extracts / pharmacology. Skin Pigmentation / drug effects

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  • [Copyright] Georg Thieme Verlag KG Stuttgart, New York.
  • (PMID = 19533579.001).
  • [ISSN] 1439-0221
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Dermatologic Agents; 0 / Melanins; 0 / Plant Extracts; 0 / Sesquiterpenes, Guaiane; 0 / torilin; 581-05-5 / alpha-MSH; C5INA23HXF / Arbutin; EC 1.14.18.1 / Monophenol Monooxygenase
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26. Sato K, Takahashi H, Iraha R, Toriyama M: Down-regulation of tyrosinase expression by acetylsalicylic acid in murine B16 melanoma. Biol Pharm Bull; 2008 Jan;31(1):33-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down-regulation of tyrosinase expression by acetylsalicylic acid in murine B16 melanoma.
  • Therefore, we investigated the effect of ASA on melanin production using B16 murine melanoma cells and demonstrated a new biological effect of ASA.
  • In the presence of alpha-melanocyte stimulating hormone (alpha-MSH), B16 melanoma cells are stimulated to enhance melanin synthesis.
  • ASA (2 mM) inhibited alpha-MSH-enhanced melanin synthesis in melanoma more strongly than other well-known anti-melanogenic agents such as arbutin (2 mM) and kojic acid (200 microM).
  • [MeSH-major] Aspirin / pharmacology. Melanoma, Experimental / enzymology. Monophenol Monooxygenase / antagonists & inhibitors

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  • (PMID = 18175938.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Melanins; 63-84-3 / Dihydroxyphenylalanine; EC 1.14.18.1 / Monophenol Monooxygenase; R16CO5Y76E / Aspirin
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27. Yamaoka Y, Ohguchi K, Itoh T, Nozawa Y, Akao Y: Effects of theaflavins on melanin biosynthesis in mouse b16 melanoma cells. Biosci Biotechnol Biochem; 2009 Jun;73(6):1429-31
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  • [Title] Effects of theaflavins on melanin biosynthesis in mouse b16 melanoma cells.
  • In this study, we examined the effects of theaflavins, polyphenols in black tea, on alpha melanocyte-stimulating hormone (alphaMSH)-induced melanogenesis in mouse B16 melanoma cells.
  • [MeSH-major] Biflavonoids / pharmacology. Catechin / pharmacology. Melanins / biosynthesis. Melanoma, Experimental / metabolism

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  • (PMID = 19502752.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biflavonoids; 0 / DNA Primers; 0 / Melanins; 0 / RNA, Messenger; 1IA46M0D13 / theaflavin; 8R1V1STN48 / Catechin; EC 1.14.18.1 / Monophenol Monooxygenase
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28. Arung ET, Yoshikawa K, Shimizu K, Kondo R: Isoprenoid-substituted flavonoids from wood of Artocarpus heterophyllus on B16 melanoma cells: cytotoxicity and structural criteria. Fitoterapia; 2010 Mar;81(2):120-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isoprenoid-substituted flavonoids from wood of Artocarpus heterophyllus on B16 melanoma cells: cytotoxicity and structural criteria.
  • A structure-activity investigation of the effect of these isolated compounds (1-9) and structurally related compounds on B16 melanoma cells indicated that isoprenoid moiety substitutions in flavonoids enhance their cytotoxicity, and that the position of attachment and the number of isoprenoid-substituent moieties per molecule influence flavonoid cytotoxicity.
  • [MeSH-major] Artocarpus / chemistry. Flavonoids / pharmacology. Melanoma, Experimental / drug therapy. Plant Extracts / pharmacology. Skin Neoplasms / drug therapy

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  • [Copyright] 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19686821.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Plant Extracts; 0 / Terpenes
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29. Kline J, Brown IE, Zha YY, Blank C, Strickler J, Wouters H, Zhang L, Gajewski TF: Homeostatic proliferation plus regulatory T-cell depletion promotes potent rejection of B16 melanoma. Clin Cancer Res; 2008 May 15;14(10):3156-67
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  • [Title] Homeostatic proliferation plus regulatory T-cell depletion promotes potent rejection of B16 melanoma.
  • EXPERIMENTAL DESIGN: B16 melanoma cells were engineered to express the model SIYRYYGL (SIY) antigen to enable immune monitoring.
  • To determine whether Treg depletion could synergize with homeostatic proliferation, RAG2-/- mice received total or CD25-depleted T cells, followed or preceded by B16.SIY challenge.
  • RESULTS: Adoptive transfer of total splenic T cells into RAG2-/- mice moderately affected the growth rate of B16.SIY.
  • Interestingly, transfer of CD25-depleted T cells into RAG2-/- mice resulted in potent rejection of B16 melanoma in both prophylactic and short-term preimplanted tumor settings and was associated with maintained T-cell effector function.
  • [MeSH-major] Cell Proliferation. Homeostasis / immunology. Immunotherapy, Adoptive / methods. Lymphocyte Depletion. Melanoma, Experimental / therapy. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 18483384.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA97296; United States / NCI NIH HHS / CA / R01 CA118153
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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30. Sato K, Morita M, Ichikawa C, Takahashi H, Toriyama M: Depigmenting mechanisms of all-trans retinoic acid and retinol on B16 melanoma cells. Biosci Biotechnol Biochem; 2008 Oct;72(10):2589-97
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  • [Title] Depigmenting mechanisms of all-trans retinoic acid and retinol on B16 melanoma cells.
  • We assessed the effects of ATRA and retinol on melanogenesis in murine B16 melanoma cells.
  • In the present study, ATRA and retinol inhibited melanin synthesis in melanoma cells stimulated by alpha-melanocyte stimulating hormone (alpha-MSH) or 3-isobutyl-1-methylxanthine (IBMX).
  • [MeSH-major] Melanoma / metabolism. Pigmentation / drug effects. Tretinoin / pharmacology. Vitamin A / pharmacology

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  • (PMID = 18838813.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Melanins; 11103-57-4 / Vitamin A; 5688UTC01R / Tretinoin; EC 1.14.18.1 / Monophenol Monooxygenase
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31. Hongo T, Miyano-Kurosaki N, Kurosaki K, Hata A, Harigae S, Tomoda A: 2-aminophenoxazine-3-one prevents pulmonary metastasis of mouse B16 melanoma cells in mice. J Pharmacol Sci; 2010;114(1):63-8
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  • [Title] 2-aminophenoxazine-3-one prevents pulmonary metastasis of mouse B16 melanoma cells in mice.
  • 2-Aminophenoxazine-3-one (Phx-3) induced cellular apoptosis in mouse melanoma B16 cells as detected by DNA laddering and upregulated Fas expression in the cells in vitro.
  • When B16 melanoma cells were injected into the tail veins of mice, significant metastasis of the cells was indicated in the lungs, 14 days after treatment.
  • In contrast, when 0.5 mg/kg Phx-3 was administered to mice through the tail veins, once simultaneously with or every three days after the administration of B16 melanoma cells, the number of metastasized pulmonary cells was extremely reduced.
  • The present results indicate that the metastasis of mouse B16 melanoma cells to the lung was significantly inhibited in mice administered Phx-3, which activated the intrinsic and extrinsic apoptotic pathways.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Melanoma, Experimental / prevention & control. Melanoma, Experimental / secondary. Oxazines / therapeutic use

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  • (PMID = 20710120.001).
  • [ISSN] 1347-8648
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oxazines; 1916-59-2 / 3-aminophenoxazone
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32. Lv N, Koo JH, Yoon HY, Yu J, Kim KA, Choi IW, Kwon KB, Kwon KS, Kim HU, Park JW, Park BH: Effect of Angelica gigas extract on melanogenesis in B16 melanoma cells. Int J Mol Med; 2007 Nov;20(5):763-7
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  • [Title] Effect of Angelica gigas extract on melanogenesis in B16 melanoma cells.
  • During the screening of herbs for inhibition of melanogenesis, it was observed that ethanolic extract of Angelicae Gigantis Radix (AGE) effectively inhibited isobutylmethylxanthine-induced melanogenesis in B16 melanoma cells.
  • [MeSH-major] Apiaceae / chemistry. Melanins / biosynthesis. Melanoma / metabolism

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  • (PMID = 17912471.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Melanins; 0 / Plant Extracts; 0 / RNA, Messenger; 1F7A44V6OU / Colforsin; 581-05-5 / alpha-MSH; EC 1.14.18.1 / Monophenol Monooxygenase; TBT296U68M / 1-Methyl-3-isobutylxanthine
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33. Chen J, Peng H, Ou-Yang X, He X: Research on the antitumor effect of ginsenoside Rg3 in B16 melanoma cells. Melanoma Res; 2008 Oct;18(5):322-9
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  • [Title] Research on the antitumor effect of ginsenoside Rg3 in B16 melanoma cells.
  • To further explore the antitumor function of Rg3, we investigated the in-vitro and in-vivo activity of Rg3 in the treatment of B16 melanoma cells, derived from C57BL/6 mouse, capable of forming tumor colonies in the lungs following intravenous injection.
  • B16 melanoma-bearing mice were used to evaluate in vivo the antitumor activity of Rg3.
  • This research might supply valuable data for chemotherapy with Rg3 in melanoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Proliferation / drug effects. Ginsenosides / therapeutic use. Lung Neoplasms / drug therapy. Melanoma, Experimental / drug therapy

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  • (PMID = 18781130.001).
  • [ISSN] 1473-5636
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ginsenosides; 0 / Proto-Oncogene Proteins c-bcl-2; 14197-60-5 / ginsenoside Rg3; EC 3.4.22.- / Caspase 3
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34. Kim KS, Kim JA, Eom SY, Lee SH, Min KR, Kim Y: Inhibitory effect of piperlonguminine on melanin production in melanoma B16 cell line by downregulation of tyrosinase expression. Pigment Cell Res; 2006 Feb;19(1):90-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effect of piperlonguminine on melanin production in melanoma B16 cell line by downregulation of tyrosinase expression.
  • In the present study, piperlonguminine from Piper longum was discovered to inhibit melanin production in melanoma B16 cells stimulated with alpha-melanocyte stimulating hormone (alpha-MSH), 3-isobutyl-1-methylxanthine or protoporphyrin IX, where the compound exhibited stronger depigmenting efficacy than kojic acid.
  • Surprisingly, piperlonguminine did not inhibit the catalytic activity of cell-free tyrosinase from melanoma B16 cells but rather suppressed tyrosinase mRNA expression.

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  • (PMID = 16420250.001).
  • [ISSN] 0893-5785
  • [Journal-full-title] Pigment cell research
  • [ISO-abbreviation] Pigment Cell Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Diglycerides; 0 / Dioxolanes; 0 / Melanins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Phosphodiesterase Inhibitors; 0 / Plant Extracts; 0 / Protoporphyrins; 0 / RNA, Messenger; 553-12-8 / protoporphyrin IX; 581-05-5 / alpha-MSH; 86390-77-4 / 1-oleoyl-2-acetylglycerol; EC 1.14.18.1 / Monophenol Monooxygenase; HN39MC8KIO / piperlonguminine; TBT296U68M / 1-Methyl-3-isobutylxanthine
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35. Ohguchi K, Akao Y, Nozawa Y: Stimulation of melanogenesis by the citrus flavonoid naringenin in mouse B16 melanoma cells. Biosci Biotechnol Biochem; 2006 Jun;70(6):1499-501
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stimulation of melanogenesis by the citrus flavonoid naringenin in mouse B16 melanoma cells.
  • In this study, we examined the effect of naringenin on melanogenesis in mouse B16 melanoma cells.
  • [MeSH-major] Citrus / chemistry. Flavanones / pharmacology. Melanins / metabolism. Melanoma / metabolism

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  • (PMID = 16794334.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Flavanones; 0 / Melanins; HN5425SBF2 / naringenin
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36. D'Agostini C, Pica F, Febbraro G, Grelli S, Chiavaroli C, Garaci E: Antitumour effect of OM-174 and cyclophosphamide on murine B16 melanoma in different experimental conditions. Int Immunopharmacol; 2005 Jul;5(7-8):1205-12
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  • [Title] Antitumour effect of OM-174 and cyclophosphamide on murine B16 melanoma in different experimental conditions.
  • We report that OM-174, a purified water soluble diphosphorylated and triacetylated lipid A derived from E. coli, is able to reduce tumour progression and to prolong the survival of mice in the B16 melanoma experimental model.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cyclophosphamide / therapeutic use. Lipopolysaccharides / therapeutic use. Melanoma, Experimental / drug therapy

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  • (PMID = 15914325.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lipopolysaccharides; 8N3DW7272P / Cyclophosphamide; HC3530GGGG / defoslimod
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37. Sato K, Toriyama M: Effect of pyrroloquinoline quinone (PQQ) on melanogenic protein expression in murine B16 melanoma. J Dermatol Sci; 2009 Feb;53(2):140-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of pyrroloquinoline quinone (PQQ) on melanogenic protein expression in murine B16 melanoma.
  • OBJECTIVE: In this study, we assessed the effects of PQQ on melanogenic protein expression of murine B16 melanoma cells.
  • METHODS: We assessed melanin production of PQQ-treated B16 melanoma cells.
  • RESULTS: In the present study, PQQ inhibited melanin synthesis in cultured melanoma cells stimulated by either alpha-melanocyte stimulating hormone (alpha-MSH) or 3-isobutyl-1-methylxanthine (IBMX).
  • [MeSH-major] Melanins / biosynthesis. Melanoma, Experimental / enzymology. Monophenol Monooxygenase / metabolism. PQQ Cofactor / pharmacology. Pigmentation / drug effects

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  • (PMID = 19013771.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Melanins; 0 / Membrane Glycoproteins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Mitf protein, mouse; 0 / RNA, Messenger; 581-05-5 / alpha-MSH; 72909-34-3 / PQQ Cofactor; EC 1.- / Oxidoreductases; EC 1.14.18.- / Tyrp1 protein, mouse; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase; TBT296U68M / 1-Methyl-3-isobutylxanthine
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38. Ohshima Y, Tsukimoto M, Takenouchi T, Harada H, Suzuki A, Sato M, Kitani H, Kojima S: gamma-Irradiation induces P2X(7) receptor-dependent ATP release from B16 melanoma cells. Biochim Biophys Acta; 2010 Jan;1800(1):40-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] gamma-Irradiation induces P2X(7) receptor-dependent ATP release from B16 melanoma cells.
  • Here, we examined gamma-irradiation-induced ATP release and its mechanism in B16 melanoma.
  • To investigate mechanism of radiation-induced ATP release, we pharmacologically inhibited the ATP release and established stable P2X(7) receptor-knockdown B16 melanoma cells using two short hairpin RNAs targeting P2X(7) receptor.
  • Our results indicate that gamma-irradiation evokes ATP release from melanoma cells, and P2X(7) receptor channel plays a significant role in mediating the ATP release.
  • [MeSH-minor] Animals. Cell Line, Tumor. Extracellular Space / drug effects. Extracellular Space / metabolism. Extracellular Space / radiation effects. Immunoblotting. Melanoma, Experimental / genetics. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Purinergic P2 Receptor Antagonists. RNA Interference. Receptors, Purinergic P2X7. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19854240.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Purinergic P2 Receptor Antagonists; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X7; 8L70Q75FXE / Adenosine Triphosphate
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39. Voigt H, Houben R, Schrama D, Hofmann UB, Vetter-Kauczok CS, Becker JC: Matrix metalloproteinase induction in the tumor stroma does not depend on CD147 expression in murine B16 melanoma. Tumour Biol; 2007;28(4):229-37

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Matrix metalloproteinase induction in the tumor stroma does not depend on CD147 expression in murine B16 melanoma.
  • METHODS AND RESULTS: To address the impact of CD147 on MMP expression in the murine B16 melanoma model, we consequently stably knocked down CD147 expression in two B16 sublines.
  • Coculture of melanoma cells with different fibroblast cell lines demonstrated that neither CD147+ nor CD147- B16 tumor cells altered the expression of MMP-2 or MMP-9 by the fibroblasts, although we could confirm the susceptibility of these fibroblasts for MMP induction.
  • CONCLUSIONS: At least for the murine B16 melanoma model, CD147 expression on tumor cells seems not to be crucial for MMP-2, MMP-9 and MT1-MMP induction on tumor-associated stromal cells.
  • [MeSH-major] Antigens, CD147 / biosynthesis. Gene Expression Regulation, Neoplastic. Matrix Metalloproteinases / biosynthesis. Melanoma, Experimental / metabolism

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  • (PMID = 17709990.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 136894-56-9 / Antigens, CD147; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.80 / Matrix Metalloproteinase 14
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40. Matsuda H, Hirata N, Kawaguchi Y, Naruto S, Takata T, Oyama M, Iinuma M, Kubo M: Melanogenesis stimulation in murine B16 melanoma cells by Kava (Piper methysticum) rhizome extract and kavalactones. Biol Pharm Bull; 2006 Apr;29(4):834-7

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  • [Title] Melanogenesis stimulation in murine B16 melanoma cells by Kava (Piper methysticum) rhizome extract and kavalactones.
  • Melanogenesis stimulation activity of aqueous ethanolic extracts obtained from several different parts of five Piper species, namely Piper longum, P. kadsura, P. methysticum, P. betle, and P. cubeba, were examined by using cultured murine B16 melanoma cells.
  • 7,8-Epoxyyangonin (5) showed a significant stimulatory effect on melanogenesis in B16 melanoma cells.
  • [MeSH-major] Kava / chemistry. Melanins / biosynthesis. Melanoma, Experimental / metabolism

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  • (PMID = 16595931.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Lactones; 0 / Melanins; 0 / Plant Extracts
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41. Mena S, Benlloch M, Ortega A, Carretero J, Obrador E, Asensi M, Petschen I, Brown BD, Estrela JM: Bcl-2 and glutathione depletion sensitizes B16 melanoma to combination therapy and eliminates metastatic disease. Clin Cancer Res; 2007 May 1;13(9):2658-66
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  • [Title] Bcl-2 and glutathione depletion sensitizes B16 melanoma to combination therapy and eliminates metastatic disease.
  • PURPOSE: Advanced melanoma resists all current therapies, and metastases in the liver are particularly problematic.
  • Prevalent resistance factors include elevated glutathione (GSH) and increased expression of bcl-2 in melanoma cells.
  • This study determined the in vivo efficacy of combination therapies administered while GSH and Bcl-2 were individually and simultaneously decreased in metastatic melanoma lesions.
  • EXPERIMENTAL DESIGN: Highly metastatic murine B16 melanoma (B16M-F10) cells have elevated levels of both GSH and Bcl-2.
  • CONCLUSIONS: Our results suggest a new strategy to induce regression of late-stage metastatic melanoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Glutathione / antagonists & inhibitors. Melanoma, Experimental / therapy. Paclitaxel / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Skin Neoplasms / therapy. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 17473197.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thionucleotides; 0 / Tumor Necrosis Factor-alpha; 0RH81L854J / Glutamine; 85J5ZP6YSL / oblimersen; GAN16C9B8O / Glutathione; P88XT4IS4D / Paclitaxel
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42. Zhao Y, Liu J, McMartin KE: Inhibition of NADPH oxidase activity promotes differentiation of B16 melanoma cells. Oncol Rep; 2008 May;19(5):1225-30
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  • [Title] Inhibition of NADPH oxidase activity promotes differentiation of B16 melanoma cells.
  • The activity of NADPH oxidase is increased in malignant skin keratinocytes.
  • We demonstrated that inhibition of NADPH oxidase activity by diphenyleneiodonium (DPI) suppressed free radical production, inhibited cell growth and promoted cell differentiation of B16 melanoma cells, as indicated by cell morphology, increased production of melanin, and increased expression of microphthalmia-associated transcription factor (MITF).
  • In addition, the protein levels of the tumor suppressor p53 were suppressed by DPI, suggesting that p53 is activated by oxidative stress and may negatively regulate differentiation in melanoma cells.
  • Taken together, these results suggest that inhibiting NADPH oxidase activity promotes cell differentiation of B16 melanoma cells.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Differentiation. Enzyme Activation. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Melanins / metabolism. Melanoma, Experimental. Mice. Microphthalmia-Associated Transcription Factor / biosynthesis. RNA, Small Interfering / metabolism. Reactive Oxygen Species. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18425380.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Melanins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Mitf protein, mouse; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; EC 1.6.3.1 / NADPH Oxidase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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43. Ren Z, Ye X, Fang C, Lu Q, Zhao Y, Liu F, Liang M, Hu F, Chen HZ: Intratumor injection of oncolytic adenovirus expressing HSP70 prolonged survival in melanoma B16 bearing mice by enhanced immune response. Cancer Biol Ther; 2008 Feb;7(2):191-95
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  • [Title] Intratumor injection of oncolytic adenovirus expressing HSP70 prolonged survival in melanoma B16 bearing mice by enhanced immune response.
  • The HSP expression and cytopathic killing effect in mouse B16 melanoma and human PLC/PRF/5 hepatoma cells were measured after in vitro infection of adenoviruses.
  • Survival rate of immunocompetent C57/BL mice was observed following intratumor injection of recombinant adenoviruses in B16 melanoma xenograft models.
  • The Ad.CMV.HSP.IRES.E1a induced significantly higher HSP expression level than Ad.CMV.IRES.E1a in both B16 and PLC/ PRF/5 cells.
  • The cytocidal efficacy of Ad.CMV.HSP.IRES.E1a and Ad.CMV.IRES.E1a in PLC/PRF/5 cells was much higher than that in B16 cells, where the two adenoviruses showed similarly very weak oncolytic effect in vitro.
  • E1a improved animal survival rate and exhibited more potent anti-tumor efficiency than Ad.CMV.IRES.E1a in B16 xenograft models.
  • [MeSH-major] Genetic Therapy / methods. Genetic Vectors / administration & dosage. HSP70 Heat-Shock Proteins / genetics. Melanoma, Experimental / therapy. Oncolytic Virotherapy / methods

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  • [CommentIn] Cancer Biol Ther. 2008 Feb;7(2):196-7 [18347427.001]
  • (PMID = 18073525.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / HSP70 Heat-Shock Proteins; 82115-62-6 / Interferon-gamma
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44. Penafuerte C, Galipeau J: TGF beta secreted by B16 melanoma antagonizes cancer gene immunotherapy bystander effect. Cancer Immunol Immunother; 2008 Aug;57(8):1197-206
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  • [Title] TGF beta secreted by B16 melanoma antagonizes cancer gene immunotherapy bystander effect.
  • We have previously described a Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) and Interleukin 2 (IL2) fusokine (aka GIFT2) which serves as a potent anticancer cytokine and it here served as a means to understand the mechanistic underpinnings to the immune bystander effect in an immune competent model of B16 melanoma.
  • As expected, we observed that GIFT2 secreted by genetically engineered B16 tumor cells induces a bystander effect on non modified B16 cells, when admixed in a 1:1 ratio.
  • However, despite keeping the 1:1 ratio constant, the immune bystander effect was completely lost as the total B16 cell number was increased from 10(4) to 10(6) which correlated with a sharp reduction in the number of tumor-infiltrating NK cells.
  • We found that B16 secrete biologically active TGFbeta which in turn inhibited GIFT2 dependent immune cell proliferation in vitro and downregulated IL-2R beta expression and IFN gamma secretion by NK cells.
  • In vivo blockade of B16 originating TGFbeta significantly improved the immune bystander effect arising from GIFT2.
  • [MeSH-major] Bystander Effect / immunology. Genetic Therapy / methods. Immunotherapy. Melanoma, Experimental / immunology. Melanoma, Experimental / therapy. Transforming Growth Factor beta / immunology

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  • (PMID = 18214474.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Histocompatibility Antigens Class II; 0 / Interleukin-2; 0 / Interleukin-2 Receptor beta Subunit; 0 / Transforming Growth Factor beta; 82115-62-6 / Interferon-gamma; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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45. Song HS, Sim SS: Acteoside inhibits alpha-MSH-induced melanin production in B16 melanoma cells by inactivation of adenyl cyclase. J Pharm Pharmacol; 2009 Oct;61(10):1347-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acteoside inhibits alpha-MSH-induced melanin production in B16 melanoma cells by inactivation of adenyl cyclase.
  • METHODS: We used tyrosinase activity and melanin production stimulated in B16 melanoma cells by alpha-melanocyte stimulating hormone (alpha-MSH) or forskolin to measure the whitening effect of acteoside.
  • KEY FINDINGS: Acteoside did not directly inhibit mushroom tyrosinase activity, but dose-dependently inhibited tyrosinase activity and melanin production in B16 melanoma cells stimulated by 1 micromol/l alpha-MSH.
  • [MeSH-major] Adenylyl Cyclases / drug effects. Antioxidants / pharmacology. Glucosides / pharmacology. Melanoma, Experimental / enzymology. Phenols / pharmacology. alpha-MSH / antagonists & inhibitors

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  • (PMID = 19814867.001).
  • [ISSN] 2042-7158
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Biphenyl Compounds; 0 / Glucosides; 0 / Melanins; 0 / Phenols; 0 / Picrates; 0 / Reactive Oxygen Species; 1898-66-4 / 2,2-diphenyl-1-picrylhydrazyl; 1F7A44V6OU / Colforsin; 581-05-5 / alpha-MSH; 61276-17-3 / acteoside; E0399OZS9N / Cyclic AMP; EC 1.14.18.1 / Monophenol Monooxygenase; EC 4.6.1.1 / Adenylyl Cyclases
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46. Fëdorov ES, Manikhas GM, Petrishchëv NN, Dubina MV: [The role of gap junction communication in metastatic B16 melanoma in C57BL mice]. Vopr Onkol; 2006;52(4):433-7
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  • [Title] [The role of gap junction communication in metastatic B16 melanoma in C57BL mice].
  • The study is concerned with the effects of non-specific blocking gap junction communication with oleamide as well as genesis and spreading of melanoma B16 metastases to the lung in mice C57B1.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinogens. Cell Communication. Gap Junctions. Melanoma, Experimental / ultrastructure. Oleic Acids / pharmacology

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  • (PMID = 17024817.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Oleic Acids; 7L25QK8BWO / oleylamide
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47. Hao S, Ye Z, Li F, Meng Q, Qureshi M, Yang J, Xiang J: Epigenetic transfer of metastatic activity by uptake of highly metastatic B16 melanoma cell-released exosomes. Exp Oncol; 2006 Jun;28(2):126-31
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  • [Title] Epigenetic transfer of metastatic activity by uptake of highly metastatic B16 melanoma cell-released exosomes.
  • METHODS: The highly metastatic B16 melanoma cell line (BL6-10) was generated in our laboratory.
  • For phenotypic analysis BL6-10 and F1 melanoma cells were stained with FITC-conjugated anti-MHC I (H-2K(b)), MHC II (Ia(b)) and Met 72 antibodies and analyzed by flow cytometry.
  • C57BL/6 mice (8 per group) were injected (i. v.) with 0.5 x 10(6) F1, BL6-10 and F1(EXO) melanoma cells.
  • All mice inoculated with BL6-10 melanoma cells had numerous lung tumor colonies, while mice injected with F1 tumor cells were free of lung metastatic colonies.
  • [MeSH-major] Cytoplasmic Vesicles / transplantation. Lung Neoplasms / secondary. Melanoma, Experimental / pathology. Skin Neoplasms / pathology


48. Wang P, Yang X, Wu P, Zhang J, Sato T, Yamagata S, Yamagata T: GM3 signals regulating TNF-alpha expression are mediated by Rictor and Arhgdib in mouse melanoma B16 cells. Oncology; 2007;73(5-6):430-8
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  • [Title] GM3 signals regulating TNF-alpha expression are mediated by Rictor and Arhgdib in mouse melanoma B16 cells.
  • OBJECTIVE: We have previously shown GM3 to positively regulate TNF-alpha expression via a PI3K/Akt pathway in mouse melanoma B16 cells [Wang et al.: Biochem Biophys Res Commun 2007;356:438-443].
  • RESULTS: PI3K inhibitors LY294002 and LY303511 were shown to suppress TNF-alpha expression that is stimulated by GM3 in B16 cells, suggesting that the GM3 signal is located upstream of the PI3K-Akt pathway.
  • CONCLUSIONS: The GM3 signal is thus transduced in B16 cells through a PI3K, Rictor/mTOR, Akt, Arhgdib pathway, leading to stimulated expression of TNF-alpha.
  • [MeSH-major] Carrier Proteins / physiology. G(M3) Ganglioside / pharmacology. Gene Expression Regulation, Neoplastic. Melanoma, Experimental / genetics. Tumor Necrosis Factor-alpha / genetics

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  • [Copyright] 2008 S. Karger AG, Basel.
  • (PMID = 18523362.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Chromones; 0 / DNA Primers; 0 / G(M3) Ganglioside; 0 / Piperazines; 0 / RNA, Small Interfering; 0 / Rhog protein, mouse; 0 / Tumor Necrosis Factor-alpha; 0 / rictor protein, mouse; 154447-38-8 / LY 303511; EC 3.6.1.- / GTP Phosphohydrolases
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49. Hirata N, Naruto S, Ohguchi K, Akao Y, Nozawa Y, Iinuma M, Matsuda H: Mechanism of the melanogenesis stimulation activity of (-)-cubebin in murine B16 melanoma cells. Bioorg Med Chem; 2007 Jul 15;15(14):4897-902
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  • [Title] Mechanism of the melanogenesis stimulation activity of (-)-cubebin in murine B16 melanoma cells.
  • (-)-Cubebin showed a melanogenesis stimulation activity in a concentration-dependent manner in murine B16 melanoma cells without any significant effects on cell proliferation.
  • Tyrosinase activity was increased at 24-72 h after addition of cubebin to B16 cells, and then intracellular melanin amount was increased at 48-96 h after the treatment.
  • SB203580, a selective inhibitor of p38 MAPK, completely blocked cubebin-induced expression of tyrosinase mRNA in B16 cells.
  • These results suggested that cubebin increased melanogenesis in B16 cells through the enhancement of tyrosinase expression mediated by activation of p38 MAPK.
  • [MeSH-major] Lignans / pharmacology. Melanins / biosynthesis. Melanoma / metabolism

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  • (PMID = 17521910.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Lignans; 0 / Melanins; 0 / Pyridines; 0 / RNA, Messenger; 0 / SB 203580; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; J237078S8A / cubebin
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50. Berezhnaya NM, Vinnichuk YD, Belova OB: The use of doxorubicine at low doses for elevation of LAK-activity toward explants and cells of MC-rhabdomyosarcoma and B16 melanoma resistant to doxorubicin. Exp Oncol; 2008 Mar;30(1):52-5
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  • [Title] The use of doxorubicine at low doses for elevation of LAK-activity toward explants and cells of MC-rhabdomyosarcoma and B16 melanoma resistant to doxorubicin.
  • AIM: To study the influence of doxorubicin at low doses on antitumor action of activated (LAK) and non-activated lymphocytes from lymph nodes toward tumor cells of mice bearing doxorubicin-resistant and doxorubicin-sensitive transplantable MC-rhabdomyosarcoma and B16 melanoma.
  • MATERIALS AND METHODS: The study was carried out on BALB/c mice bearing MC-rhabdomyosarcoma and 57BL/6 mice bearing 16 melanoma.
  • RESULTS: At the day 7 of tumor growth in mice bearing resistant MC-rhabdomyosarcoma, non-activated lymphocytes pretreated with low-dose doxorubicin possess the highest antitumor activity, and in mice bearing doxorubicin-resistant B16 melanoma the highest antitumor activity was detected for lymphocytes after combined cultivation with IL-2 and doxorubicin.
  • At the day 14 of tumor growth, LAK obtained from lymphocytes pretreated with doxorubicin possess the highest cytotoxic activity toward resistant tumor cells both of MC-rhabdomyosarcoma and B16 melanoma.
  • CONCLUSION: To elevate antitumor activity of LAK toward MC-rhabdomyosarcoma and B16 melanoma cells, low doses of doxorubicin could be used at certain conditions of LAK generation.
  • [MeSH-major] Doxorubicin / administration & dosage. Drug Resistance, Neoplasm / drug effects. Killer Cells, Lymphokine-Activated / drug effects. Lymphocyte Activation / drug effects. Melanoma, Experimental / drug therapy. Rhabdomyosarcoma / drug therapy

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  • (PMID = 18438341.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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51. Janczak M, Kapuściński J, Olasik EM, Rózalski M, Płachcińska A, Kuśmierek J: Biodistribution of two (131)I-IMBA preparations, differently labelled, in mice with experimental B16 melanoma tumours. Nucl Med Rev Cent East Eur; 2008;11(2):48-52
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  • [Title] Biodistribution of two (131)I-IMBA preparations, differently labelled, in mice with experimental B16 melanoma tumours.
  • BACKGROUND: Numerous reports indicate that some iodinated compounds of benzamide derivatives display a strong affinity to the cells of melanoma.
  • Biodistribution of the injected compound was followed in mice with experimentally induced B16 melanoma tumours, and tumour/ tissue ratios were studied as a function of time post administration.
  • The biodistribution of (131)I-IMBA in C57 Black mice was studied in animals with experimentally induced B16 mice melanoma tumours.
  • RESULTS: The mean labelling efficiency exceeded 95 and 80 % for methods I and II, respectively, at radiochemical purity > 95% in both cases. (131)I-IMBA was vividly cumulated by melanoma tumours in mice.
  • CONCLUSIONS: High values of tumour/non-tumour ratios indicate that (131)I-IMBA could be a promising radiopharmaceutical for clinical diagnosis (staging) of melanomas in humans.
  • [MeSH-major] Benzamides / pharmacokinetics. Iodobenzenes / pharmacokinetics. Melanoma / metabolism. Melanoma / radionuclide imaging. Whole Body Imaging / methods

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  • (PMID = 19585454.001).
  • [ISSN] 1506-9680
  • [Journal-full-title] Nuclear medicine review. Central & Eastern Europe
  • [ISO-abbreviation] Nucl Med Rev Cent East Eur
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Iodobenzenes; 0 / N-(2-diethylaminoethyl)-3-iodo-4-methoxybenzamide; 0 / Radiopharmaceuticals
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52. Qin YS, Zhang X, Li L, Yu HL: [Effect of histamine on metastasis of melanoma B16 cell xenograft in C57BL/6 mice]. Ai Zheng; 2007 Aug;26(8):833-6
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  • [Title] [Effect of histamine on metastasis of melanoma B16 cell xenograft in C57BL/6 mice].
  • METHODS: Cultured melanoma B16 cells were inoculated into the left armpit of C57BL/6 mice to develop melanoma.
  • RESULTS: All the mice developed melanoma after inoculation.
  • CONCLUSION: Histamine can inhibit the metastasis of melanoma B16 cells in C57BL/6 mice either through lymphatic or hemal route, and this partly because of its inhibitory effect on tumor growth.
  • [MeSH-major] Histamine / pharmacology. Lung Neoplasms / secondary. Lymphatic Metastasis / pathology. Melanoma, Experimental / pathology. Splenic Neoplasms / secondary

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  • (PMID = 17697542.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 820484N8I3 / Histamine
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53. Murakami M, Matsuzaki F, Funaba M: Regulation of melanin synthesis by the TGF-beta family in B16 melanoma cells. Mol Biol Rep; 2009 Jul;36(6):1247-50
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  • [Title] Regulation of melanin synthesis by the TGF-beta family in B16 melanoma cells.
  • Effects of representative members of the transforming growth factor-beta (TGF-beta) family, TGF-beta1, activin A and BMP-2, on melanin content and expression of pigment-producing enzymes were examined in B16 melanoma cells.
  • As compared with parental B16 cells, the inhibitory effects of TGF-beta1 and activin A on melanin content were relative smaller in B16 F10 cells, a subline of B16 cells that contain more pigment.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. Melanins / biosynthesis. Melanocyte-Stimulating Hormones / pharmacology. Melanoma / metabolism. Transforming Growth Factor beta / pharmacology

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  • (PMID = 18600473.001).
  • [ISSN] 1573-4978
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BMP2 protein, human; 0 / Bone Morphogenetic Protein 2; 0 / Melanins; 0 / Membrane Glycoproteins; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / activin A; 104625-48-1 / Activins; 9002-79-3 / Melanocyte-Stimulating Hormones; EC 1.- / Oxidoreductases; EC 1.14.18.- / TYRP1 protein, human; EC 1.14.18.1 / Monophenol Monooxygenase
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54. Matsuda H, Hirata N, Kawaguchi Y, Yamazaki M, Naruto S, Shibano M, Taniguchi M, Baba K, Kubo M: Melanogenesis stimulation in murine b16 melanoma cells by umberiferae plant extracts and their coumarin constituents. Biol Pharm Bull; 2005 Jul;28(7):1229-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Melanogenesis stimulation in murine b16 melanoma cells by umberiferae plant extracts and their coumarin constituents.
  • ) CUSSON and C. formosanum YABE, were examined by using cultured murine B16 melanoma cells.
  • The melanogenesis stimulatory effects of sixteen coumarins (1-16) isolated from the seven Umbelliferae crude drugs were also examined.
  • [MeSH-major] Apiaceae / chemistry. Coumarins / pharmacology. Melanins / biosynthesis. Melanoma, Experimental / metabolism. Plant Extracts / pharmacology

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  • (PMID = 15997104.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Coumarins; 0 / Melanins; 0 / Plant Extracts
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55. Itzhaki O, Skutelsky E, Kaptzan T, Siegal A, Sinai J, Schiby G, Michowitz M, Huszar M, Leibovici J: Decreased DNA ploidy may constitute a mechanism of the reduced malignant behavior of B16 melanoma in aged mice. Exp Gerontol; 2008 Mar;43(3):164-75
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  • [Title] Decreased DNA ploidy may constitute a mechanism of the reduced malignant behavior of B16 melanoma in aged mice.
  • In the present study we report an incidentally found, not yet described mechanism, of the age-related reduced tumor progression, namely a decreased ploidy in B16 melanoma growing in old (near diploidy) as compared to young mice (tetraploidy).
  • Flow cytometry forward scatter data also showed a smaller cell size of melanoma cells from old mice.
  • DNA flow cytometry profile comparison demonstrated that while B16 melanoma cells from young animals contained a high percentage of tetraploid cells, those derived from old animals were mostly close to diploid.
  • The transit from tetraploidy to near euploidy in melanoma cells growing in aged mice might avoid the genetic instability inherent to tumor progression.
  • [MeSH-major] Aging / genetics. DNA, Neoplasm / analysis. Melanoma, Experimental / genetics. Ploidies

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  • (PMID = 18261868.001).
  • [ISSN] 0531-5565
  • [Journal-full-title] Experimental gerontology
  • [ISO-abbreviation] Exp. Gerontol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins c-bcl-2
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56. Sitabkhan Y, Frankfater A: Differences in the expression of cathepsin B in B16 melanoma metastatic variants depend on transcription factor Sp1. DNA Cell Biol; 2007 Sep;26(9):673-82
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  • [Title] Differences in the expression of cathepsin B in B16 melanoma metastatic variants depend on transcription factor Sp1.
  • Cathepsin B contributes to the invasiveness of B16 melanoma cells in mice, with the highly metastatic B16a melanoma producing six- to eightfold more cathepsin B mRNA and protein than the less metastatic B16F1 variant.
  • The proximal promoter region of the cathepsin B (Ctsb) gene (-149 to +94) was previously found to be capable of reproducing this pattern of differential gene activation in B16 melanoma variants.
  • The binding of B16 melanoma nuclear proteins to this promoter region has now been mapped to three GC-boxes (Sp1 transcription factor binding sites) and a potential X-box [tax response element (TRE)/c-AMP responsive element (CRE) site].
  • Promoter activity was also attenuated by mutations within the GC-rich segment between +6 and +16, but not by mutation of the putative X-box.
  • Thus, the difference in cathepsin B expression between high and low metastatic B16 melanoma variants is largely due to different levels of Sp1.
  • [MeSH-major] Cathepsin B / genetics. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Melanoma, Experimental / genetics. Sp1 Transcription Factor / metabolism

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  • (PMID = 17691867.001).
  • [ISSN] 1044-5498
  • [Journal-full-title] DNA and cell biology
  • [ISO-abbreviation] DNA Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Sp1 Transcription Factor; 148710-94-5 / Sp3 Transcription Factor; EC 3.4.22.1 / Cathepsin B
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57. Murad JM, de Souza LR, De Lucca FL: PKR activation by a non-coding RNA expressed in lymphocytes of mice bearing B16 melanoma. Blood Cells Mol Dis; 2006 Sep-Oct;37(2):128-33
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  • [Title] PKR activation by a non-coding RNA expressed in lymphocytes of mice bearing B16 melanoma.
  • In this study, we investigated the presence of ncRNAs in lymphocytes of C57BL/6 mice bearing B16 melanoma by using the differential display reverse transcription-PCR (DD-RT-PCR).
  • We detected a highly structured transcript of 220 nt with no open reading frame (ORF) which is able to activate PKR, and it is only expressed in lymphocytes of C57BL/6 mice bearing B16 melanoma.
  • [MeSH-major] Lymphocytes / metabolism. Melanoma, Experimental / metabolism. Neoplasms / metabolism. RNA, Untranslated / genetics. eIF-2 Kinase / metabolism

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  • (PMID = 16857398.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Untranslated; EC 2.7.11.1 / eIF-2 Kinase
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58. Hou CC, Chen YP, Wu JH, Huang CC, Wang SY, Yang NS, Shyur LF: A galactolipid possesses novel cancer chemopreventive effects by suppressing inflammatory mediators and mouse B16 melanoma. Cancer Res; 2007 Jul 15;67(14):6907-15
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  • [Title] A galactolipid possesses novel cancer chemopreventive effects by suppressing inflammatory mediators and mouse B16 melanoma.
  • We investigated the cancer chemopreventive bioactivity of C. rabens phytocompounds in vitro and in vivo using cell- and gene-based bioassays and a mouse B16 melanoma model.
  • The bioactive glyceroglycolipid 1,2-di-O-alpha-linolenoyl-3-O-beta-galactopyranosyl-sn-glycerol (dLGG) that was identified from C. rabens was found in vitro and in vivo to be a potent nitric oxide (NO) scavenger. dLGG treatment inhibited both mRNA and protein expression of inducible NO synthase and cyclooxygenase-2 (COX-2) in murine macrophages and inhibited COX-2 gene transcription in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated B16 cells.
  • A dLGG-enriched extract from C. rabens (10 mg/kg) markedly suppressed B16 melanoma growth in C57BL/6J mice following i.p. administration, an effect comparable with that of cisplatin, a cancer chemotherapeutic drug.
  • [MeSH-minor] Active Transport, Cell Nucleus. Animals. Asteraceae / metabolism. Cell Survival. Female. I-kappa B Kinase / metabolism. Immunohistochemistry. Inhibitory Concentration 50. Macrophages / metabolism. Melanoma, Experimental. Mice. Mice, Inbred C57BL. Plant Extracts / metabolism

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  • (PMID = 17638902.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Galactolipids; 0 / Plant Extracts; EC 2.7.11.10 / I-kappa B Kinase
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59. Lasfar A, Lewis-Antes A, Smirnov SV, Anantha S, Abushahba W, Tian B, Reuhl K, Dickensheets H, Sheikh F, Donnelly RP, Raveche E, Kotenko SV: Characterization of the mouse IFN-lambda ligand-receptor system: IFN-lambdas exhibit antitumor activity against B16 melanoma. Cancer Res; 2006 Apr 15;66(8):4468-77
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  • [Title] Characterization of the mouse IFN-lambda ligand-receptor system: IFN-lambdas exhibit antitumor activity against B16 melanoma.
  • We showed that, similar to their human orthologues, mIFN-lambda2 and mIFN-lambda3 signal through the IFN-lambda receptor complex, activate IFN stimulated gene factor 3, and are capable of inducing antiviral protection and MHC class I antigen expression in several cell types including B16 melanoma cells.
  • We then used the murine B16 melanoma model to investigate the potential antitumor activities of IFN-lambdas.
  • We developed B16 cells constitutively expressing murine IFN-lambda2 (B16.IFN-lambda2 cells) and evaluated their tumorigenicity in syngeneic C57BL/6 mice.
  • Although constitutive expression of mIFN-lambda2 in melanoma cells did not affect their proliferation in vitro, the growth of B16.IFN-lambda2 cells, when injected s.c. into mice, was either retarded or completely prevented.
  • We then developed IFN-lambda-resistant B16.IFN-lambda2 cells (B16.IFN-lambda2Res cells) and showed that their tumorigenicity was also highly impaired or completely abolished similar to B16.IFN-lambda2 cells, suggesting that IFN-lambdas engage host mechanisms to inhibit melanoma growth.

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  • (PMID = 16618774.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI051139; United States / NIAID NIH HHS / AI / R01 AI057468; United States / NIAID NIH HHS / AI / AI057468; United States / NIEHS NIH HHS / ES / ES05022
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Interferon; 9008-11-1 / Interferons
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60. Vaidya SV, Stepp SE, McNerney ME, Lee JK, Bennett M, Lee KM, Stewart CL, Kumar V, Mathew PA: Targeted disruption of the 2B4 gene in mice reveals an in vivo role of 2B4 (CD244) in the rejection of B16 melanoma cells. J Immunol; 2005 Jan 15;174(2):800-7
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  • [Title] Targeted disruption of the 2B4 gene in mice reveals an in vivo role of 2B4 (CD244) in the rejection of B16 melanoma cells.
  • To investigate the in vivo role of 2B4, wild-type and 2B4(-/-) mice were injected with CD48(+) and CD48(-) metastatic B16 melanoma cells.
  • Wild-type mice rejected CD48(+) melanoma poorly compared with CD48(-) tumor cells, suggesting that ligation of 2B4 by CD48 on melanoma cells is inhibitory.
  • In keeping with this, male 2B4(-/-) mice showed enhanced ability to reject CD48(+) melanoma cells.
  • However, female 2B4(-/-) mice poorly rejected both CD48(+) and CD48(-) melanoma cells, revealing a gender-specific and CD48-independent defect in mice lacking 2B4.
  • [MeSH-major] Antigens, CD / genetics. Graft Rejection / genetics. Graft Rejection / immunology. Killer Cells, Natural / immunology. Melanoma, Experimental / genetics. Melanoma, Experimental / immunology. Membrane Glycoproteins / deficiency. Membrane Glycoproteins / genetics. Receptors, Immunologic / deficiency. Receptors, Immunologic / genetics

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  • (PMID = 15634901.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA85753
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD48 antigen; 0 / Cd244 protein, mouse; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic
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61. Thanigaimalai P, Hoang TA, Lee KC, Bang SC, Sharma VK, Yun CY, Roh E, Hwang BY, Kim Y, Jung SH: Structural requirement(s) of N-phenylthioureas and benzaldehyde thiosemicarbazones as inhibitors of melanogenesis in melanoma B 16 cells. Bioorg Med Chem Lett; 2010 May 1;20(9):2991-3
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  • [Title] Structural requirement(s) of N-phenylthioureas and benzaldehyde thiosemicarbazones as inhibitors of melanogenesis in melanoma B 16 cells.
  • In order to define the structural requirements of phenylthiourea (PTU), a series of thiourea and thiosemicarbazone analogs were prepared and evaluated as inhibitors of melanogenesis in melanoma B16 cells.
  • [MeSH-major] Benzaldehydes / chemistry. Melanoma, Experimental / drug therapy. Peptides / chemistry. Phenylthiourea / chemistry. Thiosemicarbazones / chemistry

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  • [Copyright] 2010. Published by Elsevier Ltd.
  • (PMID = 20359890.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(4-tert-butylbenzylidene)hydrazinecarbothioamide; 0 / Benzaldehydes; 0 / Peptides; 0 / Thiosemicarbazones; 6F82C6Q54C / Phenylthiourea; EC 1.14.18.1 / Monophenol Monooxygenase; TA269SD04T / benzaldehyde
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62. Gava B, Zorzet S, Spessotto P, Cocchietto M, Sava G: Inhibition of B16 melanoma metastases with the ruthenium complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlororuthenate and down-regulation of tumor cell invasion. J Pharmacol Exp Ther; 2006 Apr;317(1):284-91
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  • [Title] Inhibition of B16 melanoma metastases with the ruthenium complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlororuthenate and down-regulation of tumor cell invasion.
  • The antimetastatic ruthenium complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlorouthenate (NAMI-A) is tested in the B16 melanoma model in vitro and in vivo.
  • Treatment of B6D2F1 mice carrying intra-footpad B16 melanoma with 35 mg/kg/day NAMI-A for 6 days reduces metastasis weight independently of whether NAMI-A is given before or after surgical removal of the primary tumor.
  • This work shows the selective effectiveness of NAMI-A on the metastatic melanoma and suggests that metastasis inhibition is due to the negative modulation of tumor cell invasion processes, a mechanism in which the reduction of the gelatinolitic activity of tumor cells plays a crucial role.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Dimethyl Sulfoxide / analogs & derivatives. Lung Neoplasms / drug therapy. Melanoma, Experimental / drug therapy. Organometallic Compounds / therapeutic use. Skin Neoplasms / drug therapy

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  • (PMID = 16368900.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Adhesion Molecules; 0 / Organometallic Compounds; 0 / imidazolium-bis(imidazole)dimethylsulfoxideimidazotetrachlororuthenate(III); YOW8V9698H / Dimethyl Sulfoxide
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63. Kushida S, Ohmae H, Kamma H, Totsuka R, Matsumura M, Takeuchi A, Saiki I, Yanagawa T, Onizawa K, Ishii T, Ohn T: Artificial cytokine storm combined with hyperthermia induces significant anti-tumor effect in mice inoculated with lewis lung carcinoma and B16 melanoma cells. Int J Hyperthermia; 2006 Dec;22(8):699-712

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Artificial cytokine storm combined with hyperthermia induces significant anti-tumor effect in mice inoculated with lewis lung carcinoma and B16 melanoma cells.
  • These cytokines in a proper combination augmented the anti-tumor effect of LH and prolonged survival time in Lewis lung carcinoma or B16 melanoma significantly.
  • Moreover, the 12-cytokine cocktail suppressed B 16 metastasis to the lung and lymph nodes, and complete regression of the tumors without regrowth occurred in 3 of 5 mice.
  • In the cured three B16 mice, there was hyperplasia of lymphatic organs with many CD3-positive T lymphocytes.
  • [MeSH-major] Carcinoma, Lewis Lung / therapy. Cytokines / therapeutic use. Hyperthermia, Induced. Immunotherapy, Active / methods. Melanoma, Experimental / therapy

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  • (PMID = 17390999.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
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64. Wu TG, Rose WA 2nd, Albrecht TB, Knutson EP, König R, Perdigão JR, Nguyen AP, Fleischmann WR Jr: IFN-alpha-induced murine B16 melanoma cancer vaccine cells: induction and accumulation of cell-associated IL-15. J Interferon Cytokine Res; 2007 Jan;27(1):13-22

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  • [Title] IFN-alpha-induced murine B16 melanoma cancer vaccine cells: induction and accumulation of cell-associated IL-15.
  • Long-term treatment of mouse cancer cells with interferon-alpha (IFN-alpha) converts parental B16 melanoma cells to B16alpha vaccine cells.
  • Inoculation of syngeneic mice with B16alpha vaccine cells triggers immunity to the parental B16 tumor that is mediated by host macrophages, T cells, and natural killer (NK) cells.
  • The release of accumulated cell-associated IL-15 may then trigger a host T cell response to tumor antigens and cause host development of immunity to the B16 tumor cells.
  • [MeSH-major] Cancer Vaccines / immunology. Interferon-alpha / physiology. Interleukin-15 / metabolism. Melanoma, Experimental / immunology. Melanoma, Experimental / metabolism

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  • (PMID = 17266439.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES06676; United States / NIEHS NIH HHS / ES / ES10018
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Interferon-alpha; 0 / Interleukin-15
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65. Kim DS, Jeong YM, Park IK, Hahn HG, Lee HK, Kwon SB, Jeong JH, Yang SJ, Sohn UD, Park KC: A new 2-imino-1,3-thiazoline derivative, KHG22394, inhibits melanin synthesis in mouse B16 melanoma cells. Biol Pharm Bull; 2007 Jan;30(1):180-3
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  • [Title] A new 2-imino-1,3-thiazoline derivative, KHG22394, inhibits melanin synthesis in mouse B16 melanoma cells.
  • Moreover, alpha-melanocyte-stimulating hormone (alpha-MSH) is known to increase melanin biosynthesis by increasing tyrosinase production, and here, we found that alpha-MSH-induced Mitf and tyrosinase increases were inhibited in B16 melanoma cells treated with KHG22394.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Extracellular Signal-Regulated MAP Kinases / metabolism. Melanoma, Experimental. Mice. Microphthalmia-Associated Transcription Factor / metabolism. Monophenol Monooxygenase / metabolism

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  • (PMID = 17202683.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Dermatologic Agents; 0 / KHG22394; 0 / Melanins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Mitf protein, mouse; 0 / Thiazoles; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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66. Sun T, Sun BC, Ni CS, Zhao XL, Wang XH, Qie S, Zhang DF, Gu Q, Qi H, Zhao N: Pilot study on the interaction between B16 melanoma cell-line and bone-marrow derived mesenchymal stem cells. Cancer Lett; 2008 May 8;263(1):35-43
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  • [Title] Pilot study on the interaction between B16 melanoma cell-line and bone-marrow derived mesenchymal stem cells.
  • Our previous study had shown that BMSCs maybe participate in angiogenesis in melanoma in vivo.
  • The aim of this study was to investigate the interaction between B16 melanoma cells and BMSCs in vitro, the mechanism of BMSCs participating in melanoma angiogenesis in vivo is unclear, so a co-culture system containing BMSCs and B16 melanoma cells, based on transwell indirect model, was established, and the interaction between BMSCs and B16 melanoma cells was studied in vitro.
  • In our study, BMSCs were generated out of bone marrow from C57 mouse, isolated BMSCs were positive for the markers CD105, CD90, CD73, CD44 and CD166 and negative for endothelial markers, which acquired endothelial phenotype (including the expression of VEGFR-1, VEGFR-2, Factor VIII) after co-culture with B16 melanoma cells; at the same time, B16 melanoma cells also up-regulated the expression of VEGF-a, VEGFR-1, VEGFR-2 and Factor VIII.
  • The proliferation rate of B16 melanoma cells and BMSCs were also found to be increased.
  • [MeSH-major] Bone Marrow Cells / cytology. Melanoma, Experimental / pathology. Mesenchymal Stromal Cells / cytology

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  • (PMID = 18234417.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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67. Lavi G, Voronov E, Dinarello CA, Apte RN, Cohen S: Sustained delivery of IL-1 Ra from biodegradable microspheres reduces the number of murine B16 melanoma lung metastases. J Control Release; 2007 Nov 6;123(2):123-30
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  • [Title] Sustained delivery of IL-1 Ra from biodegradable microspheres reduces the number of murine B16 melanoma lung metastases.
  • In vitro cytokine release and bioactivity studies in cultured melanoma B16 cells revealed the microspheres to be capable of sustained IL-1Ra release on a daily level that could inhibit cell proliferation for at least 7 days.
  • In mice injected with B16 melanoma cells, the sustained IL-1Ra delivery from biodegradable microspheres inhibited tumor growth and significantly prolonged mice survival.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Carriers. Interleukin 1 Receptor Antagonist Protein / pharmacology. Interleukin-1beta / antagonists & inhibitors. Lactic Acid / chemistry. Lung Neoplasms / prevention & control. Melanoma, Experimental / drug therapy. Microspheres. Polyglycolic Acid / chemistry. Polymers / chemistry

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  • (PMID = 17900737.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; 0 / Drug Carriers; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1beta; 0 / Polymers; 0 / Recombinant Proteins; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid
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68. Li B, Lei Z, Lichty BD, Li D, Zhang GM, Feng ZH, Wan Y, Huang B: Autophagy facilitates major histocompatibility complex class I expression induced by IFN-γ in B16 melanoma cells. Cancer Immunol Immunother; 2010 Feb;59(2):313-21
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  • [Title] Autophagy facilitates major histocompatibility complex class I expression induced by IFN-γ in B16 melanoma cells.
  • Here, we report that autophagy is a negative regulator of MHC-I antigen expression in B16 melanoma cells; however, in the presence of IFN-γ, it is converted to a positive regulator.
  • Using B16 melanoma mouse model, we further show that autophagy may enhance the cytolysis of CTL to melanoma cells at the early stage of melanoma, but impairs the cytolysis at the late stage.
  • [MeSH-major] Autophagy. Histocompatibility Antigens Class I / immunology. Interferon-gamma / immunology. Melanoma, Experimental / immunology. Skin Neoplasms / immunology

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  • (PMID = 19680649.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 82115-62-6 / Interferon-gamma
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69. Chen PF, Liu LM, Chen Z, Lin SY, Song WX, Xu YF: [Effects of ethanol extracts of Panax notoginseng on liver metastasis of B16 melanoma grafted in mice]. Zhong Xi Yi Jie He Xue Bao; 2006 Sep;4(5):500-3
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  • [Title] [Effects of ethanol extracts of Panax notoginseng on liver metastasis of B16 melanoma grafted in mice].
  • OBJECTIVE: To observe the effects of ethanol extracts of Panax notoginseng on the tumor and the liver metastasis in experimental mice grafted with B16 melanoma.
  • METHODS: B16 melanoma was transplanted in the spleen of C57BL/6 mice.
  • [MeSH-major] Liver Neoplasms / prevention & control. Melanoma, Experimental / pathology. Panax notoginseng / chemistry. Plant Extracts / therapeutic use

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  • (PMID = 16965745.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Interferon-alpha; 0 / Plant Extracts; 3K9958V90M / Ethanol
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70. Saha S, Mohanty KC, Mallick P: Gangliosides enhance migration of mouse B16-melanoma cells through artificial basement membrane alone or in presence of laminin or fibronectin. Indian J Exp Biol; 2005 Dec;43(12):1130-8

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  • [Title] Gangliosides enhance migration of mouse B16-melanoma cells through artificial basement membrane alone or in presence of laminin or fibronectin.
  • The migration of B16LuF1 cells, B16-melanoma cells of lower metastatic potential to lung was enhanced through artificial basement membrane in presence of gangliosides of B16LuF1 cells as well as gangliosides of B16-melanoma cells of higher metastatic potential to lung, namely, B16LuF5 and B16LuF10 cells.
  • Thus, gangliosides of B16 melanoma cells alone or in combination with laminin or fibronectin enhanced migration of B16 melanoma cells through artificial basement membrane, suggesting possible role of tumor gangliosides during invasion of metastatic tumor cells through basement membrane of the surrounding tissues in vivo.
  • [MeSH-major] Cell Movement / physiology. Fibronectins / physiology. G(M2) Ganglioside / physiology. G(M3) Ganglioside / physiology. Laminin / physiology. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Membranes, Artificial

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  • (PMID = 16359123.001).
  • [ISSN] 0019-5189
  • [Journal-full-title] Indian journal of experimental biology
  • [ISO-abbreviation] Indian J. Exp. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Fibronectins; 0 / G(M3) Ganglioside; 0 / Laminin; 0 / Membranes, Artificial; 19600-01-2 / G(M2) Ganglioside
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71. Wang P, Wu P, Zhang J, Sato T, Yamagata S, Yamagata T: Positive regulation of tumor necrosis factor-alpha by ganglioside GM3 through Akt in mouse melanoma B16 cells. Biochem Biophys Res Commun; 2007 May 4;356(2):438-43
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  • [Title] Positive regulation of tumor necrosis factor-alpha by ganglioside GM3 through Akt in mouse melanoma B16 cells.
  • However, we found that GM3 and TNFalpha were expressed in parallel in mouse melanoma B16 cells that were transfected with UDP-Gal:glucosylceramide beta-1,4-galactosyltransferase cDNA in a sense or antisense direction or CMP-NeuAc:lactosylceramide alpha-2,3-sialyltransferase siRNA.
  • TNFalpha expression was increased by addition of GM3 to the B16 transfectants and decreased after treatment with D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol, an inhibitor of glucosylceramide synthesis.
  • These results clearly indicate that GM3 positively regulates TNFalpha expression in B16 cells.
  • GM3 was shown to increase phosphorylation of Akt in B16 cells and the B16-derived transfectants.
  • Treatment of B16 cells with siRNA targeted to Akt1/2 resulted in TNFalpha suppression, indicating that Akt plays an important role in regulation of TNFalpha expression.
  • [MeSH-major] G(M3) Ganglioside / pharmacology. Melanoma / pathology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / physiology. Skin Neoplasms / pathology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17367758.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androstadienes; 0 / Chromones; 0 / G(M3) Ganglioside; 0 / Morpholines; 0 / Piperazines; 0 / Tumor Necrosis Factor-alpha; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 154447-38-8 / LY 303511; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; XVA4O219QW / wortmannin
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72. Ni CS, Zhao N, Sun T, Zhao XL, Wang XH, Gu Q, Sun BC: [Pilot study of differentiation of bone marrow derived mesenchymal stem cells into endothelial cells induced by B16 melanoma cells in vitro]. Zhonghua Bing Li Xue Za Zhi; 2009 Jun;38(6):402-7
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  • [Title] [Pilot study of differentiation of bone marrow derived mesenchymal stem cells into endothelial cells induced by B16 melanoma cells in vitro].
  • The aim of the study was to investigate the induction process of BMSC by B16 melanoma cells in vitro and to analyze the role of VEGF-a in the process.
  • METHODS: A co-culture system containing BMSC and B16 melanoma cells based on transwell indirect model was established, and the induction process of BMSC by B16 melanoma cells was studied in vitro.
  • BMSC expressed CD105, CD90, CD73, CD44 and CD166, and acquired expressin of endothelial phenotype markers including VEGFR-1, VEGFR-2 and Factor VIII after co-culture with B16 melanoma cells for 48 hours.
  • In the co-culture system, B16 melanoma cells also up-regulated the expression of VEGF-a.
  • [MeSH-major] Bone Marrow Cells / cytology. Endothelial Cells / cytology. Melanoma, Experimental / pathology. Mesenchymal Stromal Cells / cytology. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19781348.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 9001-27-8 / Factor VIII; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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73. Shin JH, Choi GS, Kang WH, Myung KB: Sphingosine 1-phosphate triggers apoptotic signal for B16 melanoma cells via ERK and caspase activation. J Korean Med Sci; 2007 Apr;22(2):298-304
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  • [Title] Sphingosine 1-phosphate triggers apoptotic signal for B16 melanoma cells via ERK and caspase activation.
  • In this study, we investigated the effects of S1P on the cell growth, melanogenesis, and apoptosis of cultured B16 mouse melanoma cells.
  • In results, S1P was found to induce apoptosis in B16 melanoma cells in a dose- and time-dependent manner, but exerted minimal effects on melanogenesis.
  • Although receptors of sphingosine 1-phosphate (endothelial differentiation gene 1 [Edg]/S1P(1), Edg5/S1P(2), Edg3/S1P(3)) were expressed in B16 melanoma cells, they were shown not to be associated with S1P-induced apoptosis.
  • In addition, pertussis toxin did not block the apoptotic effects of S1P on B16 melanoma cells.
  • Interestingly, the ERK pathway inhibitor, UO126, reversed the apoptotic effects of S1P on B16 melanoma cells.
  • These results suggest that S1P induced apoptosis of B16 melanoma cells via an Edg receptor-independent, pertussis toxin-insensitive pathway, and appears to be associated with the ERK and caspase-3 activation.
  • [MeSH-major] Apoptosis / drug effects. Caspase 3 / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Lysophospholipids / administration & dosage. Melanoma / enzymology. Melanoma / pathology. Sphingosine / analogs & derivatives

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  • (PMID = 17449940.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Lysophospholipids; 26993-30-6 / sphingosine 1-phosphate; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / Caspase 3; NGZ37HRE42 / Sphingosine
  • [Other-IDs] NLM/ PMC2693598
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74. Benlloch M, Ortega A, Ferrer P, Segarra R, Obrador E, Asensi M, Carretero J, Estrela JM: Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cytotoxicity. J Biol Chem; 2005 Feb 25;280(8):6950-9
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  • [Title] Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cytotoxicity.
  • Highly metastatic B16 melanoma (B16M)-F10 cells, as compared with the low metastatic B16M-F1 line, have higher GSH content and preferentially overexpress BCL-2.
  • [MeSH-major] Apoptosis. Endothelium / cytology. Glutathione / metabolism. Melanoma, Experimental / pathology. Neoplasm Metastasis. gamma-Glutamyltransferase / antagonists & inhibitors

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  • (PMID = 15561710.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / multidrug resistance-associated protein 1; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator; CJ0O37KU29 / Verapamil; EC 2.3.2.2 / gamma-Glutamyltransferase; GAN16C9B8O / Glutathione
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75. Guan S, Su W, Wang N, Li P, Wang Y: A potent tyrosinase activator from Radix Polygoni multiflori and its melanogenesis stimulatory effect in B16 melanoma cells. Phytother Res; 2008 May;22(5):660-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A potent tyrosinase activator from Radix Polygoni multiflori and its melanogenesis stimulatory effect in B16 melanoma cells.
  • All the compounds were tested in B16 melanoma cells, the anthraquinones were found to inhibit cell proliferation at a concentration of 0.1-2.5 microg/mL, and THSG was found to be non-cytotoxic at a concentration of 0.1-12.5 microg/mL.
  • THSG significantly increased the activity of murine tyrosinase and stimulated melanin biosynthesis in B16 melanoma cells.
  • [MeSH-minor] Animals. Anthraquinones / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Glucosides / pharmacology. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Mice. Stilbenes / pharmacology

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  • (PMID = 18389468.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2,3,5,4'-tetrahydroxystilbene-2-O-glucoside; 0 / Anthraquinones; 0 / Glucosides; 0 / Melanins; 0 / Plant Extracts; 0 / Stilbenes; EC 1.14.18.1 / Monophenol Monooxygenase
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76. Suzuki S, Heldin CH, Heuchel RL: Platelet-derived growth factor receptor-beta, carrying the activating mutation D849N, accelerates the establishment of B16 melanoma. BMC Cancer; 2007;7:224

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Platelet-derived growth factor receptor-beta, carrying the activating mutation D849N, accelerates the establishment of B16 melanoma.
  • METHODS: B16 melanoma cells lacking PDGFR-beta expression and either mock-transfected or engineered to express PDGF-BB, were injected alone or in combination with matrigel into mice carrying the activated PDGFR-beta (D849N) and into wild type mice.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Melanoma, Experimental / genetics. Mutation / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics

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  • [Cites] J Biol Chem. 2004 Oct 8;279(41):42516-27 [15284236.001]
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  • (PMID = 18076756.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2234427
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77. Alshamsan A, Hamdy S, Samuel J, El-Kadi AO, Lavasanifar A, Uludağ H: The induction of tumor apoptosis in B16 melanoma following STAT3 siRNA delivery with a lipid-substituted polyethylenimine. Biomaterials; 2010 Feb;31(6):1420-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The induction of tumor apoptosis in B16 melanoma following STAT3 siRNA delivery with a lipid-substituted polyethylenimine.
  • In this study, we investigated the potential of nanoparticles based on polyethylenimine (PEI) modified with stearic acid (StA), to deliver siRNA for efficient STAT3 downregulation in B16 melanoma cells.
  • The B16 cells were targeted with approximately 6-200 nm of siRNA complexes for 36 h.
  • Compared to the PEI complexes, the PEI-StA complexes showed higher potency in STAT3 silencing in B16 cells accompanied by a significant induction of IL-6 secretion and a reduction of VEGF production.
  • When the cells were treated with 50 nm of siRNA complexes on a daily basis, the cell viability was dramatically reduced reaching only to 16% after the third daily dose of PEI-StA complexes, as compared to the 69% viability observed with the PEI complexes at an equivalent time period.
  • [MeSH-major] Apoptosis / drug effects. Lipids / chemistry. Melanoma / genetics. Melanoma / therapy. Polyethyleneimine / chemistry. RNA, Small Interfering / administration & dosage. RNA, Small Interfering / genetics. STAT3 Transcription Factor / genetics

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  • [Copyright] (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19913908.001).
  • [ISSN] 1878-5905
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP 42407; Canada / Canadian Institutes of Health Research / / MOP 74452
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Lipids; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 9002-98-6 / Polyethyleneimine
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78. Sheng FX, Fan JH, Wang DM, Zhao BC, Cui XY, Tian YX: [Secretory expression vector V-pLNCX-s-hri inhibits the growth of mouse B16 melanoma]. Ai Zheng; 2009 Mar;28(3):236-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Secretory expression vector V-pLNCX-s-hri inhibits the growth of mouse B16 melanoma].
  • This study was to construct V-pLNCX-s-hri, a secretory expression vector, and explore its inhibition effects on the growth of mouse B16 melanoma cells.
  • The model of B16 melanoma-carrying mouse was established and received different treatments.
  • RESULTS: The infection efficiency of V-pLNCX-s-hri on cultured B16 cells reached 38.5%.
  • mRNA and protein levels of hRI were detected in B16 cells infected by V-pLNCX-s-hri.
  • The hRI content in the supernatant of infected B16 cells reached 0.228 microg/mL.
  • CONCLUSIONS: V-pLNCX-s-hri can effectively infect B16 cells and induce high expression of hRI.
  • V-pLNCX-s-hri is superior to V-pLNCX-hri in inhibiting the growth of B16 cells.
  • [MeSH-major] Cell Proliferation. Melanoma, Experimental / pathology. Neovascularization, Pathologic / prevention & control. Placental Hormones / biosynthesis. Ribonucleases / antagonists & inhibitors

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  • (PMID = 19619436.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Placental Hormones; 0 / RNA, Messenger; 0 / Recombinant Proteins; 120178-77-0 / placental ribonuclease inhibitor; EC 3.1.- / Ribonucleases
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79. Hayashi C, Rittling S, Hayata T, Amagasa T, Denhardt D, Ezura Y, Nakashima K, Noda M: Serum osteopontin, an enhancer of tumor metastasis to bone, promotes B16 melanoma cell migration. J Cell Biochem; 2007 Jul 1;101(4):979-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum osteopontin, an enhancer of tumor metastasis to bone, promotes B16 melanoma cell migration.
  • Serum from wild-type mice induced cell migration of B16 melanoma cells, while serum from OPN-deficient mouse suppressed this event.
  • Overexpression of OPN in these cancer cells per se promoted cell proliferation and tended to increase B16 cell migration suggesting that OPN promotes bone metastasis by playing dual roles both in host microenvironment and in tumor cell itself.
  • [MeSH-minor] 3T3 Cells. Animals. Bone Neoplasms / blood. Bone Neoplasms / secondary. Cell Line, Tumor. Cell Proliferation / drug effects. Flavonoids / pharmacology. Genotype. Melanoma, Experimental / blood. Melanoma, Experimental / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinase Kinases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serum / physiology. Transfection

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  • (PMID = 17390343.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / RNA, Messenger; 106441-73-0 / Osteopontin; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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80. Takashima K, Fujiwara H, Inada S, Atsuji K, Araki Y, Kubota T, Yamagishi H: Tracking of green fluorescent protein (GFP)-labeled LAK cells in mice carrying B16 melanoma metastases. Anticancer Res; 2006 Sep-Oct;26(5A):3327-32
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tracking of green fluorescent protein (GFP)-labeled LAK cells in mice carrying B16 melanoma metastases.
  • In the present study, an in vivo tracking study was performed using an adoptive transfer model of lymphokine-activated killer (LAK) cells induced from green mice into C57/BL6 mice with B16 melanoma metastases.
  • [MeSH-major] Green Fluorescent Proteins / pharmacokinetics. Killer Cells, Lymphokine-Activated / pathology. Lung Neoplasms / metabolism. Melanoma, Experimental / pathology

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  • (PMID = 17094448.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interleukin-2; 147336-22-9 / Green Fluorescent Proteins
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81. Tai SS, Lin CG, Wu MH, Chang TS: Evaluation of depigmenting activity by 8-hydroxydaidzein in mouse B16 melanoma cells and human volunteers. Int J Mol Sci; 2009 Oct;10(10):4257-66
Hazardous Substances Data Bank. L-Ascorbic Acid .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of depigmenting activity by 8-hydroxydaidzein in mouse B16 melanoma cells and human volunteers.
  • In this study, the compound was evaluated for in vitro cellular tyrosinase and melanogenesis inhibitory activities in mouse B16 melanoma cells and for in vivo skin-whitening activity in human volunteers.
  • Hence, 8-OHDe exhibited more than an inhibitory effects on melanin production in B16 cells 10-fold stronger than kojic acid.
  • From the results of the study, it was concluded that 8-OHDe, the potent suicide substrate of mushroom tyrosinase, has depigmenting activities in both mouse melanoma cells and in human volunteers.
  • [MeSH-minor] Adult. Animals. Ascorbic Acid / analogs & derivatives. Ascorbic Acid / chemistry. Ascorbic Acid / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Female. Healthy Volunteers. Humans. Melanins / metabolism. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Mice. Middle Aged. Monophenol Monooxygenase / antagonists & inhibitors. Monophenol Monooxygenase / metabolism

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  • (PMID = 20057943.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / 8-hydroxydaidzein; 0 / Isoflavones; 0 / Melanins; 0 / Skin Lightening Preparations; 2V52R0NHXW / ascorbic acid 2-O-glucoside; EC 1.14.18.1 / Monophenol Monooxygenase; PQ6CK8PD0R / Ascorbic Acid
  • [Other-IDs] NLM/ PMC2790106
  • [Keywords] NOTNLM ; 8-hydroxydaidzein / skin whitening / suicide substrate / tyrosinase inhibitor
  • [General-notes] NLM/ Original DateCompleted: 20100628
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82. Choi MY, Song HS, Hur HS, Sim SS: Whitening activity of luteolin related to the inhibition of cAMP pathway in alpha-MSH-stimulated B16 melanoma cells. Arch Pharm Res; 2008 Sep;31(9):1166-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Whitening activity of luteolin related to the inhibition of cAMP pathway in alpha-MSH-stimulated B16 melanoma cells.
  • To examine the possibility of luteolin as a whitening agent, we measured antioxidant activity using DPPH assay, NBT/XO assay and intracellular ROS scavengning assay and depigmenting activity using tyrosinase assay, alpha-MSH-induced melanin production in B-16 cells.
  • Although luteolin did not directly inhibit tyrosinase activity, it dose-dependently inhibited both tyrosinase activity and melanin production in B16 melanoma cells stimulated by 1 microM alpha-MSH.
  • Luteolin dose-dependently inhibited cAMP levels in B16 melanoma cells stimulated by 1 microM alpha-MSH and 1 microM forskolin, which suggest that luteolin directly inhibits adenyl cyclase in B16 melanoma cells.
  • Therefore, these results suggest that whitening activity of luteolin may be due to the inhibition of adenyl cyclase involved in the signal pathway of alpha-MSH in B16 melanoma cells.
  • [MeSH-major] Cyclic AMP / physiology. Luteolin / pharmacology. Melanins / antagonists & inhibitors. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / antagonists & inhibitors. Signal Transduction / drug effects. alpha-MSH / pharmacology

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  • (PMID = 18806960.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biphenyl Compounds; 0 / Free Radical Scavengers; 0 / Melanins; 0 / Picrates; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 1898-66-4 / 2,2-diphenyl-1-picrylhydrazyl; 1F7A44V6OU / Colforsin; 581-05-5 / alpha-MSH; C5INA23HXF / Arbutin; E0399OZS9N / Cyclic AMP; EC 1.14.18.1 / Monophenol Monooxygenase; EC 1.17.3.2 / Xanthine Oxidase; KUX1ZNC9J2 / Luteolin
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83. Lee TH, Cho YH, Lee JD, Yang WI, Shin JL, Lee MG: Enhanced antitumor effect of dendritic cell based immunotherapy after intratumoral injection of radionuclide Ho-166 against B16 melanoma. Immunol Lett; 2006 Jul 15;106(1):19-26
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced antitumor effect of dendritic cell based immunotherapy after intratumoral injection of radionuclide Ho-166 against B16 melanoma.
  • Internal radiotherapy with the intratumoral injection of the beta-emitting radionuclide, Holmium (Ho)-166, into B16 melanoma resulted in a reduction in size and growth rate; however, complete remission was not always achieved.
  • Malignant melanoma was induced in mice by inoculating B16F10 cell line subcutaneously.
  • (1) non-treated (group I, n = 11), (2) treated with Ho-166 (group II, n = 16), (3) treated with immature DCs (group III, n = 8), and (4) treated with immature DCs after Ho-166 injection (group IV, n = 19).
  • Our results suggest that a combination of internal radiotherapy using Ho-166 and immature DCs could be used either to treat unresectable melanoma or as an adjuvant therapy after surgery.
  • [MeSH-major] Dendritic Cells / immunology. Immunotherapy. Melanoma / immunology. Melanoma / therapy. Piperidines / chemistry. Piperidines / therapeutic use. Thiazines / chemistry. Thiazines / therapeutic use

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  • (PMID = 16647143.001).
  • [ISSN] 0165-2478
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Piperidines; 0 / Radioisotopes; 0 / Thiazines; 115043-27-1 / Hoe 166
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84. Wang SM, Xu XY, Chen G, Yang LR: [Taohong Siwu decoction II inhibits the angiogenesis and the expressions of VEGF and KDR/FLK-1 in C57BL/6J mice bearing B16 melanoma]. Zhongguo Zhong Yao Za Zhi; 2005 Dec;30(23):1866-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Taohong Siwu decoction II inhibits the angiogenesis and the expressions of VEGF and KDR/FLK-1 in C57BL/6J mice bearing B16 melanoma].
  • OBJECTIVE: To investigate the effects of Taohong Siwu decoction II on B16 melanoma in mice and the underlying mechanism.
  • METHOD: C57BL/6J mice bearing B16 melanoma were used in this study.
  • CONCLUSION: Taohong Siwu decoction II can inhibit the growth of B16 melanoma in mice and attenuate the expressions of VEGF and KDR/FLK-1, suggesting that Taohong Siwu decoction II produces the antitumor effect via a possible antiagiogenisis mechanism.
  • [MeSH-major] Drugs, Chinese Herbal / pharmacology. Melanoma, Experimental / pathology. Neovascularization, Pathologic / pathology. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 16499030.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 0 / Taohong Siwu decoction II; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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85. Baral R, Mandal I, Chattopadhyay U: Immunostimulatory neem leaf preparation acts as an adjuvant to enhance the efficacy of poorly immunogenic B16 melanoma surface antigen vaccine. Int Immunopharmacol; 2005 Jul;5(7-8):1343-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunostimulatory neem leaf preparation acts as an adjuvant to enhance the efficacy of poorly immunogenic B16 melanoma surface antigen vaccine.
  • Immunogenecity of the poorly immunogenic B16 melanoma cell surface antigen (B16MelSAg) was enhanced by combining B16MelSAg with NLP in C57BL/6 mice, as evidenced by ELISA and flow cytometry.
  • Vaccination of mice with B16MelSAg+NLP more efficiently prevented the growth of B16 melanoma tumor than mice immunized with B16MelSAg or NLP alone.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Antigens, Neoplasm / immunology. Azadirachta. Cancer Vaccines / immunology. Melanoma, Experimental / immunology. Plant Leaves. Plant Preparations / pharmacology

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  • (PMID = 15914339.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Cancer Vaccines; 0 / Plant Preparations
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86. Kamei Y, Otsuka Y, Abe K: Comparison of the inhibitory effects of vitamin E analogues on melanogenesis in mouse B16 melanoma cells. Cytotechnology; 2009 Apr;59(3):183-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of the inhibitory effects of vitamin E analogues on melanogenesis in mouse B16 melanoma cells.
  • The effect of eight vitamin E analogues (d-alpha-, dl-alpha-, d-beta-, d-gamma-, and d-delta-tocopherols, d-alpha- and dl-alpha-tocopheryl acetates) and 2,2,5,7,8-pentamethyl-6-hydroxychroman (PMC) on melanogenesis were compared in mouse B16 melanoma cells.
  • D-beta-tocopherol at 250 mug ml(-1) inhibited not only 28% of melanin synthesis in B16 cells, but also 34% of the tyrosinase activity, a very important cascade enzyme involved in the synthesis of melanin in melanoma cells.
  • Weak activity was also observed with d-delta-tocopherol at 8 mug ml(-1) and with PMC at 16 mug ml(-1), with 19% and 25% inhibition of melanin synthesis, respectively.

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  • (PMID = 19568943.001).
  • [ISSN] 0920-9069
  • [Journal-full-title] Cytotechnology
  • [ISO-abbreviation] Cytotechnology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2774566
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87. Xu X, Wang S, Chen W, Chen G: Effects of taohong siwu decoction II in the chick chorioallantoic membrane (CAM) assay and on B16 melanoma in mice and endothelial cells ECV304 proliferation. J Tradit Chin Med; 2006 Mar;26(1):63-7

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  • [Title] Effects of taohong siwu decoction II in the chick chorioallantoic membrane (CAM) assay and on B16 melanoma in mice and endothelial cells ECV304 proliferation.
  • METHODS: The chick chorioallantoic membrane (CAM) assay was adopted to study the anti-angiogenesis action of THSWD II; the MTT test was used to investigate its effect on proliferation of the human umbilical vein endothelial cells ECV304; and the immunohistochemical method was used to observe the effect of THSWD II on the expression of kinase insert domain containing receptor/fetal liver kinase 1 (KDR/Flk-1) and the microvessel density (MVD) of B16 melanoma in mice.
  • RESULTS: After treatment with THSWD II, the blood vessel index of CAM and the absorbency of ECV304 in the THSWD II 1 mg/ml group and the 2 mg/ml group decreased significantly (P < 0.01); the weight, the expression of KDR/Flk-1 and the MVD of B16 melanoma in mice reduced significantly in the THSWD II 5 g/kg group, the 10 g/kg group and the TSHSWD 10g/kg plus cyclophosphamide group (P < 0.01).
  • CONCLUSION: THSWD II has the actions of anti-angiogenesis, and inhibiting the proliferation of ECV304 cells and the growth of B16 melanoma.

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  • (PMID = 16705858.001).
  • [ISSN] 0255-2922
  • [Journal-full-title] Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan
  • [ISO-abbreviation] J Tradit Chin Med
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drugs, Chinese Herbal; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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88. Ugen KE, Kutzler MA, Marrero B, Westover J, Coppola D, Weiner DB, Heller R: Regression of subcutaneous B16 melanoma tumors after intratumoral delivery of an IL-15-expressing plasmid followed by in vivo electroporation. Cancer Gene Ther; 2006 Oct;13(10):969-74
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  • [Title] Regression of subcutaneous B16 melanoma tumors after intratumoral delivery of an IL-15-expressing plasmid followed by in vivo electroporation.
  • In vivo electroporation has been used to efficiently deliver drugs and 'therapeutic' genes to tumors, including melanoma lesions.
  • This study reports on the effect of intratumoral delivery of an optimized DNA plasmid expressing interleukin-15 (pIL-15) on established murine melanoma tumors.
  • In this study, C57BL/6 mice were injected with B16.F10 melanoma cells and randomized into different experimental groups: untreated (P-V-E-), treated with pIL-15 (P+) or backbone plasmid (V+), with or without electroporation (E+ or E-).
  • These results demonstrate the ability of pIL-15 to mediate B16 melanoma regression, with the effect being significantly enhanced by electroporative delivery.
  • This is the first description of the ability of a naked DNA plasmid expressing IL-15 to alone mediate complete regression of B16 melanoma tumors and underscores the potential clinical use of these plasmids for the treatment of malignant tumors when delivered with in vivo electroporation.

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  • (PMID = 16763607.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / F32AI054152; United States / NIAID NIH HHS / AI / F32 AI054152; United States / NCI NIH HHS / CA / R01 CA122518-01A2; United States / NCI NIH HHS / CA / R01 CA122518; United States / NCI NIH HHS / CA / CA122518-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-15
  • [Other-IDs] NLM/ NIHMS253299; NLM/ PMC3277848
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89. Thanigaimalai P, Lee KC, Bang SC, Lee JH, Yun CY, Roh E, Hwang BY, Kim Y, Jung SH: Evaluation of 3,4-dihydroquinazoline-2(1H)-thiones as inhibitors of alpha-MSH-induced melanin production in melanoma B16 cells. Bioorg Med Chem; 2010 Feb 15;18(4):1555-62
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  • [Title] Evaluation of 3,4-dihydroquinazoline-2(1H)-thiones as inhibitors of alpha-MSH-induced melanin production in melanoma B16 cells.
  • The effect of QNTs to inhibit melanin formation in B16 melanoma cells was screened in the presence of alpha-MSH.
  • [MeSH-major] Melanins / biosynthesis. Melanoma, Experimental / metabolism. Quinazolines / pharmacology. alpha-MSH / antagonists & inhibitors

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20097083.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Melanins; 0 / Quinazolines; 581-05-5 / alpha-MSH
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90. Koo JH, Lee I, Yun SK, Kim HU, Park BH, Park JW: Saponified evening primrose oil reduces melanogenesis in B16 melanoma cells and reduces UV-induced skin pigmentation in humans. Lipids; 2010 May;45(5):401-7
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  • [Title] Saponified evening primrose oil reduces melanogenesis in B16 melanoma cells and reduces UV-induced skin pigmentation in humans.
  • In B16 melanoma cells, sap-EPO dose-dependently inhibited isobutylmethylxanthine-induced melanogenesis with no cytotoxicity.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Down-Regulation. Humans. Melanoma, Experimental. Men. Mice. Monophenol Monooxygenase / genetics. Monophenol Monooxygenase / metabolism. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Ultraviolet Rays

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  • (PMID = 20352496.001).
  • [ISSN] 1558-9307
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Melanins; 0 / Plant Oils; 0 / RNA, Messenger; EC 1.14.18.1 / Monophenol Monooxygenase
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91. Wu SP, Lee I, Ghoroghchian PP, Frail PR, Zheng G, Glickson JD, Therien MJ: Near-infrared optical imaging of B16 melanoma cells via low-density lipoprotein-mediated uptake and delivery of high emission dipole strength tris[(porphinato)zinc(II)] fluorophores. Bioconjug Chem; 2005 May-Jun;16(3):542-50
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  • [Title] Near-infrared optical imaging of B16 melanoma cells via low-density lipoprotein-mediated uptake and delivery of high emission dipole strength tris[(porphinato)zinc(II)] fluorophores.
  • The reconstituted LDL(PZn(3)) proteins can be used to deliver rapidly hundreds of copies of PZn(3) to a given murine B16 melanoma cell via LDL receptor-mediated endocytosis.
  • Confocal NIR fluorescence microscopy evinces that B16 cells can be imaged at very low doses (approximately nM) of NIRF.
  • The highly attractive photophysical properties of PZn(3) and closely related chromophores, coupled with their lack of toxicity and compatibility with uptake into apo-LDL and subsequent rapid delivery to B16 cells via LDLr-mediated endocytosis, suggest the potential utility of this platform for NIR optical imaging of cancer cells in vivo.
  • [MeSH-major] Fluorescent Dyes / metabolism. Lipoproteins, LDL / metabolism. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Metalloporphyrins / metabolism

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  • (PMID = 15898720.001).
  • [ISSN] 1043-1802
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-37199; United States / NCI NIH HHS / CA / P20-CA86255; United States / NCI NIH HHS / CA / R24-CA83105-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Lipoproteins, LDL; 0 / Metalloporphyrins; 0 / tris(porphinato)zinc(II)
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92. Wu TG, Perdigão JR, Umhoefer TK, Cao J, Ansari DA, Albrecht TB, Knutson EP, Rose WA 2nd, Jorgensen AJ, Ryan LM, Abdalla LE, Fleischmann WR Jr: Heterogeneous interleukin-15 inducibilities in murine B16 melanoma and RM-1 prostate carcinoma by interferon-alpha treatment. J Interferon Cytokine Res; 2009 Nov;29(11):719-28
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  • [Title] Heterogeneous interleukin-15 inducibilities in murine B16 melanoma and RM-1 prostate carcinoma by interferon-alpha treatment.
  • Long-term treatment of mouse cancer cells with interferon-alpha (IFN-alpha) converts parental B16 melanoma cells to B16alpha vaccine cells.
  • Inoculation of syngeneic mice with UV-irradiated B16alpha vaccine cells triggers immunity to the parental B16 tumor that is mediated by host macrophages, T cells, and NK cells.

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  • (PMID = 19642895.001).
  • [ISSN] 1557-7465
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES10018
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Interferon-alpha; 0 / Interleukin-15; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC3096523
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93. Lee J, Jung E, Park J, Jung K, Park E, Kim J, Hong S, Park J, Park S, Lee S, Park D: Glycyrrhizin induces melanogenesis by elevating a cAMP level in b16 melanoma cells. J Invest Dermatol; 2005 Feb;124(2):405-11
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  • [Title] Glycyrrhizin induces melanogenesis by elevating a cAMP level in b16 melanoma cells.
  • In this study, using B16 melanoma cells, we showed that GR activated activator protein-1 (AP-1) and cyclic response filament "CRE" promoters, but not the nuclear factor-kappaB promoter.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cyclic AMP / metabolism. Glycyrrhizic Acid / pharmacology. Melanocytes / drug effects. Melanoma. Skin Neoplasms

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  • (PMID = 15675961.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Melanins; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 6FO62043WK / Glycyrrhizic Acid; E0399OZS9N / Cyclic AMP; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.25 / MAP Kinase Kinase Kinase 1; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.6.5.2 / ras Proteins
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94. Itoh T, Furuichi Y: Hot-water extracts from adzuki beans (Vigna angularis) stimulate not only melanogenesis in cultured mouse B16 melanoma cells but also pigmentation of hair color in C3H mice. Biosci Biotechnol Biochem; 2005 May;69(5):873-82
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  • [Title] Hot-water extracts from adzuki beans (Vigna angularis) stimulate not only melanogenesis in cultured mouse B16 melanoma cells but also pigmentation of hair color in C3H mice.
  • Its distilled water fraction (WEx) was found to stimulate tyrosinase activity in cultured mouse B16 melanoma cells and hair color pigmentation in C3H mice.
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Melanoma, Experimental / metabolism. Mice. Mice, Inbred C3H. Plant Extracts / chemistry. Plant Extracts / pharmacology

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  • (PMID = 15914904.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Melanins; 0 / Plant Extracts
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95. Amarzguioui M, Peng Q, Wiiger MT, Vasovic V, Babaie E, Holen T, Nesland JM, Prydz H: Ex vivo and in vivo delivery of anti-tissue factor short interfering RNA inhibits mouse pulmonary metastasis of B16 melanoma cells. Clin Cancer Res; 2006 Jul 1;12(13):4055-61
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  • [Title] Ex vivo and in vivo delivery of anti-tissue factor short interfering RNA inhibits mouse pulmonary metastasis of B16 melanoma cells.
  • In this study, we explore the effects of ex vivo and in vivo delivery of short interfering RNA (siRNA) targeting tissue factor on B16 melanoma colonization of the lung in a murine model for metastasis.
  • EXPERIMENTAL DESIGN AND RESULTS: C57BL/6 mice were evaluated for pulmonary metastases following tail vein injection of B16 cells transfected with either active or inactive siRNA.
  • [MeSH-major] Drug Delivery Systems. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Melanoma, Experimental / drug therapy. RNA, Small Interfering / administration & dosage. Thromboplastin / genetics

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  • (PMID = 16818705.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 9035-58-9 / Thromboplastin
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96. Ehira N, Oshiumi H, Matsumoto M, Kondo T, Asaka M, Seya T: An embryo-specific expressing TGF-β family protein, growth-differentiation factor 3 (GDF3), augments progression of B16 melanoma. J Exp Clin Cancer Res; 2010;29:135
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  • [Title] An embryo-specific expressing TGF-β family protein, growth-differentiation factor 3 (GDF3), augments progression of B16 melanoma.
  • Malignant tumor cells often express embryonic antigens which share the expression with embryonic stem (ES) cells.
  • We examined the expression of ES cell-specific genes in the mouse B16 melanoma cell line to identify the factors promoting tumorigenesis.
  • We found that endogenous growth-differentiation factor 3 (GDF3) expression was induced in implant B16 tumor during tumor progression in syngenic C57BL/6 mice.
  • B16 F10, a subline with a high metastatic potential, continuously expressed GDF3 while low metastatic B16 F1 expressed comparatively decreased levels of GDF3.
  • Overexpression of GDF3 promoted growth of implanted melanoma B16 F1 and F10 in syngenic mice.
  • Such a profile was reported to be characteristic of melanoma stem cell-like cells.
  • Since GDF3-driven CD24 acts as a receptor for endogenous innate immune ligands that modulate cell proliferation, CD24 is an effective determinant of tumorigenesis in malignant cell transformation.
  • Finally, our results support the view that GDF3 has the ability to induce progression of CD24-inducible melanoma in mice.
  • [MeSH-major] Growth Differentiation Factor 3 / metabolism. Melanoma, Experimental / metabolism

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  • (PMID = 20950440.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD24; 0 / Antigens, CD44; 0 / Cd24a protein, mouse; 0 / Cd44 protein, mouse; 0 / Gdf3 protein, mouse; 0 / Growth Differentiation Factor 3
  • [Other-IDs] NLM/ PMC2972255
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97. Graves E, Ramsay E, McCarthy DO: Inhibitors of COX activity preserve muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma. Res Nurs Health; 2006 Apr;29(2):87-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitors of COX activity preserve muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma.
  • We report that indomethacin, a nonspecific inhibitor of COX, and NS398, a specific inhibitor of COX2, preserved muscle mass and reduced type 1 TNF receptors in muscles of mice bearing the Lewis lung carcinoma, but not in mice bearing the B16 melanoma.
  • [MeSH-minor] Analysis of Variance. Animals. Carcinoma, Lewis Lung. Female. Interleukin-6 / metabolism. Melanoma, Experimental. Mice. Mice, Inbred C57BL. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright 2006 Wiley Periodicals, Inc.
  • (PMID = 16532483.001).
  • [ISSN] 0160-6891
  • [Journal-full-title] Research in nursing & health
  • [ISO-abbreviation] Res Nurs Health
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Interleukin-6; 0 / Nitrobenzenes; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Sulfonamides; 0 / Tumor Necrosis Factor-alpha; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; XXE1CET956 / Indomethacin
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98. McCarthy DO, Graves E: Conjugated linoleic acid preserves muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma. Res Nurs Health; 2006 Apr;29(2):98-104
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conjugated linoleic acid preserves muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma.
  • The B16 melanoma expresses TNFa mRNA, and induced SMW with no change in muscle levels of TNFa type 1 receptor (TNFR1) protein.
  • A diet containing .5% CLA had no effect on SMW or TNFR1 in mice bearing B16 tumors.
  • [MeSH-minor] Analysis of Variance. Animals. Carcinoma, Lewis Lung. Female. Male. Melanoma, Experimental. Mice. Mice, Inbred C57BL. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright 2006 Wiley Periodicals, Inc.
  • (PMID = 16532476.001).
  • [ISSN] 0160-6891
  • [Journal-full-title] Research in nursing & health
  • [ISO-abbreviation] Res Nurs Health
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Linoleic Acids, Conjugated; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Necrosis Factor-alpha
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99. Yu J, Tian R, Xiu B, Yan J, Jia R, Zhang L, Chang AE, Song H, Li Q: Antitumor activity of T cells generated from lymph nodes draining the SEA-expressing murine B16 melanoma and secondarily activated with dendritic cells. Int J Biol Sci; 2009;5(2):135-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of T cells generated from lymph nodes draining the SEA-expressing murine B16 melanoma and secondarily activated with dendritic cells.
  • We transferred the bacterial superantigen staphylococcal enterotoxin A (SEA) gene into B16 murine melanoma tumor cells, and used them to induce TDLN (SEA TDLN) in syngeneic hosts.
  • Wild-type (wt) TDLN induced by parental B16 tumor was used as a control.
  • DC-stimulated SEA TDLN cells eliminated nearly 90% of the pulmonary metastasis in mice bearing established B16 melanoma micrometastases.
  • [MeSH-major] Dendritic Cells / physiology. Enterotoxins / metabolism. Immunotherapy, Adoptive / methods. Lymph Nodes / cytology. Melanoma, Experimental / therapy. T-Lymphocytes / physiology

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  • (PMID = 19173035.001).
  • [ISSN] 1449-2288
  • [Journal-full-title] International journal of biological sciences
  • [ISO-abbreviation] Int. J. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Enterotoxins; 37337-57-8 / enterotoxin A, Staphylococcal
  • [Other-IDs] NLM/ PMC2631223
  • [Keywords] NOTNLM ; Adoptive therapy / B16 melanoma / Staphylococcal enterotoxin A (SEA) / T lymphocyte / dendritic cells (DC)
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100. Vandercappellen J, Liekens S, Bronckaers A, Noppen S, Ronsse I, Dillen C, Belleri M, Mitola S, Proost P, Presta M, Struyf S, Van Damme J: The COOH-terminal peptide of platelet factor-4 variant (CXCL4L1/PF-4var47-70) strongly inhibits angiogenesis and suppresses B16 melanoma growth in vivo. Mol Cancer Res; 2010 Mar;8(3):322-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The COOH-terminal peptide of platelet factor-4 variant (CXCL4L1/PF-4var47-70) strongly inhibits angiogenesis and suppresses B16 melanoma growth in vivo.
  • In addition, low (7 microg total) doses of intratumoral CXCL4L1/PF-4var(47-70) inhibited B16 melanoma growth in mice more extensively than CXCL4/PF-4(47-70).
  • This antitumoral activity was predominantly mediated through inhibition of angiogenesis (without affecting blood vessel stability) and induction of apoptosis, as evidenced by immunohistochemical and fluorescent staining of B16 tumor tissue.
  • [MeSH-major] Angiostatic Proteins / pharmacology. Antineoplastic Agents / pharmacology. Melanoma, Experimental / drug therapy. Neovascularization, Pathologic / drug therapy. Peptide Fragments / pharmacology. Platelet Factor 4 / pharmacology

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  • (PMID = 20215425.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiostatic Proteins; 0 / Antineoplastic Agents; 0 / PF4V1 protein, human; 0 / Peptide Fragments; 37270-94-3 / Platelet Factor 4
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