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1. Li B, VanRoey M, Wang C, Chen TH, Korman A, Jooss K: Anti-programmed death-1 synergizes with granulocyte macrophage colony-stimulating factor--secreting tumor cell immunotherapy providing therapeutic benefit to mice with established tumors. Clin Cancer Res; 2009 Mar 1;15(5):1623-34
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  • EXPERIMENTAL DESIGN: Survival studies were done in the B16 melanoma and CT26 colon carcinoma tumor models.
  • Immune monitoring studies were done in the B16 model.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Apoptosis Regulatory Proteins / antagonists & inhibitors. Colonic Neoplasms / therapy. Granulocyte-Macrophage Colony-Stimulating Factor / physiology. Immunotherapy. Melanoma, Experimental / therapy

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  • [CommentIn] Clin Cancer Res. 2009 Mar 1;15(5):1507-9 [19240168.001]
  • (PMID = 19208793.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Apoptosis Regulatory Proteins; 0 / Cytokines; 0 / Neoplasm Proteins; 0 / PDCD1 protein, human; 0 / Programmed Cell Death 1 Receptor; 0 / Recombinant Fusion Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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2. Averill-Bates DA, Chérif A, Agostinelli E, Tanel A, Fortier G: Anti-tumoral effect of native and immobilized bovine serum amine oxidase in a mouse melanoma model. Biochem Pharmacol; 2005 Jun 15;69(12):1693-704
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  • [Title] Anti-tumoral effect of native and immobilized bovine serum amine oxidase in a mouse melanoma model.
  • The aims of the study were to evaluate the anti-tumoral activities of native and immobilized BSAO in mouse melanoma and also to determine the mechanism of tumor cell death.
  • C57BL mice received a subcutaneous injection of B16 melanoma cells to induce formation of tumors, prior to antitumor treatments with native and immobilized BSAO.
  • [MeSH-major] Amine Oxidase (Copper-Containing) / blood. Amine Oxidase (Copper-Containing) / therapeutic use. Antineoplastic Agents / therapeutic use. Enzymes, Immobilized / therapeutic use. Growth Inhibitors / therapeutic use. Melanoma, Experimental / drug therapy

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  • (PMID = 15935145.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzymes, Immobilized; 0 / Growth Inhibitors; 2FZ7Y3VOQX / Spermine; EC 1.4.3.21 / Amine Oxidase (Copper-Containing)
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3. Krieg C, Létourneau S, Pantaleo G, Boyman O: Improved IL-2 immunotherapy by selective stimulation of IL-2 receptors on lymphocytes and endothelial cells. Proc Natl Acad Sci U S A; 2010 Jun 29;107(26):11906-11
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  • Treatment of mice with high-dose IL-2 led to efficient expansion of effector immune cells expressing high levels of IL-2Rbetagamma, including CD8(+) T cells and natural killer cells, which resulted in a considerable antitumor response against s.c. and pulmonary B16 melanoma nodules.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / immunology. Antigen-Antibody Complex / administration & dosage. Antigen-Antibody Complex / immunology. Endothelial Cells / immunology. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Interleukin-2 Receptor alpha Subunit / deficiency. Interleukin-2 Receptor alpha Subunit / genetics. Interleukin-2 Receptor alpha Subunit / metabolism. Lung / cytology. Lung / immunology. Lung Neoplasms / immunology. Lung Neoplasms / secondary. Lung Neoplasms / therapy. Lymphocytes / immunology. Melanoma, Experimental / immunology. Melanoma, Experimental / secondary. Melanoma, Experimental / therapy. Mice. Mice, Inbred C57BL. Mice, Knockout. Pulmonary Edema / etiology. Pulmonary Edema / immunology. Recombinant Proteins / administration & dosage. Recombinant Proteins / adverse effects. Recombinant Proteins / therapeutic use

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  • (PMID = 20547866.001).
  • [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
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigen-Antibody Complex; 0 / Homeodomain Proteins; 0 / IL2 protein, human; 0 / Il2ra protein, mouse; 0 / Interleukin-2; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin-2; 0 / Recombinant Proteins; 128559-51-3 / RAG-1 protein
  • [Other-IDs] NLM/ PMC2900642
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4. Robey IF, Baggett BK, Kirkpatrick ND, Roe DJ, Dosescu J, Sloane BF, Hashim AI, Morse DL, Raghunand N, Gatenby RA, Gillies RJ: Bicarbonate increases tumor pH and inhibits spontaneous metastases. Cancer Res; 2009 Mar 15;69(6):2260-8
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  • In tail vein injections of alternative cancer models, bicarbonate had mixed results, inhibiting the formation of metastases from PC3M prostate cancer cells, but not those of B16 melanoma.

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  • (PMID = 19276390.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA077575-09; United States / NCI NIH HHS / CA / R01 CA077575; United States / NCI NIH HHS / CA / CA 077575; United States / NCI NIH HHS / CA / R01 CA077575-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 8MDF5V39QO / Sodium Bicarbonate; EC 3.4.22.1 / Cathepsin B
  • [Other-IDs] NLM/ NIHMS179466; NLM/ PMC2834485
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5. Begley J, Vo DD, Morris LF, Bruhn KW, Prins RM, Mok S, Koya RC, Garban HJ, Comin-Anduix B, Craft N, Ribas A: Immunosensitization with a Bcl-2 small molecule inhibitor. Cancer Immunol Immunother; 2009 May;58(5):699-708
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, the addition of ABT-737 to either a vaccine strategy involving priming with TRP-2 melanoma antigen peptide-pulsed DC and boosting with recombinant Listeria monocytogenes expressing the same melanoma antigen, or the adoptive transfer of TCR transgenic cells, did not result in superior antitumor activity against B16 murine melanoma.
  • In vitro studies failed to demonstrate increased cytotoxic lytic activity when testing the combination of ABT-737 with lymphokine activated killer (LAK) cells, or the death receptor agonists Fas, TRAIL-ligand or TNF-alpha against the CT26 and B16 cell lines.
  • In conclusion, the Bcl-2 inhibitor ABT-737 sensitized cancer cells to the antitumor effect of antigen-specific immunotherapy in a vaccine model for the CT26 colon carcinoma in vivo but not in two immunotherapy strategies against B16 melanoma.
  • [MeSH-major] Biphenyl Compounds / therapeutic use. Cancer Vaccines / therapeutic use. Colonic Neoplasms / therapy. Immunotherapy / methods. Melanoma, Experimental / therapy. Neoplasm Proteins / antagonists & inhibitors. Nitrophenols / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Sulfonamides / therapeutic use

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  • (PMID = 18807035.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA127565
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antigens, CD95; 0 / Antigens, Neoplasm; 0 / Biphenyl Compounds; 0 / Cancer Vaccines; 0 / Neoplasm Proteins; 0 / Nitrophenols; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Death Domain; 0 / Recombinant Fusion Proteins; 0 / Sulfonamides; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
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6. Zhang X, Moyana T, Quereshi M, Xiang J: Conversion of tolerogenic CD4-8- dendritic cells to immunogenic ones inducing efficient antitumor immunity. Cancer Biother Radiopharm; 2006 Feb;21(1):74-80
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  • Vaccination of mice with converted CD4-8- DCs induced strong OVA-specific cytotoxic T-lymphocyte (CTL) responses and protective immunity against OVA-expressing BL6-10OVA B16 melanoma.
  • [MeSH-major] Antigens, CD4 / immunology. Antigens, CD8 / immunology. Dendritic Cells / immunology. Lymphoma, T-Cell / immunology. Melanoma, Experimental / immunology

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  • (PMID = 16480334.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8
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7. Arora A, Su G, Mathiowitz E, Reineke J, Chang AE, Sabel MS: Neoadjuvant intratumoral cytokine-loaded microspheres are superior to postoperative autologous cellular vaccines in generating systemic anti-tumor immunity. J Surg Oncol; 2006 Oct 1;94(5):403-12
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  • METHODS: C57BL6 mice with established B16 melanomas underwent a single intralesional injection of IL-12, TNF-alpha or GM-CSF PLAM, alone or in combination.
  • Adjuvant therapy, using irradiated B16 cells in combination with equivalent doses of IL-12 and TNF-alpha, failed to generate a similar T-cell response or prevent re-challenge.
  • [MeSH-major] Cancer Vaccines / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Immunotherapy, Adoptive. Interleukin-12 / administration & dosage. Melanoma, Experimental / immunology. Melanoma, Experimental / therapy. Tumor Necrosis Factor-alpha / administration & dosage

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16967445.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA102602-01
  • [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 / Cancer Vaccines; 0 / Polymers; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 26100-51-6 / poly(lactic acid); 33X04XA5AT / Lactic Acid; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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8. Kaptzan T, Skutelsky E, Itzhaki O, Sinai J, Huszar M, Siegal A, Ben-Zvi R, Jossiphov J, Michowitz M, Schiby G, Leibovici J: Efficacy of anti-angiogenic treatment of tumors in old versus young mice. Mech Ageing Dev; 2006 Apr;127(4):398-409
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  • TNP-470 treatment resulted in an inhibitory effect on B16 melanoma in both young and old mice but the effect was more pronounced in old animals.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Lymphoma / drug therapy. Melanoma, Experimental / drug therapy. Neoplasms / drug therapy

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  • (PMID = 16476469.001).
  • [ISSN] 0047-6374
  • [Journal-full-title] Mechanisms of ageing and development
  • [ISO-abbreviation] Mech. Ageing Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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9. Lin Y, Dubinsky WP, Ho DH, Felix E, Newman RA: Determinants of human and mouse melanoma cell sensitivities to oleandrin. J Exp Ther Oncol; 2008;7(3):195-205
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Determinants of human and mouse melanoma cell sensitivities to oleandrin.
  • Oleandrin, a cardiac glycoside component of Nerium oleander, has been shown to induce apoptosis in malignant cells.
  • Using human BRO and mouse B16 melanoma cell lines, we explored several possible determinants of cell sensitivity to oleandrin and compared with ouabain.
  • Oleandrin and ouabain induced apoptosis was detected in BRO cells while no evidence of cell death was observed in B16 cells even at concentrations 1000-fold higher than that used for BRO cells.
  • Partially purified Na+, K(+)-ATPase from human BRO cells was inhibited at a concentration that was 1000-fold less than that was required to inhibit mouse B16 enzyme to the same extent.
  • Using Western blot analyses, human BRO cells were found to express both the sensitive alpha3 isoform and the less sensitive alpha1 isoform of Na+, K(+)-ATPase while mouse B16 cells expressed only the alpha1 isoform.
  • These data suggest that differential expressions of Na+, K(+)-ATPase activities and its isoforms in BRO and B16 cells as well as cellular drug uptake may be important determinants of tumor cell sensitivity to cardiac glycosides.
  • [MeSH-major] Cardenolides / pharmacology. Cardiac Glycosides / pharmacology. Cell Proliferation / drug effects. Melanoma, Experimental / pathology. Sodium-Potassium-Exchanging ATPase / metabolism

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  • (PMID = 19066128.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cardenolides; 0 / Cardiac Glycosides; 0 / Enzyme Inhibitors; 0 / Protein Isoforms; 5ACL011P69 / Ouabain; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase; II95UDU7I4 / oleandrin
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10. 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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11. Yang J, Jin G, Liu X, Liu S: Therapeutic effect of pEgr-IL18-B7.2 gene radiotherapy in B16 melanoma-bearing mice. Hum Gene Ther; 2007 Apr;18(4):323-32
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  • [Title] Therapeutic effect of pEgr-IL18-B7.2 gene radiotherapy in B16 melanoma-bearing mice.
  • After the introduction of pEgr-IL18-B7.2 into B16 melanoma cells, followed by X-ray irradiation, higher expression levels of B7.2 and IL18 compared with control were found both by flow cytometry and enzyme-linked immunosorbent assay.
  • It was shown that even low-dose irradiation was able to induce their expression, which could be tightly regulated either by giving cells different doses of radiation or the same dose at different time points. pEgr-IL18-B7.2 was then packaged with liposome and injected into melanoma tumor-bearing mice.
  • B16 tumor growth slowed significantly when treated with pEgr-IL18-B7.2 plus X-radiation versus either treatment separately.
  • [MeSH-major] Antigens, CD86 / genetics. Genetic Therapy / methods. Interleukin-18 / genetics. Melanoma, Experimental / therapy. Skin Neoplasms / therapy

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  • (PMID = 17411412.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD86; 0 / CD86 protein, human; 0 / Interleukin-18; 0 / Tumor Necrosis Factor-alpha
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12. Hussein MR: Tumour-associated macrophages and melanoma tumourigenesis: integrating the complexity. Int J Exp Pathol; 2006 Jun;87(3):163-76
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  • [Title] Tumour-associated macrophages and melanoma tumourigenesis: integrating the complexity.
  • The macrophage (TAMs) content of melanoma ranges from 0 to 30% and their density increases with increasing tumour thickness.
  • The melanoma cells and TAMs seem to interact with each other through the release of soluble factors that either prevent or enhance tumour growth.
  • For instance, syngeneic macrophages from tumour-bearing mice can inhibit melanoma growth in the nude mice more than the control macrophages.
  • Alternatively, metastatic B16 melanoma cells can produce some macrophage cytotoxic substances that help tumour cells not only escape the host immunosurveillance system but also prevent distant metastasis.
  • Together, these observations suggest opposing effects for these soluble factors in melanoma.
  • To date, little is available in the literature about the interactions between TAMs and melanoma cells.
  • [MeSH-major] Antigen-Presenting Cells / immunology. Antigens, Neoplasm / immunology. Macrophages / physiology. Melanoma, Experimental / immunology

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  • (PMID = 16709225.001).
  • [ISSN] 0959-9673
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
  • [Number-of-references] 74
  • [Other-IDs] NLM/ PMC2517364
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13. Riddle DS, Sanz L, Chong H, Thompson J, Vile RG: Tumor cell surface display of immunoglobulin heavy chain Fc by gene transfer as a means to mimic antibody therapy. Hum Gene Ther; 2005 Jul;16(7):830-44
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  • In vitro, Fc receptor-positive natural killer (NK) cells specifically recognized and lysed B16 melanoma cells expressing surface IgFc.
  • Macrophages bound to B16-Fc cells significantly more than to parental B16 cells and surface IgFc expression promoted formation of the terminal complement pore complex leading to cell lysis and death.
  • Expression of IgFc dramatically delayed the ability of B16 cells to form tumors in vivo, attributable largely to the effects of NK cells.
  • Furthermore, fluorescence-activated cell-sorting analysis showed that cells from outgrowth B16 IgFc tumors had lost all IgFc expression.
  • [MeSH-major] Genetic Therapy. Immunoglobulin Fc Fragments / genetics. Immunoglobulin Heavy Chains / genetics. Melanoma, Experimental / therapy

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  • (PMID = 16000065.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA94180-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin Heavy Chains
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14. 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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  • [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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15. 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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16. Akihisa T, Noto T, Takahashi A, Fujita Y, Banno N, Tokuda H, Koike K, Suzuki T, Yasukawa K, Kimura Y: Melanogenesis inhibitory, anti-inflammatory, and chemopreventive effects of limonoids from the seeds of Azadirachta indicia A. Juss. (neem). J Oleo Sci; 2009;58(11):581-94
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  • Upon evaluation of compounds 1-32 on the melanogenesis in the B16 melanoma cells, five compounds, 20, 26, 27, 29, and 31, exhibited marked inhibitory effect (74-91% reduction of melanin content at 25 microg/mL) with no or almost no toxicity to the cells.
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor / methods. Magnetic Resonance Spectroscopy. Melanoma, Experimental / metabolism. Melanoma, Experimental / prevention & control. Mice. Plant Extracts / chemistry. Plant Extracts / isolation & purification. Plant Extracts / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 19844073.001).
  • [ISSN] 1347-3352
  • [Journal-full-title] Journal of oleo science
  • [ISO-abbreviation] J Oleo Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents, Phytogenic; 0 / Limonins; 0 / Melanins; 0 / Plant Extracts
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17. Chen LG, Chang WL, Lee CJ, Lee LT, Shih CM, Wang CC: Melanogenesis inhibition by gallotannins from Chinese galls in B16 mouse melanoma cells. Biol Pharm Bull; 2009 Aug;32(8):1447-52
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  • [Title] Melanogenesis inhibition by gallotannins from Chinese galls in B16 mouse melanoma cells.
  • In a B16 mouse melanoma cell culture assay, Chinese galls dose-dependently inhibited melanin biosynthesis.
  • Using ultraviolet A (UVA) or alpha-melanocyte-stimulating hormone (alpha-MSH) to stimulate B16 cells after Chinese gall treatment, the melanin biosynthesis of B16 cells was inhibited in a dose-dependent manner.
  • The active compounds of Chinese galls were isolated by column chromatography, and the melanin biosynthesis inhibition in B16 melanoma cells was measured.
  • [MeSH-minor] Animals. Aphids / growth & development. Biphenyl Compounds / chemistry. Cell Line, Tumor. Dose-Response Relationship, Drug. Free Radicals / chemistry. Hyperpigmentation / drug therapy. Hyperpigmentation / metabolism. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Mice. Monophenol Monooxygenase / antagonists & inhibitors. Picrates / chemistry. Plant Leaves / chemistry. Plant Leaves / parasitology. Ultraviolet Rays

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  • (PMID = 19652388.001).
  • [ISSN] 1347-5215
  • [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 / Biphenyl Compounds; 0 / Drugs, Chinese Herbal; 0 / Free Radical Scavengers; 0 / Free Radicals; 0 / Hydrolyzable Tannins; 0 / Melanins; 0 / Picrates; 1898-66-4 / 2,2-diphenyl-1-picrylhydrazyl; EC 1.14.18.1 / Monophenol Monooxygenase
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18. Ali S, Mulryan K, Taher T, Stern PL: Immunotherapy success in prophylaxis cannot predict therapy: prime-boost vaccination against the 5T4 oncofoetal antigen. Cancer Immunol Immunother; 2007 Feb;56(2):165-80
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  • We have investigated the tumour therapeutic efficacy of homologous and heterologous prime-boost vaccine strategies against the 5T4 oncofoetal antigen, using both replication defective adenovirus expressing human 5T4 (Ad5T4), and retrovirally transduced DC lines (DCh5T4) in a subcutaneous B16 melanoma model (B16h5T4).
  • [MeSH-major] Antigens, Neoplasm / immunology. Cancer Vaccines / immunology. Melanoma, Experimental / prevention & control. Melanoma, Experimental / therapy. Vaccination / methods

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  • (PMID = 16758205.001).
  • [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 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Interleukin-2 Receptor alpha Subunit; 0 / oncofetal antigens
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19. Wolf M, Bauder-Wüst U, Haberkorn U, Mier W, Eisenhut M: Alkylating benzamides with melanoma cytotoxicity: role of melanin, tyrosinase, intracellular pH and DNA interaction. Melanoma Res; 2005 Oct;15(5):383-91
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  • [Title] Alkylating benzamides with melanoma cytotoxicity: role of melanin, tyrosinase, intracellular pH and DNA interaction.
  • N-(2-Dialkylaminoethyl)benzamides have been shown to selectively accumulate in melanoma metastases with high uptake capacity.
  • It has been demonstrated that this significant targeting effect improves the cytotoxicity against melanoma cells.
  • Although these agents are not accumulated by non-melanoma cells, they have been found to be toxic.
  • An investigation of the influence of the melanin content on the cytotoxicity of these substances in B16 melanoma and Morris hepatoma (MH3924A) cells was performed, together with their influence on melanosomal pH and tyrosinase activity.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Benzamides / pharmacology. DNA / metabolism. Melanins / metabolism. Melanoma, Experimental / drug therapy. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / metabolism

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  • (PMID = 16179865.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Drug Carriers; 0 / Melanins; 18D0SL7309 / Chlorambucil; 9007-49-2 / DNA; EC 1.14.18.1 / Monophenol Monooxygenase
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20. Pandha HS, Heinemann L, Simpson GR, Melcher A, Prestwich R, Errington F, Coffey M, Harrington KJ, Morgan R: Synergistic effects of oncolytic reovirus and cisplatin chemotherapy in murine malignant melanoma. Clin Cancer Res; 2009 Oct 1;15(19):6158-66
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  • [Title] Synergistic effects of oncolytic reovirus and cisplatin chemotherapy in murine malignant melanoma.
  • PURPOSE: To test combination treatment schedules of reovirus and cisplatin chemotherapy in human and murine melanoma cell lines and murine models of melanoma and to investigate the possible mechanisms of synergistic antitumor effects.
  • Single agent and combination therapy effects were tested in vivo in two immunocompetent models of murine melanoma.
  • RESULTS: Variable degrees of synergistic cytotoxicity between live reovirus and several chemotherapy agents were observed in B16.F10 mouse melanoma cells, most significantly with cisplatin (combination index of 0.42 +/- 0.03 at ED(50)).
  • CONCLUSION: The combination of reovirus and several chemotherapeutic agents synergistically enhanced cytotoxicity in human and murine melanoma cell lines in vitro and murine tumors in vivo.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Melanoma, Experimental / therapy. Oncolytic Virotherapy. Reoviridae / physiology

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  • (PMID = 19773377.001).
  • [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 Kingdom / Cancer Research UK / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin
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21. Du W, Takuwa N, Yoshioka K, Okamoto Y, Gonda K, Sugihara K, Fukamizu A, Asano M, Takuwa Y: S1P(2), the G protein-coupled receptor for sphingosine-1-phosphate, negatively regulates tumor angiogenesis and tumor growth in vivo in mice. Cancer Res; 2010 Jan 15;70(2):772-81
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  • Lewis lung carcinoma or B16 melanoma cells implanted in S1P(2)-deficient (S1P(2)(-/-)) mice displayed accelerated tumor growth and angiogenesis with enhanced association of vascular smooth muscle cells and pericytes.
  • [MeSH-major] Carcinoma, Lewis Lung / blood supply. Melanoma, Experimental / blood supply. Receptors, Lysosphingolipid / biosynthesis


22. Hata K, Hori K, Murata J, Takahashi S: Remodeling of actin cytoskeleton in lupeol-induced B16 2F2 cell differentiation. J Biochem; 2005 Oct;138(4):467-72
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  • [Title] Remodeling of actin cytoskeleton in lupeol-induced B16 2F2 cell differentiation.
  • Lupeol induces the formation of dendrites in B16 2F2 melanoma cells.
  • The remodeling of cytoskeletal components contributes to the dendricity of melanoma cells.
  • We studied the effects of lupeol on the remodeling of cytoplasmic filaments in B16 2F2 cells.
  • We examined the activation of cofilin, an actin-depolymerizing factor, in lupeol-treated B16 2F2 cells by western blotting.
  • At 10 microM, lupeol markedly inhibited the haptotaxis of B16 2F2 cells to fibronectin.
  • Additionally, lupeol strongly inhibited the migration of human melanoma and neuroblastoma cells, and weakly suppressed the migration of lung adenocarcinoma cells.
  • The results suggest that lupeol suppresses the migration of malignant melanoma cells by disassembling the actin cytoskeleton.
  • [MeSH-major] Actin Cytoskeleton / drug effects. Actin Depolymerizing Factors / metabolism. Cell Differentiation / drug effects. Melanoma, Experimental / pathology. Triterpenes / pharmacology

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  • (PMID = 16272141.001).
  • [ISSN] 0021-924X
  • [Journal-full-title] Journal of biochemistry
  • [ISO-abbreviation] J. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Actin Depolymerizing Factors; 0 / Pentacyclic Triterpenes; 0 / Triterpenes; O268W13H3O / lupeol
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23. Feinmesser M, Raiter A, Hardy B: Prevention of melanoma metastases in lungs of BAT treated and peptide immunized mice. Int J Oncol; 2006 Oct;29(4):911-7
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  • [Title] Prevention of melanoma metastases in lungs of BAT treated and peptide immunized mice.
  • Anti-tumor activity was obtained in mice inoculated with B16 melanoma by either a single injection with BAT or immunization with peptide A.
  • The aim of this study was to follow and compare histopathologically the process of prevention of melanoma metastases in lungs of treated and immunized mice.
  • Histological examination of tumor inoculated mice on day 10 revealed the existence of microscopic melanoma lesions (0.01-0.012 mm) that increased gradually in number and size and on day 21, most of the metastases were large and spanned entire lobes, from the pleura to the hilum, measuring up to 3.5 mm and coexisting with scattered, small metastases showing the same morphology and pattern of lung involvement.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lung / immunology. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Melanoma, Experimental / pathology. Peptides / administration & dosage

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  • (PMID = 16964387.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / BAT monoclonal antibody; 0 / Peptides
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24. Merle P, Morvan D, Caillaud D, Demidem A: Chemotherapy-induced bystander effect in response to several chloroethylnitrosoureas: an origin independent of DNA damage? Anticancer Res; 2008 Jan-Feb;28(1A):21-7
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  • Chloroethylnitrosourea (CENU) chemotherapy is used for the treatment of melanoma tumors.
  • We recently showed in murine experiments using a parental double B16 melanoma tumor model that, after treatment of primary tumors with cystemustine (CENU agent), untreated secondary tumors exhibited growth inhibition and metabolism disorders.
  • To see whether chemotherapy-induced bystander effects were induced with other members of the CENU family, we compared three CENU(s) used in melanoma treatment: cystemustine, carmustine and fotemustine.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. DNA Damage. Melanoma, Experimental / drug therapy. Nitrosourea Compounds / pharmacology. Vinyl Chloride / analogs & derivatives

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  • (PMID = 18383820.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Nitrosourea Compounds; 0 / Organophosphorus Compounds; 0 / Phospholipids; 79955-36-5 / N'-(2-chloroethyl)-N-(2-(methylsulfonyl)ethyl)-N'-nitrosourea; GAN16C9B8O / Glutathione; GQ7JL9P5I2 / fotemustine; U68WG3173Y / Carmustine; WD06X94M2D / Vinyl Chloride
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25. Negroiu G, Dwek RA, Petrescu SM: Tyrosinase-related protein-2 and -1 are trafficked on distinct routes in B16 melanoma cells. Biochem Biophys Res Commun; 2005 Mar 25;328(4):914-21
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  • [Title] Tyrosinase-related protein-2 and -1 are trafficked on distinct routes in B16 melanoma cells.
  • [MeSH-major] Intramolecular Oxidoreductases / metabolism. Melanoma, Experimental / metabolism. Membrane Glycoproteins / metabolism. Oxidoreductases / metabolism. Protein Transport

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  • (PMID = 15707965.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 886U3H6UFF / Chloroquine; 906O0YJ6ZP / Monensin; EC 1.- / Oxidoreductases; EC 1.14.18.- / TYRP1 protein, human; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
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26. Airoldi I, Di Carlo E, Cocco C, Taverniti G, D'Antuono T, Ognio E, Watanabe M, Ribatti D, Pistoia V: Endogenous IL-12 triggers an antiangiogenic program in melanoma cells. Proc Natl Acad Sci U S A; 2007 Mar 6;104(10):3996-4001
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  • [Title] Endogenous IL-12 triggers an antiangiogenic program in melanoma cells.
  • This latter phenotype may be related to (i) impairment of host IL-12-mediated immunosurveillance and/or (ii) IL-12 inability to inhibit directly the growth of IL-12 unresponsive malignant cells.
  • To address this issue, we transplanted IL-12R(+) B16 melanoma cells into syngeneic Il12rb2 KO mice with the following rationale: (i) these mice have severe defects in IFN-gamma production, as well as in cytotoxic T lymphocyte and natural killer cell cytotoxicity, and (ii) they produce but do not use IL-12 that can potentially bind to and target tumor cells only.
  • Il12rb2 KO mice displayed higher endogenous serum levels of IL-12 and developed smaller B16 tumors than WT animals.
  • Such effects depended on direct activity of endogenous IL-12 on tumor cells in KO mice, and hydrodynamic delivered IL-12 caused further reduced tumorigenicity of B16 cells in these mice.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Interleukin-12 / physiology. Melanoma / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Apoptosis. Chickens. Genes, Tumor Suppressor. Melanoma, Experimental / metabolism. Mice. Mice, Knockout. Neovascularization, Pathologic. Receptors, Interleukin-12 / metabolism. Recombinant Proteins / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 17360466.001).
  • [ISSN] 0027-8424
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Receptors, Interleukin-12; 0 / Recombinant Proteins; 187348-17-0 / Interleukin-12
  • [Other-IDs] NLM/ PMC1820697
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27. Crich SG, Lanzardo S, Alberti D, Belfiore S, Ciampa A, Giovenzana GB, Lovazzano C, Pagliarin R, Aime S: Magnetic resonance imaging detection of tumor cells by targeting low-density lipoprotein receptors with Gd-loaded low-density lipoprotein particles. Neoplasia; 2007 Dec;9(12):1046-56
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  • Their LDL adducts are taken up by human hepatoblastoma G2 (HepG2) and melanoma B16 tumor cells when added to the incubation medium.
  • Furthermore, it has been found that HepG2 hepatoma cells can internalize higher amounts of Gd-AAZTAC17 than B16 cells and the involvement of LDL receptors (LDLRs) has been demonstrated in competition assays with free LDL.
  • Gd-AAZTAC17/LDL adduct proved to be an efficient probe in the magnetic resonance (MR) visualization of subcutaneous tumors in animal models obtained by injecting B16 melanoma cells into the right flank of mice.
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / chemistry. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor / chemistry. Cell Line, Tumor / transplantation. Colorimetry. Drug Carriers. Humans. Lipid Bilayers. Liver Neoplasms / chemistry. Liver Neoplasms / pathology. Melanoma, Experimental / chemistry. Melanoma, Experimental / pathology. Mice. Mice, Inbred C57BL. Microscopy, Confocal / methods. Neoplasm Transplantation. Particle Size. Protein Binding. Specific Pathogen-Free Organisms

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  • (PMID = 18084612.001).
  • [ISSN] 1476-5586
  • [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] Canada
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Drug Carriers; 0 / Gd-AA2TAC17; 0 / Gd-DO3A-diph; 0 / Lipid Bilayers; 0 / Lipoproteins, LDL; 0 / Organometallic Compounds; 0 / Receptors, LDL
  • [Other-IDs] NLM/ PMC2134901
  • [Keywords] NOTNLM ; Gd complexes / LDL / Magnetic resonance imaging / dual imaging probe / tumor
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28. Kanzaki M, Okamoto T, Mitsui H, Shibagaki N, Shimada S: A novel immunotherapeutic approach to melanoma-bearing hosts with protein-transduction domain-containing immunogenic foreign antigens. J Dermatol Sci; 2010 Nov;60(2):84-94
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  • [Title] A novel immunotherapeutic approach to melanoma-bearing hosts with protein-transduction domain-containing immunogenic foreign antigens.
  • OBJECTIVE AND METHODS: We investigated and compared the antitumor effects by intratumoral (i.t.) injections of rR9-containing natural tumor-associated autoantigen (TAA) and other rR9-containing proteins, including rR9-OVA, into B16 melanoma.
  • RESULTS: Our results clearly demonstrate that multiple i.t. injections of rR9-OVA, but not rR9-containing TAA, elicited strong antitumor effects in B16-bearing mice, and resulted in complete tumor regression in some (50%) animals.
  • These antitumor effects were abrogated by depletion of CD8(+) T cells, and SIINFEKL-specific CTL lysed rR9-OVA-treated B16 cells in vitro. I.t. injections with rR9-OVA altered the proportion of CD4(+) T cell subsets in B16-bearing mice.
  • Interestingly, B16-tumor growth at the untreated site was also reduced following multiple injections of rR9-OVA at the other B16 tumor site.
  • Finally, we confirmed that mice that had rejected B16 tumors by i.t. injections of rR9-OVA subsequently acquired CTL activities to Trp2-epitope/B16 cells.
  • CONCLUSION: Multiple i.t. injections of rR9-PTD-containing immunogenic foreign Ags elicit strong antitumor effects, and thereby may provide important clinical benefits to melanoma patients.
  • [MeSH-major] Antigens / therapeutic use. Antigens, Neoplasm / therapeutic use. Immunotherapy, Active / methods. Melanoma, Experimental / drug therapy. Melanoma, Experimental / immunology. Neoplasm Proteins / therapeutic use

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  • [Copyright] Copyright © 2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20864317.001).
  • [ISSN] 1873-569X
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, Neoplasm; 0 / Neoplasm Proteins; 0 / Oligopeptides; 0 / Recombinant Proteins; 0 / nonaarginine; 9006-59-1 / Ovalbumin
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29. Behzadi M, Demidem A, Morvan D, Schwartz L, Stepien G, Steyaert JM: A model of phospholipid biosynthesis in tumor in response to an anticancer agent in vivo. J Integr Bioinform; 2010;7(3)
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  • In a second step we applied our model to experimental data of proton HRMAS NMR spectroscopy for solid B16 melanoma and Lewis lung (3LL) 3LL carcinoma cells treated by Chloroethyl Nitrosourea (CENU).

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  • (PMID = 20375456.001).
  • [ISSN] 1613-4516
  • [Journal-full-title] Journal of integrative bioinformatics
  • [ISO-abbreviation] J Integr Bioinform
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phosphatidylcholines; 0 / Phosphatidylethanolamines; 0 / Phospholipids; 2365-30-2 / 1-(2-chloroethyl)-1-nitrosourea; 39382-08-6 / phosphatidylethanolamine; P8M1T4190R / Ethylnitrosourea
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30. Galili U, Wigglesworth K, Abdel-Motal UM: Intratumoral injection of alpha-gal glycolipids induces xenograft-like destruction and conversion of lesions into endogenous vaccines. J Immunol; 2007 Apr 1;178(7):4676-87
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  • Efficacy of this treatment was demonstrated in alpha1,3-galactosyltransferase knockout mice producing anti-Gal and bearing B16 melanoma or B16/OVA producing OVA as a surrogate tumor Ag.
  • [MeSH-major] Glycolipids / administration & dosage. Immunotherapy / methods. Melanoma, Experimental / therapy. Skin Neoplasms / therapy. Trisaccharides / administration & dosage

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  • (PMID = 17372027.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Glycolipids; 0 / Trisaccharides; 0 / alpha-galactosyl epitope; 9006-59-1 / Ovalbumin; EC 2.4.1.- / Galactosyltransferases; EC 2.4.1.87 / N-acetyllactosaminide alpha-1,3-galactosyltransferase
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31. 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
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  • [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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32. Thanigaimalai P, Lee KC, Bang SC, Lee JH, Yun CY, Roh E, Hwang BY, Kim Y, Jung SH: Inhibitory effect of novel tetrahydropyrimidine-2(1H)-thiones on melanogenesis. Bioorg Med Chem; 2010 Feb;18(3):1135-42
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  • The series of imidazoldine-2-thiones 2 and tetrahydropyrimidine-2-thiones 3 were discovered as inhibitor of alpha-MSH-induced melanin production in melanoma B16 cells.

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20044259.001).
  • [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 / Pyrimidines; 0 / Thiones; 581-05-5 / alpha-MSH; EC 1.14.18.1 / Monophenol Monooxygenase
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33. 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
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  • [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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34. Kamiryo Y, Yajima T, Saito K, Nishimura H, Fushimi T, Ohshima Y, Tsukamoto Y, Naito S, Yoshikai Y: Soluble branched (1,4)-beta-D-glucans from Acetobacter species enhance antitumor activities against MHC class I-negative and -positive malignant melanoma through augmented NK activity and cytotoxic T-cell response. Int J Cancer; 2005 Jul 10;115(5):769-76
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  • [Title] Soluble branched (1,4)-beta-D-glucans from Acetobacter species enhance antitumor activities against MHC class I-negative and -positive malignant melanoma through augmented NK activity and cytotoxic T-cell response.
  • In the present study, we examined the effects of oral administration of AC-1 on protection against 2 types of murine B16 melanoma lines, major histocompatibility complex (MHC) class I-negative B16L and MHC class I gene-transfected B16K(b) cells.
  • [MeSH-major] Acetobacter / chemistry. Glucans / pharmacology. Killer Cells, Natural / immunology. Melanoma / pathology. Skin Neoplasms / pathology. T-Lymphocytes, Cytotoxic / immunology

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15729692.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucans; 0 / HLA Antigens
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35. Li Y, Gonzalez S, Terwey TH, Wolchok J, Li Y, Aranda I, Toledo-Crow R, Halpern AC: Dual mode reflectance and fluorescence confocal laser scanning microscopy for in vivo imaging melanoma progression in murine skin. J Invest Dermatol; 2005 Oct;125(4):798-804
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  • [Title] Dual mode reflectance and fluorescence confocal laser scanning microscopy for in vivo imaging melanoma progression in murine skin.
  • B16 melanoma cells and B16-enhanced green fluorescent protein (EGFP) cells were inoculated intradermally into transgenic C57BL/6-TgN (ACTbEGFP) 10sb and non-transgenic C57BL/6 mice, respectively.
  • In fluorescence mode, B16 melanoma cells appeared as dark objects in the bright background of the GFP expressing murine cells of the C57BL/6 transgenic mouse, and the B16-EGFP melanoma cells had a bright signal within a dark background in C57BL/6 mice.
  • [MeSH-major] Melanoma, Experimental / pathology. Skin Neoplasms / pathology

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  • (PMID = 16185281.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA08748
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins
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36. Yang JY, Koo JH, Song YG, Kwon KB, Lee JH, Sohn HS, Park BH, Jhee EC, Park JW: Stimulation of melanogenesis by scoparone in B16 melanoma cells. Acta Pharmacol Sin; 2006 Nov;27(11):1467-73
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  • [Title] Stimulation of melanogenesis by scoparone in B16 melanoma cells.
  • AIM: The effect of coumarin derivatives on melanogenesis was investigated in B16 murine melanoma cells.
  • [MeSH-major] Coumarins / pharmacology. Melanins / metabolism. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / metabolism

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  • (PMID = 17049123.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Coumarins; 0 / Isoquinolines; 0 / Melanins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; EC 1.- / Oxidoreductases; EC 1.14.18.- / Tyrp1 protein, mouse; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase; H5841PDT4Y / scoparone
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37. Fushimi T, O'Connor TP, Crystal RG: Adenoviral gene transfer of stromal cell-derived factor-1 to murine tumors induces the accumulation of dendritic cells and suppresses tumor growth. Cancer Res; 2006 Apr 1;66(7):3513-22
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  • When syngeneic murine CT26 colon carcinoma tumors (BALB/c) and B16 melanoma and Lewis lung cell carcinoma (C57Bl/6) were injected with AdSDF-1alpha (5 x 10(8) plaque-forming units), there was an accumulation of dendritic cells and CD8(+) cells within the tumor and significant inhibition of tumor growth compared with tumors injected with PBS or AdNull (control vector).
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / immunology. Adenoviridae / genetics. Animals. Carcinoma, Lewis Lung / genetics. Carcinoma, Lewis Lung / immunology. Cell Growth Processes / immunology. Chemokine CXCL12. Colonic Neoplasms / genetics. Colonic Neoplasms / immunology. Female. Gene Transfer Techniques. Genetic Vectors / genetics. Immunity, Cellular / genetics. Immunity, Cellular / immunology. Lymph Nodes / immunology. Melanoma, Experimental / genetics. Melanoma, Experimental / immunology. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout

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  • (PMID = 16585175.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 75192
  • [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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse
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38. Wondrak GT, Jacobson MK, Jacobson EL: Antimelanoma activity of apoptogenic carbonyl scavengers. J Pharmacol Exp Ther; 2006 Feb;316(2):805-14
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  • Here, we demonstrate the tumor cell-specific apoptogenicity of carbonyl scavengers, which act by covalently trapping RCS, against human (A375, G361, and LOX) and murine (B16) melanoma cell lines.
  • Indeed, in various melanoma cell lines, carbonyl scavenger-induced apoptosis was antagonized by pretreatment with the membrane-permeable RCS phenylglyoxal (PG).
  • Consistent with RCS inhibition of mitochondrial apoptosis in melanoma cells, staurosporine-induced apoptosis also was suppressed by PG pretreatment.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Free Radical Scavengers / pharmacology. Melanoma / pathology

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  • (PMID = 16210394.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA106677; United States / NCI NIH HHS / CA / CA43894; United States / NCI NIH HHS / CA / CA99469; United States / NCI NIH HHS / CA / P01CA27502; United States / NIEHS NIH HHS / ES / P30-ES06694; United States / NCI NIH HHS / CA / P30CA023074
  • [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 / Antineoplastic Agents; 0 / Free Radical Scavengers; 0 / alpha-dicarbonyl methylglyoxal; 50NP6JJ975 / Glyoxal
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39. McQuade P, Miao Y, Yoo J, Quinn TP, Welch MJ, Lewis JS: Imaging of melanoma using 64Cu- and 86Y-DOTA-ReCCMSH(Arg11), a cyclized peptide analogue of alpha-MSH. J Med Chem; 2005 Apr 21;48(8):2985-92
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  • [Title] Imaging of melanoma using 64Cu- and 86Y-DOTA-ReCCMSH(Arg11), a cyclized peptide analogue of alpha-MSH.
  • Early detection of melanoma is essential, since a patient's prognosis with metastatic melanoma is poor.
  • The goal of this current study was to label DOTA-ReCCMSH(Arg(11)) with beta(+)-emitting radionuclides, to determine if the high sensitivity of positron emission tomography (PET) imaging would aid in the detection of malignant melanoma.
  • Biodistribution and small animal PET imaging were carried out in mice implanted with B16/F1 murine melanoma tumor and compared with data obtained in the same animal model with [(18)F]FDG.
  • The data obtained suggests that DOTA-ReCCMSH(Arg(11)), when labeled with beta(+)-emitting radionuclides, has the potential for early detection of malignant melanoma by exploiting the sensitivity and high resolution of PET.
  • [MeSH-major] Melanoma, Experimental / metabolism. Organometallic Compounds / chemistry. Peptides, Cyclic / chemistry. Radiopharmaceuticals / chemistry. alpha-MSH / analogs & derivatives. alpha-MSH / chemistry

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  • (PMID = 15828837.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 P30 CA91842; United States / NCI NIH HHS / CA / 1 R24 CA83060; United States / NCI NIH HHS / CA / 1 R24 CA86307; United States / NCI NIH HHS / CA / P50-CA-10313-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1,4,7,10-tetraazacyclododecane 1,4,7,10-tetraacetic acid (ReO-acetyl(Cys(3,4,10),Phe(7),Arg(7))alpha-MSH(3-13)); 0 / Copper Radioisotopes; 0 / Organometallic Compounds; 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 0 / Receptor, Melanocortin, Type 1; 0 / Yttrium Radioisotopes; 581-05-5 / alpha-MSH
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40. Zhong Z, Kusznieruk KP, Popov IA, Riordan NH, Izadi H, Yijian L, Sher S, Szczurko OM, Agadjanyan MG, Tullis RH, Harandi A, Reznik BN, Mamikonyan GV, Ichim TE: Induction of antitumor immunity through xenoplacental immunization. J Transl Med; 2006;4:22
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  • Utilizing xenogeneic placental protein extracts as a vaccine, we have successfully induced anti-tumor immunity against B16 melanoma in C57/BL6 mice, whereas control xenogeneic extracts and B16 tumor extracts where ineffective, or actually promoted tumor growth, respectively.
  • These data suggest feasibility of using xenogeneic placental preparations as a multivalent vaccine potently targeting not just tumor antigens, but processes that are essential for tumor maintenance of malignant potential.

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  • (PMID = 16725035.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1482718
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41. Kundu S, Fan K, Cao M, Lindner DJ, Zhao ZJ, Borden E, Yi T: Novel SHP-1 inhibitors tyrosine phosphatase inhibitor-1 and analogs with preclinical anti-tumor activities as tolerated oral agents. J Immunol; 2010 Jun 01;184(11):6529-36
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  • Significantly, TPI-1 inhibited ( approximately 83%, p < 0.002) the growth of B16 melanoma tumors in mice at a tolerated oral dose in a T cell-dependent manner but had little effects on B16 cell growth in culture.
  • TPI-1 also inhibited B16 tumor growth and prolonged tumor mice survival as a tolerated s.c. agent.
  • In particular, analog TPI-1a4 as a tolerated oral agent completely inhibited the growth of K1735 melanoma tumors and was more effective than the parental lead against MC-26 colon cancer tumors in mice.

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  • (PMID = 20421638.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095020-04; United States / NHLBI NIH HHS / HL / HL079441; United States / NHLBI NIH HHS / HL / R01 HL079441-04; United States / NCI NIH HHS / CA / R01 CA096636; United States / NCI NIH HHS / CA / CA095020; United States / NCI NIH HHS / CA / R01 CA089344-05; United States / NCI NIH HHS / CA / R01 CA095020; United States / NCI NIH HHS / CA / CA096636; United States / NCI NIH HHS / CA / R01 CA096636-05; United States / NCI NIH HHS / CA / CA0890344; United States / NHLBI NIH HHS / HL / R01 HL079441
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
  • [Other-IDs] NLM/ NIHMS190683; NLM/ PMC3049920
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42. Conacci-Sorrell M, Kaplan A, Raveh S, Gavert N, Sakurai T, Ben-Ze'ev A: The shed ectodomain of Nr-CAM stimulates cell proliferation and motility, and confers cell transformation. Cancer Res; 2005 Dec 15;65(24):11605-12
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  • Nr-CAM, a cell-cell adhesion molecule of the immunoglobulin-like cell adhesion molecule family, known for its function in neuronal outgrowth and guidance, was recently identified as a target gene of beta-catenin signaling in human melanoma and colon carcinoma cells and tissue.
  • We detected a metalloprotease-mediated shedding of Nr-CAM into the culture medium of cells transfected with Nr-CAM, and of endogenous Nr-CAM in B16 melanoma cells.
  • Moreover, Nr-CAM was found in complex with alpha4beta1 integrins in melanoma cells, indicating that it can mediate, in addition to homophilic cell-cell adhesion, heterophilic adhesion with extracellular matrix receptors.
  • Suppression of Nr-CAM levels by small interfering RNA in B16 melanoma inhibited the adhesive and tumorigenic capacities of these cells.
  • [MeSH-major] Cell Adhesion Molecules / metabolism. Cell Movement. Cell Proliferation. Cell Transformation, Neoplastic. Melanoma, Experimental / pathology

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  • (PMID = 16357171.001).
  • [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 / Cell Adhesion Molecules; 0 / Culture Media, Conditioned; 0 / Enzyme Inhibitors; 0 / Integrin alpha4beta1; 0 / NRCAM protein, human; 0 / Nrcam protein, mouse; 0 / RNA, Small Interfering; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.- / Metalloproteases
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43. Parlakian A, Gomaa I, Solly S, Arandel L, Mahale A, Born G, Marazzi G, Sassoon D: Skeletal muscle phenotypically converts and selectively inhibits metastatic cells in mice. PLoS One; 2010 Feb 18;5(2):e9299
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  • Skeletal muscle is rarely a site of malignant metastasis; the molecular and cellular basis for this rarity is not understood.
  • We report that myogenic cells exert pronounced effects upon co-culture with metastatic melanoma (B16-F10) or carcinoma (LLC1) cells including conversion to the myogenic lineage in vitro and in vivo, as well as inhibition of melanin production in melanoma cells coupled with cytotoxic and cytostatic effects.
  • Tumor suppression assays reveal that the muscle-mediated tumor suppressor effects do not generate resistant clones but function through the down-regulation of the transcription factor MiTF, a master regulator of melanocyte development and a melanoma oncogene.

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  • (PMID = 20174581.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA080058; United States / NCI NIH HHS / CA / P01 CA80058
  • [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 / Culture Media, Conditioned; 0 / Desmin; 0 / Melanins; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ PMC2823787
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44. Iwai Y, Terawaki S, Honjo T: PD-1 blockade inhibits hematogenous spread of poorly immunogenic tumor cells by enhanced recruitment of effector T cells. Int Immunol; 2005 Feb;17(2):133-44
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  • In this study, we report that hematogenous spread of poorly immunogenic B16 melanoma cells to the liver was inhibited in PD-1-deficient mice.
  • As compared with wild-type mice, intrasplenic injection of B16 cells into PD-1-deficient mice showed enhanced induction of effector T cells in spleen, prolonged T cell proliferation and cytokine production, and augmented homing of effector T cells to tumor sites in the liver, resulting in accumulation of effector T cells in the tumor sites.
  • PD-1 blockade by genetic manipulation or antibody treatment inhibited not only hematogenous dissemination of B16 melanoma cells to the liver on the C57BL/6 background, but also dissemination of CT26 colon cancer cells to the lung on the BALB/c background.
  • [MeSH-major] Antigens, Surface / genetics. Antigens, Surface / physiology. Melanoma, Experimental / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 15611321.001).
  • [ISSN] 0953-8178
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Surface; 0 / Apoptosis Regulatory Proteins; 0 / Cytokines; 0 / Pdcd1 protein, mouse; 0 / Programmed Cell Death 1 Receptor
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45. Fernandes NV, Guntipalli PK, Mo H: d-δ-Tocotrienol-mediated cell cycle arrest and apoptosis in human melanoma cells. Anticancer Res; 2010 Dec;30(12):4937-44
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  • [Title] d-δ-Tocotrienol-mediated cell cycle arrest and apoptosis in human melanoma cells.
  • BACKGROUND: The rate-limiting enzyme of the mevalonate pathway, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, provides essential intermediates for the prenylation or dolichylation of growth-related proteins. d-δ-tocotrienol, a post-transcriptional down-regulator of HMG CoA reductase, suppresses the proliferation of murine B16 melanoma cells.
  • Dietary d-δ-tocotrienol suppresses the growth of implanted B16 melanomas without toxicity to host mice.
  • MATERIALS AND METHODS: The proliferation of human A2058 and A375 melanoma cells following a 72 h incubation in 96-well plates was measured by CellTiter 96® Aqueous One Solution.
  • CONCLUSION: d-δ-Tocotrienol may have potential application in melanoma chemoprevention and/or therapy.
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology. Vitamin E / analogs & derivatives

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  • (PMID = 21187473.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 1406-18-4 / Vitamin E; 1SRB74OWSI / tocotrienol, delta; 9LHU78OQFD / Lovastatin
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46. 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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  • [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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47. Chen P, Jiang X, Wei DP, Li L: [The effects of intense pulsed light and 5-aminolevulinic acid on the cultured B16 marine melanoma cells]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2010 Mar;41(2):280-3
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  • [Title] [The effects of intense pulsed light and 5-aminolevulinic acid on the cultured B16 marine melanoma cells].
  • OBJECTIVE: To investigate the effects of IPL and IPL plus 5-ALA on the proliferation, melanogenesis and tyrosinase activity of cultured B16 murine melanoma cells.
  • METHODS: B16 cells were pretreated with or without ALA and irradiated with IPL (20, 30, 40 J/cm2), also the negative control group and the positive control UVA irradiation group (3, 4, 5 J/cm2) were designed.
  • The proliferation of the treated B16 cells were evaluated with MTT method, the melanogenesis of the cells was tested with NaOH assay as well as tyrosinase activity was detected at 1 d, 2 d, 3 d, 4 d, and 5 d after irradiation.
  • RESULTS: 5 mmol/L 5-ALA did not affect the proliferation, melanogenesis and tyrosinase activity in B16 melanoma cell.
  • The cell yielding in UVA group increased significantly (P < 0.05) compared with that of negative control group after UVA irradiation (3, 4 J/cm2), but the proliferation of the treated B16 cells were suppressed after UVA irradiation (5 J/cm2).
  • IPL or IPL plus ALA have inhibitory effects on melanogenesis without any influence on cell tyrosinase activity in B16 cells.
  • CONCLUSIONS: We demonstrated that UVA could stimulate the proliferation of B16 cells, increase the melanogenesis and tyrosinase activity of the cells.
  • IPL or IPL plus ALA have inhibitory effects on melanogenesis without any influence on cell proliferation and tyrosinase activity in B16 cells.
  • [MeSH-major] Aminolevulinic Acid / pharmacology. Melanoma, Experimental / pathology. Photochemotherapy / methods. Photosensitizing Agents / pharmacology. Ultraviolet Rays

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  • (PMID = 20506653.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Melanins; 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid; EC 1.14.18.1 / Monophenol Monooxygenase
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48. Bettahi I, Dasgupta G, Renaudet O, Chentoufi AA, Zhang X, Carpenter D, Yoon S, Dumy P, BenMohamed L: Antitumor activity of a self-adjuvanting glyco-lipopeptide vaccine bearing B cell, CD4+ and CD8+ T cell epitopes. Cancer Immunol Immunother; 2009 Feb;58(2):187-200
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  • In this study, we explored a self-adjuvanting glyco-lipopeptide (GLP) as a platform for cancer vaccines using as a model MO5, an OVA-expressing mouse B16 melanoma.

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  • (PMID = 18584174.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY14900; United States / NEI NIH HHS / EY / EY16663
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Epitopes, T-Lymphocyte; 0 / Glycolipids; 0 / Lipopeptides; 82115-62-6 / Interferon-gamma; 9006-59-1 / Ovalbumin; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse
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49. Wang JF, Su RB, Wu N, Xu B, Lu XQ, Liu Y, Li J: Inhibitory effect of agmatine on proliferation of tumor cells by modulation of polyamine metabolism. Acta Pharmacol Sin; 2005 May;26(5):616-22
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  • Similar results were obtained in the transplanted B16 melanoma tumor model.
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. L-Lactate Dehydrogenase / metabolism. Male. Melanoma, Experimental / pathology. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm Transplantation. Putrescine / pharmacology

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  • (PMID = 15842783.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Polyamines; 70J407ZL5Q / Agmatine; EC 1.1.1.27 / L-Lactate Dehydrogenase; V10TVZ52E4 / Putrescine
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50. Mortensen MW, Björkdahl O, Sørensen PG, Hansen T, Jensen MR, Gundersen HJ, Bjørnholm T: Functionalization and cellular uptake of boron carbide nanoparticles. The first step toward T cell-guided boron neutron capture therapy. Bioconjug Chem; 2006 Mar-Apr;17(2):284-90
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  • Coated nanoparticles can be translocated into murine EL4 thymoma cells and B16 F10 malignant melanoma cells in amounts as high as 0.3 wt.
  • Neutron irradiation of a test system consisting of untreated B16 cells mixed with B16 cells loaded with boron carbide nanoparticles were found to inhibit the proliferative capacity of untreated cells, showing that cells loaded with boron-containing nanoparticles can hinder the growth of neighboring cells upon neutron irradiation.
  • [MeSH-minor] Animals. Cell Line, Tumor / radiation effects. Cell Proliferation. Melanoma. Mice. Molecular Structure. Particle Size

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  • (PMID = 16536457.001).
  • [ISSN] 1043-1802
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boron Compounds
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51. Kureev GV, Assesorova IuIu, Iusupova AA, Koloiarova NE, Balenkov OIu, Ibragimov FA: [The influence of soybean proteins on melanoma B-16 growth versus free-radical mechanisms in tumor-bearing animals]. Vopr Onkol; 2006;52(3):346-8
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  • [Title] [The influence of soybean proteins on melanoma B-16 growth versus free-radical mechanisms in tumor-bearing animals].
  • The influence of soybean proteins on antibody formation and free-radical mechanisms in blood serum was assessed in melanoma B-16-bearing mice.
  • [MeSH-major] Cell Division / drug effects. Free Radicals / blood. Melanoma, Experimental / pathology. Soybean Proteins / pharmacology

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  • (PMID = 17191710.001).
  • [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 / Free Radicals; 0 / Soybean Proteins
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52. 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


53. Mac Keon S, Gazzaniga S, Mallerman J, Bravo AI, Mordoh J, Wainstok R: Vaccination with dendritic cells charged with apoptotic/necrotic B16 melanoma induces the formation of subcutaneous lymphoid tissue. Vaccine; 2010 Nov 29;28(51):8162-8
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  • [Title] Vaccination with dendritic cells charged with apoptotic/necrotic B16 melanoma induces the formation of subcutaneous lymphoid tissue.
  • Mice vaccinated with DC charged with apoptotic/necrotic B16 cells (DC-Apo/Nec) are protected against B16 challenge.
  • [MeSH-major] Cancer Vaccines / immunology. Dendritic Cells / immunology. Lymphoid Tissue / physiology. Melanoma, Experimental / immunology. Melanoma, Experimental / prevention & control. Vaccination / methods

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20937314.001).
  • [ISSN] 1873-2518
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines
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54. Marttila-Ichihara F, Castermans K, Auvinen K, Oude Egbrink MG, Jalkanen S, Griffioen AW, Salmi M: Small-molecule inhibitors of vascular adhesion protein-1 reduce the accumulation of myeloid cells into tumors and attenuate tumor growth in mice. J Immunol; 2010 Mar 15;184(6):3164-73
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  • In this paper, we used anti-VAP-1 mAbs and small-molecule inhibitors of VAP-1 in B16 melanoma and EL-4 lymphoma tumor models in C57BL/6 mice.
  • In contrast, the VAP-1 inhibitors significantly reduced only the number of proangiogenic Gr-1(+)CD11b(+) myeloid cells in melanomas and lymphomas.
  • Notably, VAP-1 inhibitors, but not anti-VAP-1 Abs, retarded the growth of melanomas and lymphomas and reduced tumor neoangiogenesis.
  • [MeSH-major] Amine Oxidase (Copper-Containing) / antagonists & inhibitors. Amine Oxidase (Copper-Containing) / immunology. Cell Adhesion Molecules / antagonists & inhibitors. Cell Adhesion Molecules / immunology. Cell Migration Inhibition / immunology. Growth Inhibitors / therapeutic use. Lymphoma, T-Cell / immunology. Melanoma, Experimental / immunology. Myeloid Cells / immunology. Myeloid Cells / pathology

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  • (PMID = 20154208.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-fluoro-2-(4-methoxybenzyl)allylamine; 0 / Adjuvants, Immunologic; 0 / Antibodies, Blocking; 0 / Antibodies, Monoclonal; 0 / Cell Adhesion Molecules; 0 / Enzyme Inhibitors; 0 / Growth Inhibitors; 0 / Semicarbazides; 37QUC23K2X / carbamylhydrazine; 48G762T011 / Allylamine; EC 1.4.3.21 / Amine Oxidase (Copper-Containing); EC 1.4.3.21 / semicarbazide-sensitive amine oxidase-vascular adhesion protein-1, mouse
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55. Lutterbuese P, Brischwein K, Hofmeister R, Crommer S, Lorenczewski G, Petersen L, Lippold S, da Silva A, Locher M, Baeuerle PA, Schlereth B: Exchanging human Fcgamma1 with murine Fcgamma2a highly potentiates anti-tumor activity of anti-EpCAM antibody adecatumumab in a syngeneic mouse lung metastasis model. Cancer Immunol Immunother; 2007 Apr;56(4):459-68
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  • The anti-tumor activities of adecatumumab and mu-adecatumumab were then compared side-by-side in a lung metastasis mouse model established with a syngeneic B16 melanoma line expressing human EpCAM at physiologically relevant levels.

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  • (PMID = 16937114.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cell Adhesion Molecules; 0 / EPCAM protein, human; 0 / FCGR1A protein, human; 0 / Fc gamma receptor IIA; 0 / MT201 antibody, human; 0 / Receptors, IgG
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56. Gangjee A, Zeng Y, Ihnat M, Warnke LA, Green DW, Kisliuk RL, Lin FT: Novel 5-substituted, 2,4-diaminofuro[2,3-d]pyrimidines as multireceptor tyrosine kinase and dihydrofolate reductase inhibitors with antiangiogenic and antitumor activity. Bioorg Med Chem; 2005 Sep 15;13(18):5475-91
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  • Compounds 18 and 32 were also evaluated in a B16 melanoma mouse model and were found to be more active as antitumor agents than methotrexate.
  • In addition, both 18 and 32 were also active in decreasing lung metastases in a mouse model of B16 melanomas.

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  • (PMID = 16039863.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09885; United States / NCI NIH HHS / CA / CA10914
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Folic Acid Antagonists; 0 / Pyrimidines; EC 1.5.1.3 / Tetrahydrofolate Dehydrogenase; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; YL5FZ2Y5U1 / Methotrexate
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57. Mishra RK, Singhal JP, Datt M, Banthia AK: Amidated pectin based hydrogels: synthesis, characterization and cytocompatibility study. J Appl Biomater Biomech; 2007 May-Aug;5(2):88-94
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  • The hydrogels demonstrated good water holding properties and were found to be compatible with B-16 melanoma cells and human blood.

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  • (PMID = 20799178.001).
  • [ISSN] 1722-6899
  • [Journal-full-title] Journal of applied biomaterials & biomechanics : JABB
  • [ISO-abbreviation] J Appl Biomater Biomech
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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58. Wang L, Yi T, Kortylewski M, Pardoll DM, Zeng D, Yu H: IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway. J Exp Med; 2009 Jul 6;206(7):1457-64
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  • We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL-17(-/-) mice but drastically accelerated in IFN-gamma(-/-) mice, contributed to by elevated intratumoral IL-17, indicating a role of IL-17 in promoting tumor growth.

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  • (PMID = 19564351.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA115815; United States / NIAID NIH HHS / AI / R01 AI066008; United States / NCI NIH HHS / CA / R01CA122976; United States / NCI NIH HHS / CA / R01 CA122976; United States / NCI NIH HHS / CA / R01 CA115815
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-17; 0 / Interleukin-6; 0 / STAT3 Transcription Factor; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2715087
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59. Chen X, Wang X, Wang Y, Yang L, Hu J, Xiao W, Fu A, Cai L, Li X, Ye X, Liu Y, Wu W, Shao X, Mao Y, Wei Y, Chen L: Improved tumor-targeting drug delivery and therapeutic efficacy by cationic liposome modified with truncated bFGF peptide. J Control Release; 2010 Jul 1;145(1):17-25
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  • Then we characterized the tbFGF-modified liposome (tbFGF-LPs) and examined internalization of doxorubicin in tumor cells (TRAMP-C1, B16) and HUVEC cells in vitro.
  • In vivo, we evaluated the biodistribution and antitumor efficacy of tbFGF-LPs-DOX and tbFGF-LPs-PTX in C57BL/6J mice bearing TRAMP-C1 prostate carcinoma and B16 melanoma, respectively.
  • The tbFGF-LPs-DOX significantly improved the uptake of doxorubicin in TRAMP-C1, B16 and HUVEC cells, respectively.
  • Biodistribution study in B16 tumor-bearing mice showed that tbFGF-LPs-PTX achieved 7.1-fold (72.827+/-7.321mgh/L vs 10.292+/-0.775mgh/L, mean+/-SD, P<0.01) accumulation of paclitaxel in tumor tissue than those of free paclitaxel.
  • More importantly, treatment of tumor-bearing mice with tbFGF-LPs-DOX and tbFGF-LPs-PTX showed the significant inhibition in tumor growth and improvement in survival rate as compared with mice treated with free and liposomal drugs in TRAMP-C1 and B16 tumor models, respectively.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Carriers / chemistry. Fibroblast Growth Factor 2 / chemistry. Melanoma, Experimental / drug therapy. Prostatic Neoplasms / drug therapy

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  • [Copyright] 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20307599.001).
  • [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 / Cations; 0 / Drug Carriers; 0 / Liposomes; 0 / Receptors, Fibroblast Growth Factor; 103107-01-3 / Fibroblast Growth Factor 2; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
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61. Rodríguez-Cuesta J, Hernando FL, Mendoza L, Gallot N, de Cerio AA, Martínez-de-Tejada G, Vidal-Vanaclocha F: Candida albicans enhances experimental hepatic melanoma metastasis. Clin Exp Metastasis; 2010;27(1):35-42
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  • [Title] Candida albicans enhances experimental hepatic melanoma metastasis.
  • In this study, a well-established model of IL-18-dependent hepatic melanoma metastasis was used to study whether C. albicans can alter the ability of murine B16 melanoma (B16M) cells to colonize the liver.
  • [MeSH-major] Candidiasis / complications. Liver Neoplasms, Experimental / microbiology. Liver Neoplasms, Experimental / secondary. Melanoma, Experimental / microbiology. Melanoma, Experimental / secondary

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  • (PMID = 20035374.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Inflammation Mediators; 0 / Interleukin-18; 0 / Tumor Necrosis Factor-alpha; R9400W927I / Ketoconazole
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62. Umeshappa CS, Huang H, Xie Y, Wei Y, Mulligan SJ, Deng Y, Xiang J: CD4+ Th-APC with acquired peptide/MHC class I and II complexes stimulate type 1 helper CD4+ and central memory CD8+ T cell responses. J Immunol; 2009 Jan 1;182(1):193-206
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  • CD4(+) Th-APC with acquired pMHC II and I were capable of stimulating CD4(+) Th1 and central memory CD8(+)44(+)CD62L(high)IL-7R(+) T cell responses leading to antitumor immunity against OVA-expressing mouse B16 melanoma.
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigens, CD44 / biosynthesis. Cell Line, Tumor. Cytotoxicity Tests, Immunologic. L-Selectin / biosynthesis. Melanoma, Experimental. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Molecular Sequence Data. Receptors, Interleukin-7 / biosynthesis

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  • (PMID = 19109150.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Histocompatibility Antigens Class I; 0 / Histocompatibility Antigens Class II; 0 / Peptide Fragments; 0 / Receptors, Interleukin-7; 126880-86-2 / L-Selectin
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63. Seledtsov VI, Niza NA, Felde MA, Shishkov AA, Samarin DM, Seledtsova GV, Seledtsov DV: Xenovaccinotherapy for colorectal cancer. Biomed Pharmacother; 2007 Feb-Apr;61(2-3):125-30
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  • The objectives of this phase I-II trial were to assess the toxicity, immunological and clinical responses induced in 37 patients with stage IV colorectal cancer by the subcutaneous administration of a xenogenic polyantigenic vaccine (XPV) prepared from disrupted murine melanoma (B16) and carcinoma (LLC) cells.
  • A significant increase in cell-mediated immunoreactivity to both LLC and B16 antigens (Ags) occurred in the patients after inducing vaccinations, as determined by delayed-type hypersensitivity (DTH) skin reactions, as well as by blood lymphocyte proliferation responses.
  • [MeSH-minor] Adult. Aged. Animals. Antineoplastic Agents / therapeutic use. Carcinoma. Drug Synergism. Female. Humans. Immunity, Cellular / drug effects. Immunoglobulin G / drug effects. Immunoglobulin G / metabolism. Injections, Subcutaneous. Interferon-gamma / blood. Interferon-gamma / drug effects. Interleukin-4 / blood. Male. Melanoma. Mice. Middle Aged. Neoplasm Staging. Survival Analysis. Th1 Cells / drug effects. Th1 Cells / metabolism. Th2 Cells / drug effects. Th2 Cells / metabolism. Vaccination

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  • (PMID = 17258887.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Case Reports; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Immunoglobulin G; 0 / Interleukin-2; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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64. Ouyang GF, Saio M, Suwa T, Imai H, Nakagawa J, Nonaka K, Umemura N, Kijima M, Takami T: Interleukin-2 augmented activation of tumor associated macrophage plays the main role in MHC class I in vivo induction in tumor cells that are MHC negative in vitro. Int J Oncol; 2006 May;28(5):1201-8
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  • In this study, we utilized Interleukin-2 (IL-2) cDNA-introduced B16 melanoma cells (B16/IL-2) and vehicle-alone control cells (B16/mock) to examine whether TAM could contribute to the induction of MHC class I on B16 cells in vivo.
  • Interestingly, although B16/mock and B16/IL-2 did not express MHC class I in vitro, MHC class I was strongly expressed in vivo in B16/IL-2 in comparison to B16/mock.
  • Although in vivo treatment of anti-NK1.1 antibody abolished MHC expression in B16/mock in vivo, the same treatment did not influence MHC expression in B16/IL-2.
  • Interestingly, both anti-asialo GM1 and anti-CD11b treatment strongly decreased MHC expression in B16/IL-2.
  • TAM expressed both asialo GM1 and CD11b antigen, and TAM recovered from B16/IL-2 produced interferon gamma (IFNgamma) 6 times more than that from B16/mock.
  • In addition, TAM recovered from B16/IL-2 secreted 33.64 times more IFNgamma in response to in vitro administration of IL-2.
  • TAM recovered from IL-2 expressed middle affinity receptor of IL-2 (CD122 and CD132) while that from B16/mock expressed low affinity receptor (CD25 and CD132).
  • Finally, we observed that B16 cells became apoptotic with IFNgamma treatment in vitro.
  • [MeSH-major] Histocompatibility Antigens Class I / genetics. Interleukin-2 / pharmacology. Macrophages / immunology. Melanoma, Experimental / immunology

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  • (PMID = 16596236.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Histocompatibility Antigens Class I; 0 / Interleukin-2
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65. Kai H, Baba M, Okuyama T: Inhibitory effect of Cucumis sativus on melanin production in melanoma B16 cells by downregulation of tyrosinase expression. Planta Med; 2008 Dec;74(15):1785-8
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  • [Title] Inhibitory effect of Cucumis sativus on melanin production in melanoma B16 cells by downregulation of tyrosinase expression.
  • MeOH extracts of leaves and stems inhibited melanin production in B16 cells.
  • These extracts did not affect the activity of mushroom tyrosinase or crude enzyme lysate from B16 cells.
  • [MeSH-major] Cucumis sativus. Melanins / biosynthesis. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / metabolism. Plant Extracts / pharmacology

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  • (PMID = 19009501.001).
  • [ISSN] 0032-0943
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Melanins; 0 / Plant Extracts; 0 / Pyrones; 6K23F1TT52 / kojic acid; EC 1.14.18.1 / Monophenol Monooxygenase
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66. Guo RR, Liu Y, Lu WL, Zhao JH, Wang XQ, Zhang H, Wang JC, Zhang X, Zhang Q: A recombinant peptide, hirudin, potentiates the inhibitory effects of stealthy liposomal vinblastine on the growth and metastasis of melanoma. Biol Pharm Bull; 2008 Apr;31(4):696-702
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  • [Title] A recombinant peptide, hirudin, potentiates the inhibitory effects of stealthy liposomal vinblastine on the growth and metastasis of melanoma.
  • In vitro cytotoxicity, cell adhesion to extracellular matrix (ECM) proteins, and cell invasion and migration assays were performed on human A375 melanoma cell line.
  • Furthermore, administered at the initial implantation of murine B16 melanoma cells, hirudin evidently delayed the growth of tumor, and depressed the occurrence of experimental lung metastasis.
  • In conclusion, administration of recombinant hirudin followed by giving stealthy liposomal vinblastine may be beneficial for inhibiting the growth and metastasis of melanoma in vivo.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Hirudins / pharmacology. Melanoma / drug therapy. Protease Inhibitors / pharmacology. Vinblastine / pharmacology
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Drug Carriers. Drug Screening Assays, Antitumor. Drug Synergism. Extracellular Matrix Proteins / chemistry. Homeostasis / drug effects. Humans. Liposomes. Male. Melanoma, Experimental / drug therapy. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness / prevention & control. Neoplasm Metastasis / prevention & control. Particle Size. Recombinant Proteins / pharmacology. Tetrazolium Salts. Thiazoles

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  • (PMID = 18379065.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Drug Carriers; 0 / Extracellular Matrix Proteins; 0 / Hirudins; 0 / Liposomes; 0 / Protease Inhibitors; 0 / Recombinant Proteins; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; 5V9KLZ54CY / Vinblastine
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67. Mousa SA, Linhardt R, Francis JL, Amirkhosravi A: Anti-metastatic effect of a non-anticoagulant low-molecular-weight heparin versus the standard low-molecular-weight heparin, enoxaparin. Thromb Haemost; 2006 Dec;96(6):816-21
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  • Using the B16 melanoma mouse model of metastasis, subcutaneous (s.c.) injection of NA-LMWH or enoxaparin (10 mg/kg), three hours before intravenous (i.v.) injection of metastatic melanoma cells, followed by daily doses for 14 days, reduced lung tumor formation by 70% (P < 0.001). I.v. injection of tumor cells resulted in a significant (50-62%, P < 0.01) fall in platelet counts.

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  • (PMID = 17139378.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL052622-09; United States / NHLBI NIH HHS / HL / R01 HL052622; United States / NHLBI NIH HHS / HL / R01 HL062244; United States / NHLBI NIH HHS / HL / HL062244-07; United States / NHLBI NIH HHS / HL / HL052622-09; United States / NIGMS NIH HHS / GM / GM038060-19; United States / NIGMS NIH HHS / GM / R01 GM038060; United States / NIGMS NIH HHS / GM / R01 GM038060-19; United States / NHLBI NIH HHS / HL / R01 HL062244-07
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antineoplastic Agents; 0 / Enoxaparin; 0 / Factor Xa Inhibitors; 0 / Heparin, Low-Molecular-Weight; 0 / Lipoproteins; 0 / NA-LMWH; 0 / lipoprotein-associated coagulation inhibitor; 9001-26-7 / Prothrombin; 9002-04-4 / Factor IIa
  • [Other-IDs] NLM/ NIHMS75576; NLM/ PMC4114246
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68. Nakamura S, Chen G, Nakashima S, Matsuda H, Pei Y, Yoshikawa M: Brazilian natural medicines. IV. New noroleanane-type triterpene and ecdysterone-type sterol glycosides and melanogenesis inhibitors from the roots of Pfaffia glomerata. Chem Pharm Bull (Tokyo); 2010 May;58(5):690-5
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  • The ethyl acetate and 1-butanol soluble fractions of the roots of Pfaffia glomerata were found to show inhibitory effects on melanogenesis in theophylline-stimulated B16 melanoma 4A5 cells.
  • [MeSH-major] Amaranthaceae / chemistry. Antineoplastic Agents. Ecdysterone / chemistry. Glycosides / chemistry. Melanoma, Experimental. Oleanolic Acid / chemistry. Plant Roots / chemistry

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  • (PMID = 20460798.001).
  • [ISSN] 1347-5223
  • [Journal-full-title] Chemical & pharmaceutical bulletin
  • [ISO-abbreviation] Chem. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glycosides; 0 / Plant Extracts; 0 / Sterols; 5289-74-7 / Ecdysterone; 6SMK8R7TGJ / Oleanolic Acid
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69. Kurisu S, Suetsugu S, Yamazaki D, Yamaguchi H, Takenawa T: Rac-WAVE2 signaling is involved in the invasive and metastatic phenotypes of murine melanoma cells. Oncogene; 2005 Feb 17;24(8):1309-19
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  • [Title] Rac-WAVE2 signaling is involved in the invasive and metastatic phenotypes of murine melanoma cells.
  • We show that WAVEs, especially WAVE2, are essential for invasion and metastasis of melanoma cells.
  • Malignant B16F10 mouse melanoma cells expressed more WAVE1 and WAVE2 proteins and showed higher Rac activity than B16 parental cells, which are neither invasive nor metastatic.
  • In addition, ectopic expression of both RacCA and WAVE2 in B16 cells resulted in further increase in the invasiveness than that observed in B16 cells expressing only RacCA.
  • [MeSH-major] Melanoma, Experimental / metabolism. Microfilament Proteins / physiology. Neoplasm Invasiveness. Neoplasm Metastasis. rac GTP-Binding Proteins / physiology

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  • (PMID = 15608687.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Drug Combinations; 0 / Laminin; 0 / Microfilament Proteins; 0 / Proteoglycans; 0 / RNA, Small Interfering; 0 / Wasf1 protein, mouse; 0 / Wasf2 protein, mouse; 0 / Wiskott-Aldrich Syndrome Protein Family; 119978-18-6 / matrigel; 9007-34-5 / Collagen; EC 3.6.5.2 / rac GTP-Binding Proteins
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70. Itoh K, Hirata N, Masuda M, Naruto S, Murata K, Wakabayashi K, Matsuda H: Inhibitory effects of Citrus hassaku extract and its flavanone glycosides on melanogenesis. Biol Pharm Bull; 2009 Mar;32(3):410-5
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  • The CH-ext showed inhibition of melanogenesis without any effects on cell proliferation in cultured murine B16 melanoma cells after glucosamine exposure.

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  • (PMID = 19252287.001).
  • [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 / Antioxidants; 0 / Flavanones; 0 / Free Radical Scavengers; 0 / Glycosides; 0 / Melanins; 0 / Plant Extracts; 0 / Solvents; 3K9958V90M / Ethanol; EC 1.14.18.1 / Monophenol Monooxygenase
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71. 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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72. Meyer S, Hafner C, Guba M, Flegel S, Geissler EK, Becker B, Koehl GE, Orsó E, Landthaler M, Vogt T: Ephrin-B2 overexpression enhances integrin-mediated ECM-attachment and migration of B16 melanoma cells. Int J Oncol; 2005 Nov;27(5):1197-206
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  • [Title] Ephrin-B2 overexpression enhances integrin-mediated ECM-attachment and migration of B16 melanoma cells.
  • We have previously shown that ephrin-B2 mRNA is overexpressed in advanced malignant melanomas (MM).
  • Using a wild-type ephrin-B2-negative B16 mouse MM subclone we show that overexpression of ephrin-B2 leads to the formation of multiple lamellipodia, enhanced polymerisation of actin fibers, and induction of focal adhesion complexes with constitutive activation of focal adhesion kinase.
  • Consequently, ephrin-B2-overexpressing B16 cells display a significant increase of beta1-integrin-mediated attachment to matrix components, preferentially laminin and fibronectin.
  • [MeSH-major] Ephrin-B2 / biosynthesis. Extracellular Matrix / physiology. Melanoma / pathology. Skin Neoplasms / pathology

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  • (PMID = 16211213.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Ephrin-B2
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73. LeBlanc R, Dickson J, Brown T, Stewart M, Pati HN, VanDerveer D, Arman H, Harris J, Pennington W, Holt HL Jr, Lee M: Synthesis and cytotoxicity of epoxide and pyrazole analogs of the combretastatins. Bioorg Med Chem; 2005 Nov 1;13(21):6025-34
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  • The relatively coplanar conformation of a 3',3'',4',4'',5',5''-hexamethoxypyrazole 17 was in good agreement with the shape for 3',3'',4',4'',5'-pentamethoxypyrazole 16, which was determined from molecular mechanics optimization.
  • In vitro cytotoxicity of each class of compounds was obtained using a 72 h continuous exposure MTT assay against two murine cancer cell lines; B16 melanoma and L1210 leukemia.
  • In the majority of cases, the pyrazoles are generally more active than the epoxides, with the most active, 5-(3''-amino-4''-methoxyphenyl)-3-(3',4',5'-trimethoxyphenyl)pyrazole 21, possessing an IC(50) value of 5 and 2.4 microM (B16 and L1210, respectively).

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  • (PMID = 16055334.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / RR 16461-10
  • [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] England
  • [Chemical-registry-number] 0 / Bibenzyls; 0 / Epoxy Compounds; 0 / Pyrazoles; 0 / Stilbenes; 3QD5KJZ7ZJ / pyrazole; 82855-09-2 / combretastatin
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74. Simmons AD, Li B, Gonzalez-Edick M, Lin C, Moskalenko M, Du T, Creson J, VanRoey MJ, Jooss K: GM-CSF-secreting cancer immunotherapies: preclinical analysis of the mechanism of action. Cancer Immunol Immunother; 2007 Oct;56(10):1653-65
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  • To further define the mechanism of GM-CSF-secreting cancer immunotherapies, immunohistochemistry studies were performed using the B16F10 melanoma tumor model.
  • To evaluate the scope of the immune response generated by GM-CSF-secreting cancer immunotherapies, several related B16 melanoma tumor cell subclones that exist as a result of genetic drift in the original cell line were used to challenge mice previously immunized with GM-CSF-secreting B16F10 cells.
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Dendritic Cells / immunology. Disease Models, Animal. Female. Melanoma, Experimental. Mice. Mice, Inbred C57BL. Recombinant Proteins. T-Lymphocytes / immunology

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  • (PMID = 17410360.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Recombinant Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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75. Schumacher LY, Vo DD, Garban HJ, Comin-Anduix B, Owens SK, Dissette VB, Glaspy JA, McBride WH, Bonavida B, Economou JS, Ribas A: Immunosensitization of tumor cells to dendritic cell-activated immune responses with the proteasome inhibitor bortezomib (PS-341, Velcade). J Immunol; 2006 Apr 15;176(8):4757-65
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  • We established a murine model to test whether the proteasome inhibitor bortezomib could sensitize established B16 melanoma tumors to dendritic cell (DC)-activated immune effector cells.
  • B16 tumors had significantly decreased tumor outgrowth when treated with a combination of bortezomib and DC, regardless of whether the DC were loaded or not with a tumor Ag.
  • NF-kappaB nuclear transcription factor assay and gene-expression profiling of B16 treated with bortezomib was consistent with inhibition of NF-kappaB target genes leading to a proapoptotic phenotype.
  • In vitro lytic assays demonstrated that TNF-alpha, but not perforin, Fas-ligand, or TRAIL, was responsible for bortezomib-sensitized B16 cytotoxicity.
  • [MeSH-major] Boronic Acids / pharmacology. Dendritic Cells / immunology. Melanoma, Experimental / immunology. Melanoma, Experimental / therapy. Protease Inhibitors / pharmacology. Pyrazines / pharmacology

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  • (PMID = 16585569.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI-28697; United States / NCI NIH HHS / CA / CA-16042; United States / NCI NIH HHS / CA / K12 CA76905; United States / NCI NIH HHS / CA / K23 CA93376; United States / NCI NIH HHS / CA / P50 CA086306; United States / NCI NIH HHS / CA / R01 CA77623; United States / NCI NIH HHS / CA / R01 CA79976; United States / NCI NIH HHS / CA / T32 CA75956
  • [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 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 0 / Tumor Necrosis Factor-alpha; 69G8BD63PP / Bortezomib
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76. Maksimovic-Ivanic D, Mijatovic S, Miljkovic D, Harhaji-Trajkovic L, Timotijevic G, Mojic M, Dabideen D, Cheng KF, McCubrey JA, Mangano K, Al-Abed Y, Libra M, Garotta G, Stosic-Grujicic S, Nicoletti F: The antitumor properties of a nontoxic, nitric oxide-modified version of saquinavir are independent of Akt. Mol Cancer Ther; 2009 May;8(5):1169-78
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  • In contrast to Saq, Saq-NO had no effect on the viability of primary cells and drastically reduced B16 melanoma growth in syngeneic C57BL/6 mice.
  • Saq-NO blocked the proliferation of C6 and B16 cells, up-regulated p53 expression, and promoted the differentiation of these two cell types into oligodendrocytes or Schwann-like cells, respectively.

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  • (PMID = 19417156.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytostatic Agents; 31C4KY9ESH / Nitric Oxide; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; L3JE09KZ2F / Saquinavir
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77. Kashiwagi H, McDunn JE, Goedegebuure PS, Gaffney MC, Chang K, Trinkaus K, Piwnica-Worms D, Hotchkiss RS, Hawkins WG: TAT-Bim induces extensive apoptosis in cancer cells. Ann Surg Oncol; 2007 May;14(5):1763-71
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  • We examined whether this construct (TAT-Bim) induced apoptosis in several cancer cell lines (T-cell lymphoma (EL4), pancreatic cancer (Panc-02), and melanoma (B16)) and whether TAT-Bim treatment synergized with radiation.
  • TAT-Bim significantly slowed tumor growth in murine models of pancreatic cancer and melanoma.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / pharmacology. Gene Products, tat / metabolism. Lymphoma, T-Cell / therapy. Melanoma / therapy. Membrane Proteins / pharmacology. Pancreatic Neoplasms / therapy. Proto-Oncogene Proteins / pharmacology

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  • (PMID = 17206479.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA082841; United States / NIGMS NIH HHS / GM / GM044118; United States / NIGMS NIH HHS / GM / GM055194; United States / NCI NIH HHS / CA / P50 CA94056
  • [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 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Gene Products, tat; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins
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78. Rice JR, Gerberich JL, Nowotnik DP, Howell SB: Preclinical efficacy and pharmacokinetics of AP5346, a novel diaminocyclohexane-platinum tumor-targeting drug delivery system. Clin Cancer Res; 2006 Apr 1;12(7 Pt 1):2248-54
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  • EXPERIMENTAL DESIGN: Antitumor activity was assessed in mice bearing B16F10 melanoma and M5076 and 2008 ovarian carcinomas.
  • When given at their respective maximum tolerated doses, the antitumor activity of AP5346 was superior to that of oxaliplatin against both the B16 melanoma and 2008 human ovarian carcinoma.
  • AP5346 delivered 16.3-fold more Pt to the tumor and 14.2-fold more Pt to tumor DNA than oxaliplatin based on AUC((1-168)).
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacokinetics. Drug Delivery Systems. Melanoma / drug therapy. Organoplatinum Compounds / pharmacokinetics. Ovarian Neoplasms / drug therapy

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  • (PMID = 16609041.001).
  • [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; 0 / Organoplatinum Compounds; 0 / ProLindac; 9007-49-2 / DNA
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79. Buhtoiarov IN, Lum H, Berke G, Paulnock DM, Sondel PM, Rakhmilevich AL: CD40 ligation activates murine macrophages via an IFN-gamma-dependent mechanism resulting in tumor cell destruction in vitro. J Immunol; 2005 May 15;174(10):6013-22
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  • Intraperitoneal injection of anti-CD40 mAb into C57BL/6 mice resulted in activation of peritoneal macrophages capable of suppressing B16 melanoma cell proliferation in vitro, an effect that was greatly enhanced by LPS and observed against several murine and human tumor cell lines.
  • [MeSH-major] Antigens, CD40 / immunology. Antigens, CD40 / metabolism. Interferon-gamma / physiology. Macrophage Activation / immunology. Macrophages, Peritoneal / immunology. Macrophages, Peritoneal / metabolism. Melanoma, Experimental / immunology. Melanoma, Experimental / prevention & control

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  • (PMID = 15879094.001).
  • [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 / R01 CA087025; United States / NIGMS NIH HHS / GM / T32 GM008692; United States / NCI NIH HHS / CA / CA87025
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD40; 0 / Ligands; 82115-62-6 / Interferon-gamma
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80. Li D, Wang H, Xiang JJ, Deng N, Wang PP, Kang YL, Tao J, Xu M: Monoclonal antibodies targeting basic fibroblast growth factor inhibit the growth of B16 melanoma in vivo and in vitro. Oncol Rep; 2010 Aug;24(2):457-63
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  • [Title] Monoclonal antibodies targeting basic fibroblast growth factor inhibit the growth of B16 melanoma in vivo and in vitro.
  • Up-regulated basic fibroblast growth factor (bFGF or FGF-2) plays an important role in the development and metastasis of melanoma; therefore, neutralizing antibodies to bFGF may suppress melanoma growth.
  • Anti-bFGF mAbs significantly inhibit the proliferation and induce apoptosis of B16 cells, and show inhibitory effects on the migration of B16F10 cells and the tube formation of human umbilical vein endothelial cells (HUVECs) in vitro.
  • Treatment of B16 melanoma spheroids with anti-bFGF mAbs in vivo results in significant reduction in tumor size and prolonged survival time of animals.
  • Our data indicate that anti-bFGF mAbs are potential therapeutic candidates for melanoma therapy by effectively suppressing the melanoma growth through inhibition of angiogenesis and induction of apoptosis in the tumor.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Cell Proliferation / drug effects. Fibroblast Growth Factor 2 / antagonists & inhibitors. Melanoma, Experimental / pathology

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  • (PMID = 20596633.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 103107-01-3 / Fibroblast Growth Factor 2
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81. Abramov VV, Gontova IA, Ignat'ev IM, Gel'fgat EL, Kozlov VA: [Functional asymmetry of the brain hemispheres: the role in pathogenesis of ectromelia and melanoma in (CBAxC57BL/6)F1 mice]. Ross Fiziol Zh Im I M Sechenova; 2009 Jul;95(7):688-93
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  • [Title] [Functional asymmetry of the brain hemispheres: the role in pathogenesis of ectromelia and melanoma in (CBAxC57BL/6)F1 mice].
  • The role of functional asymmetry of the brain hemispheres in development of ectromelia and melanoma at (CBAxC57BL/6)F1 mice was investigated.
  • It has been established, that mice with domination of motor functions in the left hemisphere ("right-handed") are more resistant against infection with ectromelia virus, and melanoma B-16 grows more slowly in these mice as compated with animals with domination of motor functions of the right hemisphere ("left-handed").
  • Hence, for the first time the role of functional nervous asymmetry in pathogenesis of ectromelia and melanoma (B-16) in mice (CBAxC57BL/6)F1 is established.

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  • (PMID = 19803455.001).
  • [ISSN] 0869-8139
  • [Journal-full-title] Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova
  • [ISO-abbreviation] Ross Fiziol Zh Im I M Sechenova
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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82. Mastrofrancesco A, Kokot A, Eberle A, Gibbons NC, Schallreuter KU, Strozyk E, Picardo M, Zouboulis CC, Luger TA, Böhm M: KdPT, a tripeptide derivative of alpha-melanocyte-stimulating hormone, suppresses IL-1 beta-mediated cytokine expression and signaling in human sebocytes. J Immunol; 2010 Aug 1;185(3):1903-11
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  • Importantly, KdPT did not bind to MC-1Rs, as demonstrated by blocking experiments with a peptide analog of Agouti signaling protein and by binding assays using MC-1R-expressing B16 melanoma cells.
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. DNA-Binding Proteins / physiology. Humans. I-kappa B Kinase / antagonists & inhibitors. I-kappa B Kinase / metabolism. I-kappa B Proteins / antagonists & inhibitors. I-kappa B Proteins / metabolism. Interleukin-6 / antagonists & inhibitors. Interleukin-8 / antagonists & inhibitors. Melanoma, Experimental. Mice

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  • (PMID = 20610647.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / Immunosuppressive Agents; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Peptide Fragments; 117027-34-6 / interleukin 1beta (193-195); 139874-52-5 / NF-kappaB inhibitor alpha; 581-05-5 / alpha-MSH; EC 2.7.11.10 / I-kappa B Kinase
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83. Abduvaliev AA, Gil'dieva MS: [Differential trypan blue staining of tumor cells for the determination of apoptosis]. Klin Lab Diagn; 2006 Feb;(2):36-8
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  • The paper also gives data of the comparative studies of the content of apoptotic cells in experimental melanoma B-16 though differential trypan blue staining and classical morphostructural analysis.
  • [MeSH-major] Apoptosis. Breast Neoplasms / pathology. Coloring Agents. Immunohistochemistry. Melanoma / pathology. Trypan Blue

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  • (PMID = 16610632.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Coloring Agents; I2ZWO3LS3M / Trypan Blue
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84. Prakash J, Beljaars L, Harapanahalli AK, Zeinstra-Smith M, de Jager-Krikken A, Hessing M, Steen H, Poelstra K: Tumor-targeted intracellular delivery of anticancer drugs through the mannose-6-phosphate/insulin-like growth factor II receptor. Int J Cancer; 2010 Apr 15;126(8):1966-81
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  • M6P-HSA specifically bound and internalized into M6P/IGF-IIR-expressing B16 melanoma cells as demonstrated with radioactive studies and anti-HSA immunostaining.
  • In B16 tumor-bearing mice, Dox-HSA-M6P significantly inhibited the tumor growth whereas an equimolar dose of free doxorubicin did not show any anti-tumor effect.

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  • (PMID = 19795464.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; 0 / Mannosephosphates; 0 / Receptor, IGF Type 2; 0 / Serum Albumin; 3672-15-9 / mannose-6-phosphate; 80168379AG / Doxorubicin
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85. Genady AR: Promising carboranylquinazolines for boron neutron capture therapy: synthesis, characterization, and in vitro toxicity evaluation. Eur J Med Chem; 2009 Jan;44(1):409-16
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  • In vitro toxicity was performed with B16 melanoma cells and showed that the connection of hydrophilic nido-carborane to quinazoline moiety decreases the compound's toxicity.
  • [MeSH-minor] Cell Line, Tumor. Humans. Melanoma, Experimental / drug therapy. Spectrum Analysis. Structure-Activity Relationship

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  • (PMID = 18407378.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boranes; 0 / Quinazolines
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86. Funaba M, Murakami M, Ikeda T, Ogawa K, Tsuchida K, Sugino H: Identification of tocopherol-associated protein as an activin/TGF-beta-inducible gene in mast cells. Biochim Biophys Acta; 2006 Aug;1763(8):900-6
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  • Activin A-induced Tap expression was detected in BMMC but not in RAW264 macrophage-like cells, B16 melanoma cells or P19 embryonic carcinoma cells.

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  • (PMID = 16872693.001).
  • [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 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Benzamides; 0 / Carrier Proteins; 0 / DNA, Complementary; 0 / Dioxoles; 0 / Lipoproteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Smad3 Protein; 0 / Smad3 protein, mouse; 0 / Tgfb1 protein, mouse; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / activin A; 0 / tocopherol-associated protein, mouse; 104625-48-1 / Activins; 93443-12-0 / Inhibin-beta Subunits; EC 2.7.11.30 / Activin Receptors, Type I
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87. Ty N, Dupeyre G, Chabot GG, Seguin J, Quentin L, Chiaroni A, Tillequin F, Scherman D, Michel S, Cachet X: Structure-activity relationships of indole compounds derived from combretastatin A4: synthesis and biological screening of 5-phenylpyrrolo[3,4-a]carbazole-1,3-diones as potential antivascular agents. Eur J Med Chem; 2010 Sep;45(9):3726-39
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  • Intermediate tetrahydro[3,4-a]carbazoles and their corresponding carbazoles were submitted to biological screening tests involved in antivascular action, including the cytotoxicity against murine B16 melanoma cells, the rounding up of endothelial cells (EA.hy 926) and the inhibition of tubulin polymerization.

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  • [Copyright] 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20538383.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Stilbenes; 0 / Tubulin; 0P2197HHHN / carbazole; I5590ES2QZ / fosbretabulin
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88. Trabado S, Nguyen Van Binh P, Martin C, Lafarge-Frayssinet C, Thevenin M, Baudouin F, Warnet JM, Duc HT: Modulated expression of cell surface molecules and in vivo outgrowth of modified melanoma cells. Biomed Pharmacother; 2006 Dec;60(10):693-7
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  • [Title] Modulated expression of cell surface molecules and in vivo outgrowth of modified melanoma cells.
  • Modulation of cell surface molecules involved in immune recognition and cellular interactions (class I major histocompatibility complex or MHC-I, B7.1 or CD80, integrin alpha4 or CD49d, tetraspanins CD9, CD81) was examined in modified B16 melanoma cells displaying either inhibited IGF-I expression or transfected OVA encoding gene.
  • However downregulation of tetraspanin CD9 was observed in modified IGF-I but not in OVA encoding gene inserted melanoma cells.
  • Inoculated into syngeneic recipients, the modified melanoma cells exhibited significant delayed outgrowth with a reduction in the percentage of lethal tumors observed essentially in hosts injected with inhibited IGF-I expression cells.
  • [MeSH-major] Antigens, Surface / metabolism. Melanoma, Experimental / metabolism

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  • (PMID = 17071049.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antigens, CD; 0 / Antigens, CD80; 0 / Antigens, CD81; 0 / Antigens, CD9; 0 / Antigens, Surface; 0 / Cd81 protein, mouse; 0 / Cd9 protein, mouse; 0 / DNA, Antisense; 0 / Histocompatibility Antigens Class I; 0 / Membrane Glycoproteins; 143198-26-9 / Integrin alpha4; 3XQ2233B0B / Hygromycin B; 67763-96-6 / Insulin-Like Growth Factor I; 9006-59-1 / Ovalbumin
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89. Saji H, Song W, Furumoto K, Kato H, Engleman EG: Systemic antitumor effect of intratumoral injection of dendritic cells in combination with local photodynamic therapy. Clin Cancer Res; 2006 Apr 15;12(8):2568-74
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  • EXPERIMENTAL DESIGN: BALB/c or C57Bl/6 mice were injected s.c. with CT26 colorectal carcinoma cells and B16 melanoma cells, respectively, and following 10 to 12 days of tumor growth, the tumors were treated with PDT alone or PDT followed by IT-DC or IT-PBS.
  • RESULTS: Whereas neither PDT nor IT-DC alone was effective, PDT + IT-DC eradicated both CT26 and B16 tumors in a significant proportion of animals and prolonged the survival of mice of which the tumors were not cured.

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  • [CommentIn] Clin Cancer Res. 2006 Apr 15;12(8):2385-9 [16638842.001]
  • (PMID = 16638867.001).
  • [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 / NHLBI NIH HHS / HL / HL57443; United States / NCI NIH HHS / CA / K08CA105064
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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90. Klages K, Mayer CT, Lahl K, Loddenkemper C, Teng MW, Ngiow SF, Smyth MJ, Hamann A, Huehn J, Sparwasser T: Selective depletion of Foxp3+ regulatory T cells improves effective therapeutic vaccination against established melanoma. Cancer Res; 2010 Oct 15;70(20):7788-99
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  • [Title] Selective depletion of Foxp3+ regulatory T cells improves effective therapeutic vaccination against established melanoma.
  • We showed that Foxp3(+) Treg depletion induced partial regression of established ovalbumin (OVA)-expressing B16 melanoma, which was associated with an increased intratumoral accumulation of activated CD8(+) cytotoxic T cells.
  • [MeSH-major] Forkhead Transcription Factors / deficiency. Lymphocyte Depletion / methods. Melanoma / immunology. Melanoma, Experimental / immunology. T-Lymphocytes, Regulatory / immunology

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  • [Copyright] ©2010 AACR.
  • (PMID = 20924102.001).
  • [ISSN] 1538-7445
  • [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 / Autoantigens; 0 / Cancer Vaccines; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Foxp3 protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 9006-59-1 / Ovalbumin
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91. Søndergaard H, Galsgaard ED, Bartholomaeussen M, Straten PT, Odum N, Skak K: Intratumoral interleukin-21 increases antitumor immunity, tumor-infiltrating CD8+ T-cell density and activity, and enlarges draining lymph nodes. J Immunother; 2010 Apr;33(3):236-49
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  • In this study, we have compared the efficacy of subcutaneous and intratumoral (IT) administration of IL-21 protein in two syngeneic mouse tumor models, RenCa renal cell carcinoma and B16 melanoma, and investigated the mechanisms by which IL-21 enhances CD8 T-cell-mediated antitumor immunity.

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  • (PMID = 20445344.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukins; 0 / interleukin-21; 82115-62-6 / Interferon-gamma; EC 3.4.21.- / Granzymes
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92. Inglefield JR, Dumitru CD, Alkan SS, Gibson SJ, Lipson KE, Tomai MA, Larson CJ, Vasilakos JP: TLR7 agonist 852A inhibition of tumor cell proliferation is dependent on plasmacytoid dendritic cells and type I IFN. J Interferon Cytokine Res; 2008 Apr;28(4):253-63
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  • In vivo, six doses of 852A administration significantly delayed the onset of lung colonies in a B16 melanoma model.
  • [MeSH-minor] Aminoquinolines / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Culture Media, Conditioned / pharmacology. Humans. Leukocytes, Mononuclear / drug effects. Lung / drug effects. Lung / pathology. Melanoma / pathology. Mice. Oligodeoxyribonucleotides / pharmacology. Subcellular Fractions / drug effects

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  • (PMID = 18439103.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / CpG ODN 2216; 0 / Culture Media, Conditioned; 0 / Interferon Type I; 0 / N-(4-(4-amino-2-ethyl-1H-imidazo(4,5c)quinolin-1-yl)butyl)methanesulfonamide; 0 / Oligodeoxyribonucleotides; 0 / Quinolines; 0 / Sulfonamides; 0 / TLR7 protein, human; 0 / Toll-Like Receptor 7; 99011-02-6 / imiquimod
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93. Chopra A, Kim TS, O-Sullivan I, Martinez D, Cohen EP: Combined therapy of an established, highly aggressive breast cancer in mice with paclitaxel and a unique DNA-based cell vaccine. Int J Cancer; 2006 Jun 1;118(11):2888-98
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  • The immunity was specific, as immunization with a vaccine prepared by transfer of DNA from B16 melanoma cells into the fibroblasts failed to induce immunity to the breast cancer.

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  • (PMID = 16380982.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / 1 R01 DE013970-O1A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cancer Vaccines; 0 / Vaccines, DNA; P88XT4IS4D / Paclitaxel
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94. Chen JX, Gao Y, Liu JW, Tian YX, Zhao J, Cui XY: Antitumor effects of human ribonuclease inhibitor gene transfected on B16 melanoma cells. Int J Biochem Cell Biol; 2005 Jun;37(6):1219-31
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  • [Title] Antitumor effects of human ribonuclease inhibitor gene transfected on B16 melanoma cells.
  • In order to further understand the function of ribonuclease inhibitor and investigate the relationship with tumor growth, our study established a transfection of human ribonuclease inhibitor cDNA into the murine B16 cells by the retroviral packaging cell line PA317.
  • Mice that were injected with the B16 cells transfected RI cDNA showed a significant inhibition of the tumor growth with lighter tumor weight, lower density of microvessels, longer latent periods, and survival time than those in the other two control groups.
  • [MeSH-major] Melanoma, Experimental / pathology. Placental Hormones / genetics. Placental Hormones / pharmacology

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  • (PMID = 15778086.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Placental Hormones; 120178-77-0 / placental ribonuclease inhibitor; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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95. Huo L, Yao H, Wang X, Wong GW, Kung HF, Lin MC: Inhibition of melanoma growth by subcutaneous administration of hTERTC27 viral cocktail in C57BL/6 mice. PLoS One; 2010;5(9):e12705
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  • [Title] Inhibition of melanoma growth by subcutaneous administration of hTERTC27 viral cocktail in C57BL/6 mice.
  • METHODOLOGY/PRINCIPAL FINDING: Immunocompetent C57BL/6 mice were used for mouse B16 melanoma model.
  • Mice bearing B16 melanoma were administered rAAV-/rAdv viral cocktail expressing hTERTC27, and tumor growth was monitored after viral cocktail treatment.
  • B16 tumor growth was significantly inhibited by subcutaneous administration of a single dose of 1.5×10(11) vg rAAV-hTERTC27 and 2.5×10(9) pfu rAdv-hTERTC27 viral cocktail (rAAV-/rAdv-hTERTC27).
  • The population and cytotoxicity of NK cells in the mice were significantly augmented by rAAV-/rAdv-hTERTC27 treatment, and selective depletion of the NK cell population in mice by intraperitoneal injection of anti-GM1 antibody abrogated the growth suppression of melanoma induced by rAAV-/rAdv-hTERTC27 administration.
  • CONCLUSION: Activation of NK cells by administration of rAAV-/rAdv-hTERTC27 is critical for growth suppression of melanoma in mouse model.
  • [MeSH-major] Cell Proliferation. Down-Regulation. Melanoma / drug therapy. Melanoma / physiopathology. Telomerase / administration & dosage. Telomerase / genetics

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  • (PMID = 20856939.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2938346
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96. Wagner AY, Holle E, Holle L, Yu X, Schwamberger G: Immunological tolerance and tumor rejection in embryo-aggregated chimeric mice - lessons for tumor immunity. BMC Cancer; 2008;8:370
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  • Here, we have enlisted the aid of a unique set of embryo-aggregated lineage chimeric mice derived from C57/BL6 and FVB donors to study the interplay between local and systemic tumor immunity and tolerance in rejection of mouse B16 melanoma cells, syngeneic to the C57/BL6 donor strain.
  • Chimeric mice were analyzed for s.c. growth of B16 tumors in comparison to their respective donor strains as well as normal F1 hybrids, and the relative frequencies of cellular components of the immune system by FACS analysis of peripheral blood or lymph node cells.
  • RESULTS: B16 tumors grew significantly faster in mice with full chimerism in their skin as compared to syngeneic C57 or semi-syngeneic C57 x FVB F1 hosts.
  • CONCLUSION: Our data suggest a complex interplay between mechanisms of local peripheral tolerance and innate antitumor mechanisms possibly involving NK cell allorecognition as a basis for the differential growth or rejection of B16 tumors in these unique chimeric mice, which we suggest to constitute a valuable new model system for the study of immune-mediated tumor rejection.
  • [MeSH-major] Graft Rejection / immunology. Immune Tolerance. Melanoma, Experimental / immunology

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  • (PMID = 19087311.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2628932
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97. Seo N, Ito T, Wang N, Yao X, Tokura Y, Furukawa F, Takigawa M, Kitanaka S: Anti-allergic Psidium guajava extracts exert an antitumor effect by inhibition of T regulatory cells and resultant augmentation of Th1 cells. Anticancer Res; 2005 Nov-Dec;25(6A):3763-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In a study of tumor immunity, mice pretreated with the extracts exhibited retarded growth of s.c. inoculated B16 melanoma cells.
  • [MeSH-minor] Animals. Bidens. Female. Melanoma, Experimental / drug therapy. Melanoma, Experimental / immunology. Mice. Mice, Inbred BALB C. Th2 Cells / drug effects. Th2 Cells / immunology

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  • (PMID = 16302737.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Plant Extracts
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98. Choi J, Bae SJ, Ha YM, No JK, Lee EK, Lee JS, Song S, Lee H, Suh H, Yu BP, Chung HY: A newly synthesized, potent tyrosinase inhibitor: 5-(6-hydroxy-2-naphthyl)-1,2,3-benzenetriol. Bioorg Med Chem Lett; 2010 Aug 15;20(16):4882-4
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  • Our expectation was confirmed by the experimentations with B16 melanoma cells in which 5HNB inhibited melanin production.
  • [MeSH-minor] Agaricales / enzymology. Animals. Kinetics. Melanins / biosynthesis. Melanoma, Experimental / metabolism. Mice. Pyrones / pharmacology. Stilbenes / pharmacology

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • [ErratumIn] Bioorg Med Chem Lett. 2011 Jan 1;21(1):606
  • (PMID = 20619644.001).
  • [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 / 5-(6-hydroxy-2-naphthyl)-1,2,3-benzenetriol; 0 / Enzyme Inhibitors; 0 / Melanins; 0 / Naphthols; 0 / Pyrones; 0 / Stilbenes; 01Y4A2QXY0 / Pyrogallol; 6K23F1TT52 / kojic acid; EC 1.14.18.1 / Monophenol Monooxygenase; Q369O8926L / resveratrol
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99. Busch C, Drews U, Garbe C, Eisele SR, Oppitz M: Neural crest cell migration of mouse B16-F1 melanoma cells transplanted into the chick embryo is inhibited by the BMP-antagonist noggin. Int J Oncol; 2007 Dec;31(6):1367-78
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  • [Title] Neural crest cell migration of mouse B16-F1 melanoma cells transplanted into the chick embryo is inhibited by the BMP-antagonist noggin.
  • Melanoma cells are derived from the neural crest and characterized by high migratory potential and invasive growth.
  • To test the analogies between malignant and embryonic cell migration, in previous studies we transplanted melanoma cells and non-transformed mouse neural stem cells into the neural crest compartment of the chick embryo.
  • Human and mouse melanoma cells spontaneously migrated along the neural crest pathways while emigration of neural stem cells was dependent on pre-treatment with BMP-2 (bone morphogenetic protein-2).
  • We tested whether the spontaneous neural crest cell migration of melanoma cells was dependent on their endogenously expressed BMP and could be inhibited by noggin.
  • Mouse B16-F1 melanoma cells transfected with GFP-VASP (vasodilator-stimulated phosphoprotein) were cultured as aggregates and treated with BMP-2 or noggin.
  • Untreated and BMP-2-treated melanoma cells emigrated from the neural tube along with the chick host neural crest cells.
  • We conclude that spontaneous emigration of melanoma cells depends on their constitutive overexpression of BMP, and that noggin efficiently suppresses the emigration of melanoma cells in the embryonic micro-environment, thus rendering noggin a promising agent for the inhibition of melanoma cell migration in vivo.
  • [MeSH-major] Bone Morphogenetic Proteins / antagonists & inhibitors. Carrier Proteins / pharmacology. Melanoma, Experimental / pathology. Neural Crest / cytology
  • [MeSH-minor] Animals. Antigens, Neoplasm. Bone Morphogenetic Protein 2. Cadherins / analysis. Cell Aggregation / drug effects. Cell Movement / drug effects. Chick Embryo. Melanoma-Specific Antigens. Mice. Neoplasm Proteins / analysis. Neoplasm Transplantation. Transforming Growth Factor beta / pharmacology. Vimentin / analysis

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  • (PMID = 17982664.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / BMP2 protein, human; 0 / Bmp2 protein, mouse; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Proteins; 0 / Cadherins; 0 / Carrier Proteins; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Transforming Growth Factor beta; 0 / Vimentin; 148294-77-3 / noggin protein
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100. Shi G, Mao J, Yu G, Zhang J, Wu J: Tumor vaccine based on cell surface expression of DcR3/TR6. J Immunol; 2005 Apr 15;174(8):4727-35
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  • The cell surface TR6-based tumor vaccine was also effective against low antigenicity tumors, such as B16 melanoma; co-administration of bacillus Calmette-Guérin further enhanced the vaccine's efficacy.

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  • (PMID = 15814697.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Immunologic Factors; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human
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