[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 1409
1. Benlloch M, Ortega A, Ferrer P, Segarra R, Obrador E, Asensi M, Carretero J, Estrela JM: Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cytotoxicity. J Biol Chem; 2005 Feb 25;280(8):6950-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cytotoxicity.
  • Highly metastatic B16 melanoma (B16M)-F10 cells, as compared with the low metastatic B16M-F1 line, have higher GSH content and preferentially overexpress BCL-2.
  • [MeSH-major] Apoptosis. Endothelium / cytology. Glutathione / metabolism. Melanoma, Experimental / pathology. Neoplasm Metastasis. gamma-Glutamyltransferase / antagonists & inhibitors

  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15561710.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / multidrug resistance-associated protein 1; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator; CJ0O37KU29 / Verapamil; EC 2.3.2.2 / gamma-Glutamyltransferase; GAN16C9B8O / Glutathione
  •  go-up   go-down


2. Lee YS, Kim DW, Kim S, Choi HI, Lee Y, Kim CD, Lee JH, Lee SD, Lee YH: Downregulation of NFAT2 promotes melanogenesis in B16 melanoma cells. Anat Cell Biol; 2010 Dec;43(4):303-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of NFAT2 promotes melanogenesis in B16 melanoma cells.
  • Western blot analysis was performed to investigate the expression of NFAT2 protein in B16 melanoma cells.
  • Our data showed that NFAT2 expression was increased in the hypopigmented B16 cells, while tyrosinase and MITF expression was decreased.
  • To investigate the potential role of NFAT2, the recombinant adenovirus expressing microRNA specific for NFAT2 was transduced into the cultured B16 melanoma cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9575-80 [11493684.001]
  • [Cites] Oncogene. 2001 Apr 30;20(19):2476-89 [11402342.001]
  • [Cites] Dev Cell. 2005 May;8(5):665-76 [15866158.001]
  • [Cites] FASEB J. 2007 Apr;21(4):976-94 [17242160.001]
  • [Cites] Dev Genes Evol. 2008 Jan;218(1):23-32 [18175145.001]
  • [Cites] Cell. 2008 Jan 25;132(2):299-310 [18243104.001]
  • [Cites] Mol Biol Rep. 2009 Jul;36(6):1247-50 [18600473.001]
  • [Cites] FASEB J. 2008 Dec;22(12):4218-27 [18708588.001]
  • [Cites] Br J Cancer. 2009 Oct 20;101(8):1448-55 [19724275.001]
  • [Cites] Immunol Rev. 2009 Sep;231(1):160-73 [19754896.001]
  • [Cites] Immunol Rev. 2009 Sep;231(1):210-24 [19754899.001]
  • [Cites] Am J Transl Res. 2009;1(2):184-202 [19956430.001]
  • [Cites] Nature. 2010 May 20;465(7296):368-72 [20485437.001]
  • [Cites] Blood. 2010 Sep 16;116(11):e18-25 [20511541.001]
  • [Cites] J Cell Sci. 1994 Jan;107 ( Pt 1):205-11 [8175909.001]
  • [Cites] J Dermatol Sci. 1997 Mar;14(3):199-206 [9138477.001]
  • [Cites] Front Biosci. 2006;11:2157-73 [16720302.001]
  • [Cites] Carcinogenesis. 2007 Oct;28(10):2218-26 [17522069.001]
  • [Cites] J Mol Cell Cardiol. 2009 Sep;47(3):400-10 [19540841.001]
  • [Cites] J Cell Physiol. 1990 Feb;142(2):334-41 [2303529.001]
  • [Cites] Lab Invest. 1987 Jun;56(6):684-6 [3599911.001]
  • [Cites] Transplantation. 1995 Aug 27;60(4):362-8 [7652766.001]
  • [Cites] J Biol Chem. 1996 Nov 8;271(45):28052-6 [8910416.001]
  • [Cites] Nature. 1997 Jan 9;385(6612):172-6 [8990122.001]
  • [Cites] Annu Rev Immunol. 1999;17:149-87 [10358756.001]
  • [Cites] Pigment Cell Res. 2000;13 Suppl 8:98-102 [11041365.001]
  • [Cites] Am J Physiol Cell Physiol. 2003 Jun;284(6):C1593-603 [12734112.001]
  • (PMID = 21267404.001).
  • [ISSN] 2093-3673
  • [Journal-full-title] Anatomy & cell biology
  • [ISO-abbreviation] Anat Cell Biol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC3026182
  • [Keywords] NOTNLM ; B16 melanoma cells / Cyclosprorin A / Melanocyte / Melanogenesis / NFAT2
  •  go-up   go-down


3. Koo JH, Kim HT, Yoon HY, Kwon KB, Choi IW, Jung SH, Kim HU, Park BH, Park JW: Effect of xanthohumol on melanogenesis in B16 melanoma cells. Exp Mol Med; 2008 Jun 30;40(3):313-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of xanthohumol on melanogenesis in B16 melanoma cells.
  • Xanthohumol (XH), the principal prenylflavonoid of the hop plant (Humulus lupulus L.), dose-dependently inhibited isobutylmethylxanthine (IBMX)-induced melanogenesis in B16 melanoma cells, with little cytotoxicity at the effective concentrations.
  • [MeSH-minor] 1-Methyl-3-isobutylxanthine / pharmacology. Animals. Cell Line. Cell Survival / drug effects. Colforsin / pharmacology. Dose-Response Relationship, Drug. Down-Regulation. Drug Antagonism. Flavonoids. Intramolecular Oxidoreductases / antagonists & inhibitors. Intramolecular Oxidoreductases / biosynthesis. Melanoma, Experimental. Membrane Glycoproteins / antagonists & inhibitors. Membrane Glycoproteins / biosynthesis. Mice. Microphthalmia-Associated Transcription Factor / antagonists & inhibitors. Microphthalmia-Associated Transcription Factor / biosynthesis. Monophenol Monooxygenase / antagonists & inhibitors. Monophenol Monooxygenase / biosynthesis. Monophenol Monooxygenase / genetics. Oxidoreductases / antagonists & inhibitors. Oxidoreductases / biosynthesis. Signal Transduction / drug effects. alpha-MSH / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Investig Dermatol Symp Proc. 1999 Sep;4(1):24-8 [10537003.001]
  • [Cites] Mol Pharmacol. 1970 Nov;6(6):597-603 [4322367.001]
  • [Cites] Pigment Cell Res. 2000 Apr;13(2):60-9 [10841026.001]
  • [Cites] Pigment Cell Res. 2000 Aug;13(4):230-40 [10952390.001]
  • [Cites] Pigment Cell Res. 2000 Aug;13(4):248-52 [10952392.001]
  • [Cites] J Agric Food Chem. 2000 Sep;48(9):3876-84 [10995285.001]
  • [Cites] Pigment Cell Res. 2000;13 Suppl 8:94-7 [11041364.001]
  • [Cites] Exp Mol Med. 2001 Sep 30;33(3):131-5 [11642548.001]
  • [Cites] Mol Cancer Ther. 2002 Sep;1(11):959-69 [12481418.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Feb 7;301(2):610-6 [12565907.001]
  • [Cites] Phytochemistry. 2004 May;65(10):1317-30 [15231405.001]
  • [Cites] Nature. 1970 Aug 15;227(5259):680-5 [5432063.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] FEBS Lett. 1985 Apr 22;183(2):430-2 [2985438.001]
  • [Cites] Biosci Biotechnol Biochem. 1997 Jan;61(1):158-9 [9028043.001]
  • [Cites] Pigment Cell Res. 1997 Oct;10(5):288-97 [9359624.001]
  • [Cites] Antiviral Res. 2004 Dec;64(3):189-94 [15550272.001]
  • [Cites] In Vivo. 2005 Jan-Feb;19(1):103-7 [15796161.001]
  • [Cites] J Antimicrob Chemother. 2005 Jun;55(6):883-7 [15824094.001]
  • [Cites] Mol Nutr Food Res. 2005 Sep;49(9):837-43 [15995977.001]
  • [Cites] Mol Nutr Food Res. 2005 Sep;49(9):861-7 [16092070.001]
  • [Cites] Pigment Cell Res. 2006 Apr;19(2):146-53 [16524430.001]
  • [Cites] Trends Mol Med. 2006 Sep;12(9):406-14 [16899407.001]
  • [Cites] Acta Pharmacol Sin. 2006 Nov;27(11):1467-73 [17049123.001]
  • [Cites] Phytother Res. 2006 Nov;20(11):921-34 [16841367.001]
  • [Cites] Pigment Cell Res. 2006 Dec;19(6):550-71 [17083484.001]
  • [Cites] Nature. 2007 Feb 22;445(7130):843-50 [17314970.001]
  • [Cites] FASEB J. 2007 Apr;21(4):976-94 [17242160.001]
  • [Cites] Mutat Res. 2007 Aug 15;632(1-2):1-8 [17590382.001]
  • [Cites] Dermatol Clin. 2007 Jul;25(3):283-91, vii [17662894.001]
  • [Cites] J Biol Chem. 2007 Sep 21;282(38):27557-61 [17635904.001]
  • [Cites] Apoptosis. 2007 Nov;12(11):1953-63 [17874298.001]
  • [Cites] Int J Mol Med. 2007 Nov;20(5):763-7 [17912471.001]
  • [Cites] Methods Enzymol. 1987;142:165-9 [3037257.001]
  • [Cites] Int J Biochem. 1987;19(12):1141-7 [3125075.001]
  • [Cites] J Biol Chem. 1993 Jun 5;268(16):11742-9 [7685020.001]
  • [Cites] J Biol Chem. 1994 Oct 28;269(43):27080-7 [7929451.001]
  • [Cites] EMBO J. 1994 Dec 15;13(24):5818-25 [7813420.001]
  • [Cites] Recent Prog Horm Res. 1996;51:287-317; discussion 318 [8701084.001]
  • [Cites] Exp Cell Res. 2000 Mar 15;255(2):135-43 [10694430.001]
  • (PMID = 18587269.001).
  • [ISSN] 1226-3613
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Melanins; 0 / Membrane Glycoproteins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Mitf protein, mouse; 0 / Propiophenones; 1F7A44V6OU / Colforsin; 581-05-5 / alpha-MSH; EC 1.- / Oxidoreductases; EC 1.14.18.- / Tyrp1 protein, mouse; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase; T4467YT1NT / xanthohumol; TBT296U68M / 1-Methyl-3-isobutylxanthine
  • [Other-IDs] NLM/ PMC2679287
  •  go-up   go-down


Advertisement
4. Chen PF, Liu LM, Chen Z, Lin SY, Song WX, Xu YF: [Effects of ethanol extracts of Panax notoginseng on liver metastasis of B16 melanoma grafted in mice]. Zhong Xi Yi Jie He Xue Bao; 2006 Sep;4(5):500-3
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of ethanol extracts of Panax notoginseng on liver metastasis of B16 melanoma grafted in mice].
  • OBJECTIVE: To observe the effects of ethanol extracts of Panax notoginseng on the tumor and the liver metastasis in experimental mice grafted with B16 melanoma.
  • METHODS: B16 melanoma was transplanted in the spleen of C57BL/6 mice.
  • RESULTS: The high-, medium-, and low-doses of the extracts and the interferon-alpha (IFN-alpha) can improve the quality of life of the experimental mice.
  • CONCLUSION: The ethanol extracts of Panax notoginseng can improve the quality of life of the experimental mice and inhibit the growth of tumor and the liver metastasis.
  • [MeSH-major] Liver Neoplasms / prevention & control. Melanoma, Experimental / pathology. Panax notoginseng / chemistry. Plant Extracts / therapeutic use

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. ETHANOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16965745.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Interferon-alpha; 0 / Plant Extracts; 3K9958V90M / Ethanol
  •  go-up   go-down


5. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


6. Gava B, Zorzet S, Spessotto P, Cocchietto M, Sava G: Inhibition of B16 melanoma metastases with the ruthenium complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlororuthenate and down-regulation of tumor cell invasion. J Pharmacol Exp Ther; 2006 Apr;317(1):284-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of B16 melanoma metastases with the ruthenium complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlororuthenate and down-regulation of tumor cell invasion.
  • The antimetastatic ruthenium complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlorouthenate (NAMI-A) is tested in the B16 melanoma model in vitro and in vivo.
  • Treatment of B6D2F1 mice carrying intra-footpad B16 melanoma with 35 mg/kg/day NAMI-A for 6 days reduces metastasis weight independently of whether NAMI-A is given before or after surgical removal of the primary tumor.
  • This work shows the selective effectiveness of NAMI-A on the metastatic melanoma and suggests that metastasis inhibition is due to the negative modulation of tumor cell invasion processes, a mechanism in which the reduction of the gelatinolitic activity of tumor cells plays a crucial role.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Dimethyl Sulfoxide / analogs & derivatives. Lung Neoplasms / drug therapy. Melanoma, Experimental / drug therapy. Organometallic Compounds / therapeutic use. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. DIMETHYL SULFOXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16368900.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Adhesion Molecules; 0 / Organometallic Compounds; 0 / imidazolium-bis(imidazole)dimethylsulfoxideimidazotetrachlororuthenate(III); YOW8V9698H / Dimethyl Sulfoxide
  •  go-up   go-down


7. Harhaji Lj, Mijatović S, Maksimović-Ivanić D, Stojanović I, Momcilović M, Maksimović V, Tufegdzić S, Marjanović Z, Mostarica-Stojković M, Vucinić Z, Stosić-Grujicić S: Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: in vitro and in vivo study. Food Chem Toxicol; 2008 May;46(5):1825-33
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-tumor effect of Coriolus versicolor methanol extract against mouse B16 melanoma cells: in vitro and in vivo study.
  • In the present study we investigated the anti-tumor effect of C. versicolor methanol extract (which contains terpenoids and polyphenols) on B16 mouse melanoma cells both in vitro and in vivo.
  • In vitro treatment of the cells with the methanol extract (25-1600 microg/ml) reduced melanoma cell viability in a dose-dependent manner.
  • Furthermore, in the presence of the methanol extract (200 microg/ml, concentration IC(50)) the proliferation of B16 cells was arrested in the G(0)/G(1) phase of the cell cycle, followed by both apoptotic and secondary necrotic cell death.
  • 50 mg/kg, for 14 days) inhibited tumor growth in C57BL/6 mice inoculated with syngeneic B16 tumor cells.
  • Moreover, peritoneal macrophages collected 21 days after tumor implantation from methanol extract-treated animals exerted stronger tumoristatic activity ex vivo than macrophages from control melanoma-bearing mice.
  • Taken together, our results demonstrate that C. versicolor methanol extract exerts pronounced anti-melanoma activity, both directly through antiproliferative and cytotoxic effects on tumor cells and indirectly through promotion of macrophage anti-tumor activity.
  • [MeSH-major] Agaricales / chemistry. Melanoma, Experimental / drug therapy

  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • Hazardous Substances Data Bank. METHANOL .
  • Hazardous Substances Data Bank. Trypan blue .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18313195.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Phenols; 0 / Solvents; 0 / Terpenes; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; EC 1.1.1.27 / L-Lactate Dehydrogenase; I2ZWO3LS3M / Trypan Blue; Y4S76JWI15 / Methanol
  •  go-up   go-down


8. Toomey D, Conroy H, Jarnicki AG, Higgins SC, Sutton C, Mills KH: Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma. Vaccine; 2008 Jun 25;26(27-28):3540-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic vaccination with dendritic cells pulsed with tumor-derived Hsp70 and a COX-2 inhibitor induces protective immunity against B16 melanoma.
  • Therapeutic administration of DC pulsed in vitro with Hsp70 in the presence of a COX-2 inhibitor significantly reduced progression of B16 tumors in mice and significantly enhanced survival.
  • [MeSH-major] Cyclooxygenase 2 Inhibitors / pharmacology. Dendritic Cells / immunology. HSP70 Heat-Shock Proteins / immunology. Immunotherapy, Adoptive / methods. Melanoma, Experimental / immunology. Melanoma, Experimental / therapy

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18479787.001).
  • [ISSN] 0264-410X
  • [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, CD40; 0 / Antigens, CD80; 0 / Cyclooxygenase 2 Inhibitors; 0 / HSP70 Heat-Shock Proteins; 0 / Interleukin-6; 130068-27-8 / Interleukin-10
  •  go-up   go-down


9. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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


10. Janczak M, Kapuściński J, Olasik EM, Rózalski M, Płachcińska A, Kuśmierek J: Biodistribution of two (131)I-IMBA preparations, differently labelled, in mice with experimental B16 melanoma tumours. Nucl Med Rev Cent East Eur; 2008;11(2):48-52
MedlinePlus Health Information. consumer health - Melanoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biodistribution of two (131)I-IMBA preparations, differently labelled, in mice with experimental B16 melanoma tumours.
  • BACKGROUND: Numerous reports indicate that some iodinated compounds of benzamide derivatives display a strong affinity to the cells of melanoma.
  • Biodistribution of the injected compound was followed in mice with experimentally induced B16 melanoma tumours, and tumour/ tissue ratios were studied as a function of time post administration.
  • The biodistribution of (131)I-IMBA in C57 Black mice was studied in animals with experimentally induced B16 mice melanoma tumours.
  • RESULTS: The mean labelling efficiency exceeded 95 and 80 % for methods I and II, respectively, at radiochemical purity > 95% in both cases. (131)I-IMBA was vividly cumulated by melanoma tumours in mice.
  • CONCLUSIONS: High values of tumour/non-tumour ratios indicate that (131)I-IMBA could be a promising radiopharmaceutical for clinical diagnosis (staging) of melanomas in humans.
  • [MeSH-major] Benzamides / pharmacokinetics. Iodobenzenes / pharmacokinetics. Melanoma / metabolism. Melanoma / radionuclide imaging. Whole Body Imaging / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19585454.001).
  • [ISSN] 1506-9680
  • [Journal-full-title] Nuclear medicine review. Central & Eastern Europe
  • [ISO-abbreviation] Nucl Med Rev Cent East Eur
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Iodobenzenes; 0 / N-(2-diethylaminoethyl)-3-iodo-4-methoxybenzamide; 0 / Radiopharmaceuticals
  •  go-up   go-down


11. Sun T, Sun BC, Ni CS, Zhao XL, Wang XH, Qie S, Zhang DF, Gu Q, Qi H, Zhao N: Pilot study on the interaction between B16 melanoma cell-line and bone-marrow derived mesenchymal stem cells. Cancer Lett; 2008 May 8;263(1):35-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilot study on the interaction between B16 melanoma cell-line and bone-marrow derived mesenchymal stem cells.
  • Our previous study had shown that BMSCs maybe participate in angiogenesis in melanoma in vivo.
  • The aim of this study was to investigate the interaction between B16 melanoma cells and BMSCs in vitro, the mechanism of BMSCs participating in melanoma angiogenesis in vivo is unclear, so a co-culture system containing BMSCs and B16 melanoma cells, based on transwell indirect model, was established, and the interaction between BMSCs and B16 melanoma cells was studied in vitro.
  • In our study, BMSCs were generated out of bone marrow from C57 mouse, isolated BMSCs were positive for the markers CD105, CD90, CD73, CD44 and CD166 and negative for endothelial markers, which acquired endothelial phenotype (including the expression of VEGFR-1, VEGFR-2, Factor VIII) after co-culture with B16 melanoma cells; at the same time, B16 melanoma cells also up-regulated the expression of VEGF-a, VEGFR-1, VEGFR-2 and Factor VIII.
  • The proliferation rate of B16 melanoma cells and BMSCs were also found to be increased.
  • [MeSH-major] Bone Marrow Cells / cytology. Melanoma, Experimental / pathology. Mesenchymal Stromal Cells / cytology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18234417.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  •  go-up   go-down


12. Berezhnaya NM, Vinnichuk YD, Belova OB: The use of doxorubicine at low doses for elevation of LAK-activity toward explants and cells of MC-rhabdomyosarcoma and B16 melanoma resistant to doxorubicin. Exp Oncol; 2008 Mar;30(1):52-5
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of doxorubicine at low doses for elevation of LAK-activity toward explants and cells of MC-rhabdomyosarcoma and B16 melanoma resistant to doxorubicin.
  • AIM: To study the influence of doxorubicin at low doses on antitumor action of activated (LAK) and non-activated lymphocytes from lymph nodes toward tumor cells of mice bearing doxorubicin-resistant and doxorubicin-sensitive transplantable MC-rhabdomyosarcoma and B16 melanoma.
  • MATERIALS AND METHODS: The study was carried out on BALB/c mice bearing MC-rhabdomyosarcoma and 57BL/6 mice bearing 16 melanoma.
  • RESULTS: At the day 7 of tumor growth in mice bearing resistant MC-rhabdomyosarcoma, non-activated lymphocytes pretreated with low-dose doxorubicin possess the highest antitumor activity, and in mice bearing doxorubicin-resistant B16 melanoma the highest antitumor activity was detected for lymphocytes after combined cultivation with IL-2 and doxorubicin.
  • At the day 14 of tumor growth, LAK obtained from lymphocytes pretreated with doxorubicin possess the highest cytotoxic activity toward resistant tumor cells both of MC-rhabdomyosarcoma and B16 melanoma.
  • CONCLUSION: To elevate antitumor activity of LAK toward MC-rhabdomyosarcoma and B16 melanoma cells, low doses of doxorubicin could be used at certain conditions of LAK generation.
  • [MeSH-major] Doxorubicin / administration & dosage. Drug Resistance, Neoplasm / drug effects. Killer Cells, Lymphokine-Activated / drug effects. Lymphocyte Activation / drug effects. Melanoma, Experimental / drug therapy. Rhabdomyosarcoma / drug therapy

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18438341.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
  •  go-up   go-down


13. Sitabkhan Y, Frankfater A: Differences in the expression of cathepsin B in B16 melanoma metastatic variants depend on transcription factor Sp1. DNA Cell Biol; 2007 Sep;26(9):673-82
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the expression of cathepsin B in B16 melanoma metastatic variants depend on transcription factor Sp1.
  • Cathepsin B contributes to the invasiveness of B16 melanoma cells in mice, with the highly metastatic B16a melanoma producing six- to eightfold more cathepsin B mRNA and protein than the less metastatic B16F1 variant.
  • The proximal promoter region of the cathepsin B (Ctsb) gene (-149 to +94) was previously found to be capable of reproducing this pattern of differential gene activation in B16 melanoma variants.
  • The binding of B16 melanoma nuclear proteins to this promoter region has now been mapped to three GC-boxes (Sp1 transcription factor binding sites) and a potential X-box [tax response element (TRE)/c-AMP responsive element (CRE) site].
  • Promoter activity was also attenuated by mutations within the GC-rich segment between +6 and +16, but not by mutation of the putative X-box.
  • Thus, the difference in cathepsin B expression between high and low metastatic B16 melanoma variants is largely due to different levels of Sp1.
  • [MeSH-major] Cathepsin B / genetics. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. Melanoma, Experimental / genetics. Sp1 Transcription Factor / metabolism

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17691867.001).
  • [ISSN] 1044-5498
  • [Journal-full-title] DNA and cell biology
  • [ISO-abbreviation] DNA Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Sp1 Transcription Factor; 148710-94-5 / Sp3 Transcription Factor; EC 3.4.22.1 / Cathepsin B
  •  go-up   go-down


14. Gatouillat G, Balasse E, Joseph-Pietras D, Morjani H, Madoulet C: Resveratrol induces cell-cycle disruption and apoptosis in chemoresistant B16 melanoma. J Cell Biochem; 2010 Jul 1;110(4):893-902
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resveratrol induces cell-cycle disruption and apoptosis in chemoresistant B16 melanoma.
  • In this study, we show that resveratrol (0-500 microM) inhibits the growth of a doxorubicin-resistant B16 melanoma cell subline (B16/DOX) (IC(50) = 25 microM after 72 h, P < 0.05).
  • The G(1)-phase arrest of cell cycle in resveratrol-treated (10-100 microM) B16/DOX cells was followed by the induction of apoptosis, which was revealed by pyknotic nuclei and fragmented DNA.
  • Resveratrol also potentiated at subtoxic dose (25 microM for 24 h) doxorubicin cytotoxicity in the chemoresistant B16 melanoma (P < 0.01).
  • When administered to mice, resveratrol (12.5 mg/kg) reduced the growth of an established B16/DOX melanoma and prolonged survival (32% compared to untreated mice).
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Melanoma, Experimental / pathology. Stilbenes / pharmacology

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. RESVERATROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] J. Cell. Biochem. 110: 893-902, 2010. (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20564188.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Stilbenes; 80168379AG / Doxorubicin; Q369O8926L / resveratrol
  •  go-up   go-down


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


16. Murozuka Y, Kasuya MC, Kobayashi M, Watanabe Y, Sato T, Hatanaka K: Efficient sialylation on azidododecyl lactosides by using B16 melanoma cells. Chem Biodivers; 2005 Aug;2(8):1063-78

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17193190.001).
  • [ISSN] 1612-1880
  • [Journal-full-title] Chemistry & biodiversity
  • [ISO-abbreviation] Chem. Biodivers.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Glycosphingolipids
  •  go-up   go-down


17. Matsuda H, Nakashima S, Oda Y, Nakamura S, Yoshikawa M: Melanogenesis inhibitors from the rhizomes of Alpinia officinarum in B16 melanoma cells. Bioorg Med Chem; 2009 Aug 15;17(16):6048-53
BindingDB. BindingDB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Melanogenesis inhibitors from the rhizomes of Alpinia officinarum in B16 melanoma cells.
  • The 80% aqueous acetone extract from the rhizomes of Alpinia officinarum, a Chinese medicinal herb, were found to inhibit melanogenesis in theophylline-stimulated murine B16 melanoma 4A5 cells.
  • [MeSH-major] Alpinia / chemistry. Antineoplastic Agents / chemistry. Enzyme Inhibitors / chemistry. Melanoma, Experimental / drug therapy. Monophenol Monooxygenase / antagonists & inhibitors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19615910.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Kaempferols; 0 / kaempferide; 142FWE6ECS / galangin; EC 1.- / Oxidoreductases; EC 1.14.18.- / tyrosinase-related protein-1; EC 1.14.18.1 / Monophenol Monooxygenase
  •  go-up   go-down


18. Li B, Lei Z, Lichty BD, Li D, Zhang GM, Feng ZH, Wan Y, Huang B: Autophagy facilitates major histocompatibility complex class I expression induced by IFN-γ in B16 melanoma cells. Cancer Immunol Immunother; 2010 Feb;59(2):313-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autophagy facilitates major histocompatibility complex class I expression induced by IFN-γ in B16 melanoma cells.
  • Here, we report that autophagy is a negative regulator of MHC-I antigen expression in B16 melanoma cells; however, in the presence of IFN-γ, it is converted to a positive regulator.
  • Using B16 melanoma mouse model, we further show that autophagy may enhance the cytolysis of CTL to melanoma cells at the early stage of melanoma, but impairs the cytolysis at the late stage.
  • [MeSH-major] Autophagy. Histocompatibility Antigens Class I / immunology. Interferon-gamma / immunology. Melanoma, Experimental / immunology. Skin Neoplasms / immunology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19680649.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


19. Itzhaki O, Skutelsky E, Kaptzan T, Siegal A, Sinai J, Schiby G, Michowitz M, Huszar M, Leibovici J: Decreased DNA ploidy may constitute a mechanism of the reduced malignant behavior of B16 melanoma in aged mice. Exp Gerontol; 2008 Mar;43(3):164-75
MedlinePlus Health Information. consumer health - Seniors' Health.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Decreased DNA ploidy may constitute a mechanism of the reduced malignant behavior of B16 melanoma in aged mice.
  • In the present study we report an incidentally found, not yet described mechanism, of the age-related reduced tumor progression, namely a decreased ploidy in B16 melanoma growing in old (near diploidy) as compared to young mice (tetraploidy).
  • Flow cytometry forward scatter data also showed a smaller cell size of melanoma cells from old mice.
  • DNA flow cytometry profile comparison demonstrated that while B16 melanoma cells from young animals contained a high percentage of tetraploid cells, those derived from old animals were mostly close to diploid.
  • The transit from tetraploidy to near euploidy in melanoma cells growing in aged mice might avoid the genetic instability inherent to tumor progression.
  • [MeSH-major] Aging / genetics. DNA, Neoplasm / analysis. Melanoma, Experimental / genetics. Ploidies
  • [MeSH-minor] Animals. Apoptosis. Cell Size. Disease Progression. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Proto-Oncogene Proteins c-bcl-2 / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18261868.001).
  • [ISSN] 0531-5565
  • [Journal-full-title] Experimental gerontology
  • [ISO-abbreviation] Exp. Gerontol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins c-bcl-2
  •  go-up   go-down


20. Guan S, Su W, Wang N, Li P, Wang Y: A potent tyrosinase activator from Radix Polygoni multiflori and its melanogenesis stimulatory effect in B16 melanoma cells. Phytother Res; 2008 May;22(5):660-3
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A potent tyrosinase activator from Radix Polygoni multiflori and its melanogenesis stimulatory effect in B16 melanoma cells.
  • All the compounds were tested in B16 melanoma cells, the anthraquinones were found to inhibit cell proliferation at a concentration of 0.1-2.5 microg/mL, and THSG was found to be non-cytotoxic at a concentration of 0.1-12.5 microg/mL.
  • THSG significantly increased the activity of murine tyrosinase and stimulated melanin biosynthesis in B16 melanoma cells.
  • In conclusion, THSG is a potent tyrosinase activator and stimulator of melanogenesis with potential for the treatment of hypopigmentation disease.
  • [MeSH-minor] Animals. Anthraquinones / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Glucosides / pharmacology. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Mice. Stilbenes / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18389468.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2,3,5,4'-tetrahydroxystilbene-2-O-glucoside; 0 / Anthraquinones; 0 / Glucosides; 0 / Melanins; 0 / Plant Extracts; 0 / Stilbenes; EC 1.14.18.1 / Monophenol Monooxygenase
  •  go-up   go-down


21. Fujisawa Y, Nabekura T, Nakao T, Nakamura Y, Takahashi T, Kawachi Y, Otsuka F, Onodera M: The induction of tumor-specific CD4+ T cells via major histocompatibility complex class II is required to gain optimal anti-tumor immunity against B16 melanoma cell line in tumor immunotherapy using dendritic cells. Exp Dermatol; 2009 Apr;18(4):396-403
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The induction of tumor-specific CD4+ T cells via major histocompatibility complex class II is required to gain optimal anti-tumor immunity against B16 melanoma cell line in tumor immunotherapy using dendritic cells.
  • In this study, we showed the importance of antigen presentation via a major histocompatibility complex (MHC) class II molecule in cancer immunity against non-membrane bound TAAs such as the melanoma antigen gp100 by using DCs derived from MHC class II-deficient mice (C2KO).
  • The attenuated anti-tumor effect was also confirmed in a postimmunization setting where, while two of eight control mice eradicated the pre-existing melanoma cell line B16 (25%), no mice inoculated with C2KO-gp/DCs did.
  • These results suggested not only the limitation of current protocols using MHC class I-restricted tumor peptides but also the usefulness of DCs expressing gp100 in vaccine therapy against melanoma.
  • [MeSH-major] Antibodies, Neoplasm / immunology. CD4-Positive T-Lymphocytes / immunology. Genes, MHC Class II / immunology. Immunotherapy / methods. Langerhans Cells / immunology. Melanoma / immunology. Skin Neoplasms / immunology
  • [MeSH-minor] Animals. Cancer Vaccines / immunology. Cell Line, Tumor. HLA-D Antigens / genetics. HLA-D Antigens / immunology. Membrane Glycoproteins / genetics. Membrane Glycoproteins / immunology. Membrane Glycoproteins / metabolism. Mice. Mice, Inbred C57BL. Mice, Knockout. Th1 Cells / cytology. Th1 Cells / immunology. Th1 Cells / metabolism. gp100 Melanoma Antigen

  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19054057.001).
  • [ISSN] 1600-0625
  • [Journal-full-title] Experimental dermatology
  • [ISO-abbreviation] Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Cancer Vaccines; 0 / HLA-D Antigens; 0 / Membrane Glycoproteins; 0 / Si protein, mouse; 0 / gp100 Melanoma Antigen
  •  go-up   go-down


22. Murad JM, de Souza LR, De Lucca FL: PKR activation by a non-coding RNA expressed in lymphocytes of mice bearing B16 melanoma. Blood Cells Mol Dis; 2006 Sep-Oct;37(2):128-33
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PKR activation by a non-coding RNA expressed in lymphocytes of mice bearing B16 melanoma.
  • In this study, we investigated the presence of ncRNAs in lymphocytes of C57BL/6 mice bearing B16 melanoma by using the differential display reverse transcription-PCR (DD-RT-PCR).
  • We detected a highly structured transcript of 220 nt with no open reading frame (ORF) which is able to activate PKR, and it is only expressed in lymphocytes of C57BL/6 mice bearing B16 melanoma.
  • [MeSH-major] Lymphocytes / metabolism. Melanoma, Experimental / metabolism. Neoplasms / metabolism. RNA, Untranslated / genetics. eIF-2 Kinase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16857398.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Untranslated; EC 2.7.11.1 / eIF-2 Kinase
  •  go-up   go-down


23. Hou CC, Chen YP, Wu JH, Huang CC, Wang SY, Yang NS, Shyur LF: A galactolipid possesses novel cancer chemopreventive effects by suppressing inflammatory mediators and mouse B16 melanoma. Cancer Res; 2007 Jul 15;67(14):6907-15
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A galactolipid possesses novel cancer chemopreventive effects by suppressing inflammatory mediators and mouse B16 melanoma.
  • We investigated the cancer chemopreventive bioactivity of C. rabens phytocompounds in vitro and in vivo using cell- and gene-based bioassays and a mouse B16 melanoma model.
  • The bioactive glyceroglycolipid 1,2-di-O-alpha-linolenoyl-3-O-beta-galactopyranosyl-sn-glycerol (dLGG) that was identified from C. rabens was found in vitro and in vivo to be a potent nitric oxide (NO) scavenger. dLGG treatment inhibited both mRNA and protein expression of inducible NO synthase and cyclooxygenase-2 (COX-2) in murine macrophages and inhibited COX-2 gene transcription in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated B16 cells.
  • A dLGG-enriched extract from C. rabens (10 mg/kg) markedly suppressed B16 melanoma growth in C57BL/6J mice following i.p. administration, an effect comparable with that of cisplatin, a cancer chemotherapeutic drug.
  • [MeSH-minor] Active Transport, Cell Nucleus. Animals. Asteraceae / metabolism. Cell Survival. Female. I-kappa B Kinase / metabolism. Immunohistochemistry. Inhibitory Concentration 50. Macrophages / metabolism. Melanoma, Experimental. Mice. Mice, Inbred C57BL. Plant Extracts / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17638902.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Galactolipids; 0 / Plant Extracts; EC 2.7.11.10 / I-kappa B Kinase
  •  go-up   go-down


24. Sheng FX, Fan JH, Wang DM, Zhao BC, Cui XY, Tian YX: [Secretory expression vector V-pLNCX-s-hri inhibits the growth of mouse B16 melanoma]. Ai Zheng; 2009 Mar;28(3):236-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Secretory expression vector V-pLNCX-s-hri inhibits the growth of mouse B16 melanoma].
  • This study was to construct V-pLNCX-s-hri, a secretory expression vector, and explore its inhibition effects on the growth of mouse B16 melanoma cells.
  • The model of B16 melanoma-carrying mouse was established and received different treatments.
  • RESULTS: The infection efficiency of V-pLNCX-s-hri on cultured B16 cells reached 38.5%.
  • mRNA and protein levels of hRI were detected in B16 cells infected by V-pLNCX-s-hri.
  • The hRI content in the supernatant of infected B16 cells reached 0.228 microg/mL.
  • The hRI content in the peripheral blood of experimental mice was significantly higher in the V-pLNCX-s-hri group (0.249 microg/mL) than in the NS group (0.035 microg/mL), V-pLNCX group (0.028 microg/mL) and V-pLNCX-hri group (0.169 microg/mL) (P<0.01).
  • CONCLUSIONS: V-pLNCX-s-hri can effectively infect B16 cells and induce high expression of hRI.
  • V-pLNCX-s-hri is superior to V-pLNCX-hri in inhibiting the growth of B16 cells.
  • [MeSH-major] Cell Proliferation. Melanoma, Experimental / pathology. Neovascularization, Pathologic / prevention & control. Placental Hormones / biosynthesis. Ribonucleases / antagonists & inhibitors

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19619436.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Placental Hormones; 0 / RNA, Messenger; 0 / Recombinant Proteins; 120178-77-0 / placental ribonuclease inhibitor; EC 3.1.- / Ribonucleases
  •  go-up   go-down


25. Lavi G, Voronov E, Dinarello CA, Apte RN, Cohen S: Sustained delivery of IL-1 Ra from biodegradable microspheres reduces the number of murine B16 melanoma lung metastases. J Control Release; 2007 Nov 6;123(2):123-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sustained delivery of IL-1 Ra from biodegradable microspheres reduces the number of murine B16 melanoma lung metastases.
  • In vitro cytokine release and bioactivity studies in cultured melanoma B16 cells revealed the microspheres to be capable of sustained IL-1Ra release on a daily level that could inhibit cell proliferation for at least 7 days.
  • In mice injected with B16 melanoma cells, the sustained IL-1Ra delivery from biodegradable microspheres inhibited tumor growth and significantly prolonged mice survival.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Carriers. Interleukin 1 Receptor Antagonist Protein / pharmacology. Interleukin-1beta / antagonists & inhibitors. Lactic Acid / chemistry. Lung Neoplasms / prevention & control. Melanoma, Experimental / drug therapy. Microspheres. Polyglycolic Acid / chemistry. Polymers / chemistry

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LACTIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17900737.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; 0 / Drug Carriers; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1beta; 0 / Polymers; 0 / Recombinant Proteins; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid
  •  go-up   go-down


26. Vaidya SV, Stepp SE, McNerney ME, Lee JK, Bennett M, Lee KM, Stewart CL, Kumar V, Mathew PA: Targeted disruption of the 2B4 gene in mice reveals an in vivo role of 2B4 (CD244) in the rejection of B16 melanoma cells. J Immunol; 2005 Jan 15;174(2):800-7
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted disruption of the 2B4 gene in mice reveals an in vivo role of 2B4 (CD244) in the rejection of B16 melanoma cells.
  • To investigate the in vivo role of 2B4, wild-type and 2B4(-/-) mice were injected with CD48(+) and CD48(-) metastatic B16 melanoma cells.
  • Wild-type mice rejected CD48(+) melanoma poorly compared with CD48(-) tumor cells, suggesting that ligation of 2B4 by CD48 on melanoma cells is inhibitory.
  • In keeping with this, male 2B4(-/-) mice showed enhanced ability to reject CD48(+) melanoma cells.
  • However, female 2B4(-/-) mice poorly rejected both CD48(+) and CD48(-) melanoma cells, revealing a gender-specific and CD48-independent defect in mice lacking 2B4.
  • [MeSH-major] Antigens, CD / genetics. Graft Rejection / genetics. Graft Rejection / immunology. Killer Cells, Natural / immunology. Melanoma, Experimental / genetics. Melanoma, Experimental / immunology. Membrane Glycoproteins / deficiency. Membrane Glycoproteins / genetics. Receptors, Immunologic / deficiency. Receptors, Immunologic / genetics

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15634901.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA85753
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD48 antigen; 0 / Cd244 protein, mouse; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic
  •  go-up   go-down


27. Wu TG, Rose WA 2nd, Albrecht TB, Knutson EP, König R, Perdigão JR, Nguyen AP, Fleischmann WR Jr: IFN-alpha-induced murine B16 melanoma cancer vaccine cells: induction and accumulation of cell-associated IL-15. J Interferon Cytokine Res; 2007 Jan;27(1):13-22

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17266439.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES06676; United States / NIEHS NIH HHS / ES / ES10018
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Interferon-alpha; 0 / Interleukin-15
  •  go-up   go-down


28. Kim DS, Jeong YM, Park IK, Hahn HG, Lee HK, Kwon SB, Jeong JH, Yang SJ, Sohn UD, Park KC: A new 2-imino-1,3-thiazoline derivative, KHG22394, inhibits melanin synthesis in mouse B16 melanoma cells. Biol Pharm Bull; 2007 Jan;30(1):180-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new 2-imino-1,3-thiazoline derivative, KHG22394, inhibits melanin synthesis in mouse B16 melanoma cells.
  • Moreover, alpha-melanocyte-stimulating hormone (alpha-MSH) is known to increase melanin biosynthesis by increasing tyrosinase production, and here, we found that alpha-MSH-induced Mitf and tyrosinase increases were inhibited in B16 melanoma cells treated with KHG22394.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Extracellular Signal-Regulated MAP Kinases / metabolism. Melanoma, Experimental. Mice. Microphthalmia-Associated Transcription Factor / metabolism. Monophenol Monooxygenase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17202683.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Dermatologic Agents; 0 / KHG22394; 0 / Melanins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Mitf protein, mouse; 0 / Thiazoles; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  •  go-up   go-down


29. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


30. Takashima K, Fujiwara H, Inada S, Atsuji K, Araki Y, Kubota T, Yamagishi H: Tracking of green fluorescent protein (GFP)-labeled LAK cells in mice carrying B16 melanoma metastases. Anticancer Res; 2006 Sep-Oct;26(5A):3327-32
MedlinePlus Health Information. consumer health - Lung Cancer.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17094448.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interleukin-2; 147336-22-9 / Green Fluorescent Proteins
  •  go-up   go-down


31. Koo JH, Lee I, Yun SK, Kim HU, Park BH, Park JW: Saponified evening primrose oil reduces melanogenesis in B16 melanoma cells and reduces UV-induced skin pigmentation in humans. Lipids; 2010 May;45(5):401-7
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Saponified evening primrose oil reduces melanogenesis in B16 melanoma cells and reduces UV-induced skin pigmentation in humans.
  • In B16 melanoma cells, sap-EPO dose-dependently inhibited isobutylmethylxanthine-induced melanogenesis with no cytotoxicity.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Down-Regulation. Humans. Melanoma, Experimental. Men. Mice. Monophenol Monooxygenase / genetics. Monophenol Monooxygenase / metabolism. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Ultraviolet Rays

  • MedlinePlus Health Information. consumer health - Herbal Medicine.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20352496.001).
  • [ISSN] 1558-9307
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Melanins; 0 / Plant Oils; 0 / RNA, Messenger; EC 1.14.18.1 / Monophenol Monooxygenase
  •  go-up   go-down


32. Kushida S, Ohmae H, Kamma H, Totsuka R, Matsumura M, Takeuchi A, Saiki I, Yanagawa T, Onizawa K, Ishii T, Ohn T: Artificial cytokine storm combined with hyperthermia induces significant anti-tumor effect in mice inoculated with lewis lung carcinoma and B16 melanoma cells. Int J Hyperthermia; 2006 Dec;22(8):699-712

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17390999.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  •  go-up   go-down


33. Moreau MF, Papon J, Labarre P, Moins N, Borel M, Bayle M, Bouchon B, Madelmont JC: Synthesis, in vitro binding and biodistribution in B16 melanoma-bearing mice of new iodine-125 spermidine benzamide derivatives. Nucl Med Biol; 2005 May;32(4):377-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synthesis, in vitro binding and biodistribution in B16 melanoma-bearing mice of new iodine-125 spermidine benzamide derivatives.
  • In the course of our investigations aimed at improving the biological characteristics of iodobenzamides for melanoma therapeutic applications, four new derivatives containing a spermidine chain have been prepared and radiolabeled with (125)I.
  • In vitro studies showed that all compounds displayed high affinity for melanin superior to the reference compound BZA, thus validating our experimental approach.
  • In vivo biodistribution was investigated in B16 melanoma-bearing mice.
  • In view of these results, compounds 1 2 3 4 do not appear to be suitable radiopharmaceuticals for melanoma radionuclide therapy.
  • [MeSH-major] Benzamides / pharmacokinetics. Biomarkers, Tumor / metabolism. Iodine Radioisotopes / pharmacokinetics. Melanins / metabolism. Melanoma / metabolism. Spermidine / pharmacokinetics

  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878507.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Iodine Radioisotopes; 0 / Melanins; 0 / Radiopharmaceuticals; U87FK77H25 / Spermidine
  •  go-up   go-down


34. Lee J, Jung E, Park J, Jung K, Park E, Kim J, Hong S, Park J, Park S, Lee S, Park D: Glycyrrhizin induces melanogenesis by elevating a cAMP level in b16 melanoma cells. J Invest Dermatol; 2005 Feb;124(2):405-11
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glycyrrhizin induces melanogenesis by elevating a cAMP level in b16 melanoma cells.
  • In this study, using B16 melanoma cells, we showed that GR activated activator protein-1 (AP-1) and cyclic response filament "CRE" promoters, but not the nuclear factor-kappaB promoter.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cyclic AMP / metabolism. Glycyrrhizic Acid / pharmacology. Melanocytes / drug effects. Melanoma. Skin Neoplasms

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. GLYCYRRHIZIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15675961.001).
  • [ISSN] 0022-202X
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Melanins; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 6FO62043WK / Glycyrrhizic Acid; E0399OZS9N / Cyclic AMP; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.25 / MAP Kinase Kinase Kinase 1; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


35. Tai SS, Lin CG, Wu MH, Chang TS: Evaluation of depigmenting activity by 8-hydroxydaidzein in mouse B16 melanoma cells and human volunteers. Int J Mol Sci; 2009 Oct;10(10):4257-66
Hazardous Substances Data Bank. L-Ascorbic Acid .

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

  • Hazardous Substances Data Bank. Sodium ascorbate .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Regul Toxicol Pharmacol. 2001 Feb;33(1):80-101 [11259181.001]
  • [Cites] Skin Res Technol. 2009 May;15(2):218-23 [19622131.001]
  • [Cites] J Am Acad Dermatol. 1996 Jan;34(1):29-33 [8543691.001]
  • [Cites] J Nutr Sci Vitaminol (Tokyo). 1998 Jun;44(3):345-59 [9742456.001]
  • [Cites] Biosci Biotechnol Biochem. 2005 Oct;69(10):1999-2001 [16244458.001]
  • [Cites] Dermatol Surg. 2006 Mar;32(3):372-5; discussion 375 [16640681.001]
  • [Cites] J Agric Food Chem. 2007 Mar 7;55(5):2010-5 [17295516.001]
  • [Cites] Biosci Biotechnol Biochem. 2007 May;71(5):1330-3 [17485838.001]
  • [Cites] Tohoku J Exp Med. 2007 Aug;212(4):341-8 [17660699.001]
  • [Cites] Pak J Pharm Sci. 2008 Jan;21(1):45-50 [18166519.001]
  • [Cites] Exp Dermatol. 2008 May;17(5):395-404 [18177348.001]
  • [Cites] J Periodontol. 2009 Feb;80(2):317-23 [19186973.001]
  • [Cites] Int J Mol Sci. 2009 Jun;10(6):2440-75 [19582213.001]
  • [Cites] J Cosmet Sci. 2009 May-Jun;60(3):347-52 [19586602.001]
  • [Cites] J Cosmet Sci. 2009 May-Jun;60(3):353-7 [19586603.001]
  • [Cites] Skin Pharmacol. 1994;7(3):145-50 [8003336.001]
  • (PMID = 20057943.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / 8-hydroxydaidzein; 0 / Isoflavones; 0 / Melanins; 0 / Skin Lightening Preparations; 2V52R0NHXW / ascorbic acid 2-O-glucoside; EC 1.14.18.1 / Monophenol Monooxygenase; PQ6CK8PD0R / Ascorbic Acid
  • [Other-IDs] NLM/ PMC2790106
  • [Keywords] NOTNLM ; 8-hydroxydaidzein / skin whitening / suicide substrate / tyrosinase inhibitor
  • [General-notes] NLM/ Original DateCompleted: 20100628
  •  go-up   go-down


36. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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

  • MedlinePlus Health Information. consumer health - Melanoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


37. Ferrer P, Asensi M, Priego S, Benlloch M, Mena S, Ortega A, Obrador E, Esteve JM, Estrela JM: Nitric oxide mediates natural polyphenol-induced Bcl-2 down-regulation and activation of cell death in metastatic B16 melanoma. J Biol Chem; 2007 Feb 2;282(5):2880-90
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nitric oxide mediates natural polyphenol-induced Bcl-2 down-regulation and activation of cell death in metastatic B16 melanoma.
  • Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity.
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Line, Tumor. Endothelium, Vascular / physiology. Endothelium, Vascular / physiopathology. Hydrogen Peroxide / metabolism. Male. Melanoma. Mice. Mice, Inbred C57BL. Mitochondrial Membranes / physiology. Neoplasm Metastasis. Nitrates / metabolism. Nitrites / metabolism. Polyphenols. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17135264.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Nitrates; 0 / Nitrites; 0 / Phenols; 0 / Polyphenols; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 31C4KY9ESH / Nitric Oxide; BBX060AN9V / Hydrogen Peroxide
  •  go-up   go-down


38. Lee TH, Cho YH, Lee JD, Yang WI, Shin JL, Lee MG: Enhanced antitumor effect of dendritic cell based immunotherapy after intratumoral injection of radionuclide Ho-166 against B16 melanoma. Immunol Lett; 2006 Jul 15;106(1):19-26
The Lens. Cited by Patents in .

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

  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16647143.001).
  • [ISSN] 0165-2478
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Piperidines; 0 / Radioisotopes; 0 / Thiazines; 115043-27-1 / Hoe 166
  •  go-up   go-down


39. Kamei Y, Otsuka Y, Abe K: Comparison of the inhibitory effects of vitamin E analogues on melanogenesis in mouse B16 melanoma cells. Cytotechnology; 2009 Apr;59(3):183-90

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] EMBO J. 1992 Feb;11(2):527-35 [1537334.001]
  • [Cites] J Cosmet Sci. 2006 Jan-Feb;57(1):11-21 [16676120.001]
  • [Cites] EMBO J. 1994 Dec 15;13(24):5818-25 [7813420.001]
  • [Cites] J Biol Chem. 1994 Jul 8;269(27):17993-8000 [8027058.001]
  • [Cites] Free Radic Biol Med. 2000 Feb 15;28(4):643-51 [10719246.001]
  • [Cites] J Biol Chem. 2002 May 3;277(18):16340-4 [11864987.001]
  • [Cites] Arch Dermatol Res. 2002 Nov;294(8):349-54 [12420103.001]
  • [Cites] J Cosmet Sci. 2003 Mar-Apr;54(2):133-42 [12715091.001]
  • [Cites] J Chem Ecol. 2005 Feb;31(2):237-46 [15856781.001]
  • [Cites] J Ethnopharmacol. 2006 Jul 19;106(3):353-9 [16497459.001]
  • [Cites] Yakugaku Zasshi. 2006 Mar;126(3):173-7 [16508241.001]
  • [Cites] J Cosmet Sci. 2007 Jan-Feb;58(1):35-44 [17342266.001]
  • [Cites] J Toxicol Environ Health A. 2007 Mar 1;70(5):393-407 [17454565.001]
  • [Cites] EMBO J. 1992 Feb;11(2):519-26 [1537333.001]
  • [Cites] Science. 1982 Sep 17;217(4565):1163-5 [6810464.001]
  • [Cites] Br J Dermatol. 1999 Jul;141(1):20-9 [10417511.001]
  • [Cites] Pigment Cell Res. 2000;13 Suppl 8:170-4 [11041377.001]
  • [Cites] Dermatology. 2002;204(4):281-6 [12077522.001]
  • [Cites] J Biol Chem. 2004 Jan 30;279(5):3852-61 [14600146.001]
  • [Cites] Phytochemistry. 2007 Apr;68(8):1189-99 [17379263.001]
  • [Cites] Am J Chin Med. 2005;33(4):535-46 [16173528.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • (PMID = 19568943.001).
  • [ISSN] 0920-9069
  • [Journal-full-title] Cytotechnology
  • [ISO-abbreviation] Cytotechnology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2774566
  •  go-up   go-down


40. Suzuki S, Heldin CH, Heuchel RL: Platelet-derived growth factor receptor-beta, carrying the activating mutation D849N, accelerates the establishment of B16 melanoma. BMC Cancer; 2007;7:224

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):42516-27 [15284236.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Aug;15(4):275-86 [15207817.001]
  • [Cites] Lab Anim. 1988 Jul;22(3):195-201 [3172698.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):393-7 [8380638.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] Development. 1999 Jun;126(14):3047-55 [10375497.001]
  • [Cites] Physiol Rev. 1999 Oct;79(4):1283-316 [10508235.001]
  • [Cites] Methods Mol Biol. 2005;294:269-85 [15576918.001]
  • [Cites] Am J Pathol. 2006 Feb;168(2):529-41 [16436667.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1877-86 [16690964.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2929-34 [11306470.001]
  • [Cites] J Cell Biol. 2001 Apr 30;153(3):543-53 [11331305.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5476-84 [12359756.001]
  • [Cites] Am J Pathol. 2003 Jan;162(1):183-93 [12507901.001]
  • [Cites] Science. 2003 Jan 31;299(5607):708-10 [12522257.001]
  • [Cites] Gastroenterology. 2003 Sep;125(3):660-7 [12949711.001]
  • [Cites] Development. 2003 Oct;130(20):4769-84 [12952899.001]
  • [Cites] J Clin Invest. 2003 Oct;112(8):1142-51 [14561699.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2725-33 [15087386.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Aug;15(4):215-28 [15207813.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • (PMID = 18076756.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2234427
  •  go-up   go-down


41. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


42. Ni CS, Zhao N, Sun T, Zhao XL, Wang XH, Gu Q, Sun BC: [Pilot study of differentiation of bone marrow derived mesenchymal stem cells into endothelial cells induced by B16 melanoma cells in vitro]. Zhonghua Bing Li Xue Za Zhi; 2009 Jun;38(6):402-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pilot study of differentiation of bone marrow derived mesenchymal stem cells into endothelial cells induced by B16 melanoma cells in vitro].
  • The aim of the study was to investigate the induction process of BMSC by B16 melanoma cells in vitro and to analyze the role of VEGF-a in the process.
  • METHODS: A co-culture system containing BMSC and B16 melanoma cells based on transwell indirect model was established, and the induction process of BMSC by B16 melanoma cells was studied in vitro.
  • BMSC expressed CD105, CD90, CD73, CD44 and CD166, and acquired expressin of endothelial phenotype markers including VEGFR-1, VEGFR-2 and Factor VIII after co-culture with B16 melanoma cells for 48 hours.
  • In the co-culture system, B16 melanoma cells also up-regulated the expression of VEGF-a.
  • [MeSH-major] Bone Marrow Cells / cytology. Endothelial Cells / cytology. Melanoma, Experimental / pathology. Mesenchymal Stromal Cells / cytology. Vascular Endothelial Growth Factor A / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19781348.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 9001-27-8 / Factor VIII; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


43. Shin JH, Choi GS, Kang WH, Myung KB: Sphingosine 1-phosphate triggers apoptotic signal for B16 melanoma cells via ERK and caspase activation. J Korean Med Sci; 2007 Apr;22(2):298-304
MedlinePlus Health Information. consumer health - Melanoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sphingosine 1-phosphate triggers apoptotic signal for B16 melanoma cells via ERK and caspase activation.
  • In this study, we investigated the effects of S1P on the cell growth, melanogenesis, and apoptosis of cultured B16 mouse melanoma cells.
  • In results, S1P was found to induce apoptosis in B16 melanoma cells in a dose- and time-dependent manner, but exerted minimal effects on melanogenesis.
  • Although receptors of sphingosine 1-phosphate (endothelial differentiation gene 1 [Edg]/S1P(1), Edg5/S1P(2), Edg3/S1P(3)) were expressed in B16 melanoma cells, they were shown not to be associated with S1P-induced apoptosis.
  • In addition, pertussis toxin did not block the apoptotic effects of S1P on B16 melanoma cells.
  • Interestingly, the ERK pathway inhibitor, UO126, reversed the apoptotic effects of S1P on B16 melanoma cells.
  • These results suggest that S1P induced apoptosis of B16 melanoma cells via an Edg receptor-independent, pertussis toxin-insensitive pathway, and appears to be associated with the ERK and caspase-3 activation.
  • [MeSH-major] Apoptosis / drug effects. Caspase 3 / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Lysophospholipids / administration & dosage. Melanoma / enzymology. Melanoma / pathology. Sphingosine / analogs & derivatives

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] FEBS Lett. 1999 Nov 5;460(3):513-8 [10556527.001]
  • [Cites] J Cell Biochem Suppl. 1998;30-31:147-57 [9893266.001]
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):12200-6 [10766856.001]
  • [Cites] FEBS Lett. 2000 Jun 30;476(1-2):55-7 [10878250.001]
  • [Cites] FEBS Lett. 2000 Jul 7;476(3):118-23 [10913597.001]
  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34628-33 [10942778.001]
  • [Cites] Biochem J. 2000 Jul 15;349(Pt 2):385-402 [10880336.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2001;41:507-34 [11264467.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2001 Mar;363(3):358-63 [11284453.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11569-74 [11504919.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):12724-34 [11821388.001]
  • [Cites] Pharmacol Rev. 2002 Jun;54(2):265-9 [12037142.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):25851-4 [12011102.001]
  • [Cites] J Biol Chem. 2002 Oct 4;277(40):37323-30 [12138095.001]
  • [Cites] Cell Signal. 2003 Oct;15(10):919-26 [12873705.001]
  • [Cites] J Biol Chem. 2003 Oct 10;278(41):40330-6 [12835323.001]
  • [Cites] Prog Lipid Res. 1995;34(2):151-84 [7480064.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Dec 4;229(1):11-5 [8954076.001]
  • [Cites] J Biochem. 1997 May;121(5):969-73 [9192741.001]
  • [Cites] Biochem J. 1998 Mar 1;330 ( Pt 2):605-9 [9480864.001]
  • [Cites] Science. 1998 Mar 6;279(5356):1552-5 [9488656.001]
  • [Cites] J Cell Biol. 1998 Jul 13;142(1):229-40 [9660876.001]
  • [Cites] Ann N Y Acad Sci. 1998 Jun 19;845:11-8 [9668339.001]
  • [Cites] J Biol Chem. 1998 Oct 16;273(42):27104-10 [9765227.001]
  • [Cites] FASEB J. 1998 Dec;12(15):1589-98 [9837849.001]
  • [Cites] Biochem J. 1999 Jan 1;337 ( Pt 1):67-75 [9854026.001]
  • [Cites] J Biol Chem. 1999 Feb 19;274(8):4626-32 [9988698.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jun 24;260(1):203-8 [10381367.001]
  • [Cites] Oncogene. 2005 Jan 6;24(1):178-87 [15637591.001]
  • [Cites] Biochem J. 2005 Apr 15;387(Pt 2):281-93 [15801912.001]
  • [Cites] Am J Physiol Cell Physiol. 2006 Apr;290(4):C1000-8 [16267108.001]
  • [Cites] Apoptosis. 2006 Mar;11(3):337-46 [16538383.001]
  • [Cites] Neuroscience. 1999;94(2):405-15 [10579204.001]
  • (PMID = 17449940.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Lysophospholipids; 26993-30-6 / sphingosine 1-phosphate; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / Caspase 3; NGZ37HRE42 / Sphingosine
  • [Other-IDs] NLM/ PMC2693598
  •  go-up   go-down


44. Girard TJ: A factor X-TFPI hybrid protein inhibits B16 melanoma metastatic growth in mice. Thromb Res; 2007;121(3):427-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A factor X-TFPI hybrid protein inhibits B16 melanoma metastatic growth in mice.
  • [MeSH-major] Factor X / pharmacology. Lipoproteins / pharmacology. Melanoma, Experimental / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17555803.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lipoproteins; 0 / Recombinant Fusion Proteins; 0 / lipoprotein-associated coagulation inhibitor; 9001-29-0 / Factor X
  •  go-up   go-down


45. Choi MY, Song HS, Hur HS, Sim SS: Whitening activity of luteolin related to the inhibition of cAMP pathway in alpha-MSH-stimulated B16 melanoma cells. Arch Pharm Res; 2008 Sep;31(9):1166-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Whitening activity of luteolin related to the inhibition of cAMP pathway in alpha-MSH-stimulated B16 melanoma cells.
  • To examine the possibility of luteolin as a whitening agent, we measured antioxidant activity using DPPH assay, NBT/XO assay and intracellular ROS scavengning assay and depigmenting activity using tyrosinase assay, alpha-MSH-induced melanin production in B-16 cells.
  • Although luteolin did not directly inhibit tyrosinase activity, it dose-dependently inhibited both tyrosinase activity and melanin production in B16 melanoma cells stimulated by 1 microM alpha-MSH.
  • Luteolin dose-dependently inhibited cAMP levels in B16 melanoma cells stimulated by 1 microM alpha-MSH and 1 microM forskolin, which suggest that luteolin directly inhibits adenyl cyclase in B16 melanoma cells.
  • Therefore, these results suggest that whitening activity of luteolin may be due to the inhibition of adenyl cyclase involved in the signal pathway of alpha-MSH in B16 melanoma cells.
  • [MeSH-major] Cyclic AMP / physiology. Luteolin / pharmacology. Melanins / antagonists & inhibitors. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / antagonists & inhibitors. Signal Transduction / drug effects. alpha-MSH / pharmacology

  • Hazardous Substances Data Bank. ARBUTIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18806960.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biphenyl Compounds; 0 / Free Radical Scavengers; 0 / Melanins; 0 / Picrates; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 1898-66-4 / 2,2-diphenyl-1-picrylhydrazyl; 1F7A44V6OU / Colforsin; 581-05-5 / alpha-MSH; C5INA23HXF / Arbutin; E0399OZS9N / Cyclic AMP; EC 1.14.18.1 / Monophenol Monooxygenase; EC 1.17.3.2 / Xanthine Oxidase; KUX1ZNC9J2 / Luteolin
  •  go-up   go-down


46. Banciu M, Schiffelers RM, Fens MH, Metselaar JM, Storm G: Anti-angiogenic effects of liposomal prednisolone phosphate on B16 melanoma in mice. J Control Release; 2006 Jun 12;113(1):1-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-angiogenic effects of liposomal prednisolone phosphate on B16 melanoma in mice.
  • [MeSH-major] Liposomes. Melanoma, Experimental / blood supply. Melanoma, Experimental / prevention & control. Neovascularization, Pathologic / prevention & control. Prednisolone / analogs & derivatives

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16707187.001).
  • [ISSN] 0168-3659
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Liposomes; 752SY38R6C / prednisolone phosphate; 9PHQ9Y1OLM / Prednisolone
  •  go-up   go-down


47. Jeong YM, Lee JE, Kim SY, Yun HY, Baek KJ, Kwon NS, Kim DS: Enhanced effects of citrate on UVB-induced apoptosis of B16 melanoma cells. Pharmazie; 2009 Dec;64(12):829-33
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced effects of citrate on UVB-induced apoptosis of B16 melanoma cells.
  • Ultraviolet (UV) radiation is a major risk factor for the development of melanoma.
  • Thus, we investigated the effects of citrate on UVB-irradiated B16 murine melanoma cells.
  • B16 cells had more evident apoptotic features with the combination of citrate/UVB than by citrate or UVB alone; cell death of HaCaT human keratinocytes was not observed with citrate/UVB.
  • Correspondingly, cell cycle analysis showed that citrate/UVB clearly increased the sub-G0/G1 phase, which indicated apoptotic cell death of B16 cells.
  • Therefore, our study has demonstrated that sub-lethal doses of citrate enhanced the apoptotic cell death of melanoma cells under UVB irradiation.
  • From these results, we suggest that citrate might reduce the risk of developing melanoma induced by UVB.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis / radiation effects. Citrates / pharmacology. Melanoma, Experimental / pathology. Radiation-Protective Agents. Ultraviolet Rays

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20095142.001).
  • [ISSN] 0031-7144
  • [Journal-full-title] Die Pharmazie
  • [ISO-abbreviation] Pharmazie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Citrates; 0 / Radiation-Protective Agents; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases
  •  go-up   go-down


48. Tamura S, Nitoda T, Kubo I: Effects of salicylic acid on mushroom tyrosinase and B16 melanoma cells. Z Naturforsch C; 2007 Mar-Apr;62(3-4):227-33
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of salicylic acid on mushroom tyrosinase and B16 melanoma cells.
  • Neither acid showed noticeable effects on cultured murine B16-F10 melanoma cells except weak cytotoxicity.
  • [MeSH-major] Agaricales / enzymology. Melanoma / pathology. Monophenol Monooxygenase / metabolism. Salicylic Acid / pharmacology

  • MedlinePlus Health Information. consumer health - Melanoma.
  • Hazardous Substances Data Bank. SALICYLIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17542489.001).
  • [ISSN] 0939-5075
  • [Journal-full-title] Zeitschrift für Naturforschung. C, Journal of biosciences
  • [ISO-abbreviation] Z. Naturforsch., C, J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anacardic Acids; 0 / Melanins; 18654-18-7 / anacardic acid; 46627O600J / Levodopa; EC 1.14.18.1 / Monophenol Monooxygenase; O414PZ4LPZ / Salicylic Acid
  •  go-up   go-down


49. Jeong YM, Li H, Kim SY, Yun HY, Baek KJ, Kwon NS, Kim DS: Imidazole inhibits B16 melanoma cell migration via degradation of beta-catenin. J Pharm Pharmacol; 2010 Apr;62(4):491-6
MedlinePlus Health Information. consumer health - Melanoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imidazole inhibits B16 melanoma cell migration via degradation of beta-catenin.
  • OBJECTIVES: In the present study, we determined whether or not imidazole affects B16 murine melanoma cell migration to prevent melanoma metastasis.
  • METHODS: To determine the effects of imidazole on melanoma cell migration, B16 cells were treated with imidazole at various concentrations, and the migration was measured using a scratch migration assay.
  • KEY FINDINGS: Imidazole did not exhibit cytotoxic effects on B16 cells at a concentration below 100 microm.
  • Our results showed that imidazole significantly inhibits B16 cell migration.
  • It is known that the Wnt/beta-catenin signalling pathway regulates the progression of melanocytic tumours and determines the prognosis in cutaneous melanomas.
  • Moreover, inhibition of melanoma cell migration by imidazole was restored by MG132, a proteasome inhibitor, via inhibition of beta-catenin degradation.
  • CONCLUSIONS: Imidazole inhibits B16 cell migration through beta-catenin degradation, suggesting that imidazole is a potential candidate for the treatment of metastatic melanoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Movement / drug effects. Imidazoles / therapeutic use. Melanoma / drug therapy. Signal Transduction / drug effects. beta Catenin / metabolism

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20604839.001).
  • [ISSN] 2042-7158
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Imidazoles; 0 / Leupeptins; 0 / beta Catenin; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 7GBN705NH1 / imidazole
  •  go-up   go-down


50. Sanchez-Perez L, Kottke T, Diaz RM, Ahmed A, Thompson J, Chong H, Melcher A, Holmen S, Daniels G, Vile RG: Potent selection of antigen loss variants of B16 melanoma following inflammatory killing of melanocytes in vivo. Cancer Res; 2005 Mar 1;65(5):2009-17
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potent selection of antigen loss variants of B16 melanoma following inflammatory killing of melanocytes in vivo.
  • The resulting CD8+ T cell response eradicates systemically established B16 tumors.
  • In suboptimal protocols, the T cell response selected B16 variants, which grow extremely aggressively, are amelanotic and have lost expression of the tyrosinase and tyrosinase-related protein 2 (TRP-2) antigens.
  • However, expression of other melanoma-associated antigens, such as gp100, was not affected.
  • [MeSH-major] Antigens, Neoplasm / immunology. CD8-Positive T-Lymphocytes / immunology. Immunotherapy, Adoptive. Melanocytes / drug effects. Melanoma, Experimental / immunology. Tumor Escape. Vaccines, DNA / immunology
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacology. Azacitidine / pharmacology. Combined Modality Therapy. DNA Methylation / drug effects. Interferon-gamma / metabolism. Intramolecular Oxidoreductases / genetics. Intramolecular Oxidoreductases / immunology. Intramolecular Oxidoreductases / metabolism. Membrane Glycoproteins / genetics. Membrane Glycoproteins / immunology. Membrane Glycoproteins / metabolism. Mice. Mice, Inbred C57BL. Mice, Nude. Monophenol Monooxygenase / genetics. Monophenol Monooxygenase / immunology. Monophenol Monooxygenase / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / immunology. Neoplasm Proteins / metabolism. Perforin. Pore Forming Cytotoxic Proteins. Vaccination. gp100 Melanoma Antigen

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15753401.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA91956; United States / NCI NIH HHS / CA / R01 CA94180
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antimetabolites, Antineoplastic; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Pore Forming Cytotoxic Proteins; 0 / Si protein, mouse; 0 / Vaccines, DNA; 0 / gp100 Melanoma Antigen; 126465-35-8 / Perforin; 82115-62-6 / Interferon-gamma; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase; M801H13NRU / Azacitidine
  •  go-up   go-down


51. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor effects of human ribonuclease inhibitor gene transfected on B16 melanoma cells.
  • The experiment demonstrated that it might effectively inhibit tumor-induced angiogenesis and inhibit tumor growth.
  • 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


52. Yoon WJ, Kim MJ, Moon JY, Kang HJ, Kim GO, Lee NH, Hyun CG: Effect of palmitoleic acid on melanogenic protein expression in murine b16 melanoma. J Oleo Sci; 2010;59(6):315-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of palmitoleic acid on melanogenic protein expression in murine b16 melanoma.
  • [MeSH-major] Fatty Acids, Monounsaturated / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Melanins / biosynthesis. Melanoma, Experimental / metabolism

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20484837.001).
  • [ISSN] 1347-3352
  • [Journal-full-title] Journal of oleo science
  • [ISO-abbreviation] J Oleo Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Fatty Acids, Monounsaturated; 0 / Melanins; 0 / Microphthalmia-Associated Transcription Factor; 209B6YPZ4I / palmitoleic acid; EC 1.- / Oxidoreductases; EC 1.14.18.- / tyrosinase-related protein-1; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
  •  go-up   go-down


53. Ye Y, Chou GX, Wang H, Chu JH, Yu ZL: Flavonoids, apigenin and icariin exert potent melanogenic activities in murine B16 melanoma cells. Phytomedicine; 2010 Dec 15;18(1):32-5
Hazardous Substances Data Bank. APIGENIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flavonoids, apigenin and icariin exert potent melanogenic activities in murine B16 melanoma cells.
  • The compounds were first assessed with regard to their effects on tyrosinase activity in B16 cells.
  • Together these data suggest that apigenin and icariin exert potent melanogenic activities through, at least in part, upregulating the protein expression levels of melanogenic enzymes in B16 cells.
  • [MeSH-major] Apigenin / pharmacology. Enzyme Activators / pharmacology. Flavonoids / pharmacology. Melanins / metabolism. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / metabolism. Plant Extracts / pharmacology

  • Hazardous Substances Data Bank. 8-METHOXYPSORALEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier GmbH. All rights reserved.
  • (PMID = 20638260.001).
  • [ISSN] 1618-095X
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Activators; 0 / Flavonoids; 0 / Melanins; 0 / Membrane Glycoproteins; 0 / Plant Extracts; 489-32-7 / icariin; 7V515PI7F6 / Apigenin; EC 1.- / Oxidoreductases; EC 1.14.18.- / Tyrp1 protein, mouse; EC 1.14.18.1 / Monophenol Monooxygenase; U4VJ29L7BQ / Methoxsalen
  •  go-up   go-down


54. Banciu M, Metselaar JM, Schiffelers RM, Storm G: Liposomal glucocorticoids as tumor-targeted anti-angiogenic nanomedicine in B16 melanoma-bearing mice. J Steroid Biochem Mol Biol; 2008 Jul;111(1-2):101-10
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liposomal glucocorticoids as tumor-targeted anti-angiogenic nanomedicine in B16 melanoma-bearing mice.
  • The effects of all LCL-GC on the production of angiogenic/inflammatory factors in vivo in the B16.F10 murine melanoma model as well as on the viability and proliferation of tumor cells and endothelial cells in vitro were investigated.
  • The in vitro results presented herein suggest that LCL-BUP has strong cytotoxic effects on B16.F10 melanoma cells and the anti-proliferative effects of all LCL-GC towards angiogenic endothelial cells play a role in their antitumor activity.
  • [MeSH-major] Glucocorticoids / therapeutic use. Liposomes. Melanoma, Experimental / blood supply. Melanoma, Experimental / prevention & control. Neovascularization, Pathologic / prevention & control

  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. METHYLPREDNISOLONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18602825.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Liposomes; 0 / Receptors, Glucocorticoid; 51333-22-3 / Budesonide; 752SY38R6C / prednisolone phosphate; 7S5I7G3JQL / Dexamethasone; 9PHQ9Y1OLM / Prednisolone; X4W7ZR7023 / Methylprednisolone
  •  go-up   go-down


55. Xu X, Wang S, Chen W, Chen G: Effects of taohong siwu decoction II in the chick chorioallantoic membrane (CAM) assay and on B16 melanoma in mice and endothelial cells ECV304 proliferation. J Tradit Chin Med; 2006 Mar;26(1):63-7

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16705858.001).
  • [ISSN] 0255-2922
  • [Journal-full-title] Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan
  • [ISO-abbreviation] J Tradit Chin Med
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drugs, Chinese Herbal; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


56. Wang SM, Xu XY, Chen G, Yang LR: [Taohong Siwu decoction II inhibits the angiogenesis and the expressions of VEGF and KDR/FLK-1 in C57BL/6J mice bearing B16 melanoma]. Zhongguo Zhong Yao Za Zhi; 2005 Dec;30(23):1866-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Taohong Siwu decoction II inhibits the angiogenesis and the expressions of VEGF and KDR/FLK-1 in C57BL/6J mice bearing B16 melanoma].
  • OBJECTIVE: To investigate the effects of Taohong Siwu decoction II on B16 melanoma in mice and the underlying mechanism.
  • METHOD: C57BL/6J mice bearing B16 melanoma were used in this study.
  • The experimental groups were treated respectively with Taohong Siwu decoction II at doses of 2.5, 5 and 10 g x kg(-1) and cyclophosphamide at 0.05 g x kg(-1), Taohong Siwu decoction II at 10 g x kg(-1) plus cyclophosphamide at 0.025 mg x kg(-1).
  • CONCLUSION: Taohong Siwu decoction II can inhibit the growth of B16 melanoma in mice and attenuate the expressions of VEGF and KDR/FLK-1, suggesting that Taohong Siwu decoction II produces the antitumor effect via a possible antiagiogenisis mechanism.
  • [MeSH-major] Drugs, Chinese Herbal / pharmacology. Melanoma, Experimental / pathology. Neovascularization, Pathologic / pathology. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16499030.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 0 / Taohong Siwu decoction II; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


57. Baral R, Mandal I, Chattopadhyay U: Immunostimulatory neem leaf preparation acts as an adjuvant to enhance the efficacy of poorly immunogenic B16 melanoma surface antigen vaccine. Int Immunopharmacol; 2005 Jul;5(7-8):1343-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunostimulatory neem leaf preparation acts as an adjuvant to enhance the efficacy of poorly immunogenic B16 melanoma surface antigen vaccine.
  • Immunogenecity of the poorly immunogenic B16 melanoma cell surface antigen (B16MelSAg) was enhanced by combining B16MelSAg with NLP in C57BL/6 mice, as evidenced by ELISA and flow cytometry.
  • Vaccination of mice with B16MelSAg+NLP more efficiently prevented the growth of B16 melanoma tumor than mice immunized with B16MelSAg or NLP alone.
  • In another experiment, the immune sera (B16MelSAg+NLP) was mixed with B16Mel tumors and injected subcutaneously into syngenic C57BL/6 mice.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Antigens, Neoplasm / immunology. Azadirachta. Cancer Vaccines / immunology. Melanoma, Experimental / immunology. Plant Leaves. Plant Preparations / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15914339.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Cancer Vaccines; 0 / Plant Preparations
  •  go-up   go-down


58. Ugen KE, Kutzler MA, Marrero B, Westover J, Coppola D, Weiner DB, Heller R: Regression of subcutaneous B16 melanoma tumors after intratumoral delivery of an IL-15-expressing plasmid followed by in vivo electroporation. Cancer Gene Ther; 2006 Oct;13(10):969-74
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regression of subcutaneous B16 melanoma tumors after intratumoral delivery of an IL-15-expressing plasmid followed by in vivo electroporation.
  • In vivo electroporation has been used to efficiently deliver drugs and 'therapeutic' genes to tumors, including melanoma lesions.
  • This study reports on the effect of intratumoral delivery of an optimized DNA plasmid expressing interleukin-15 (pIL-15) on established murine melanoma tumors.
  • In this study, C57BL/6 mice were injected with B16.F10 melanoma cells and randomized into different experimental groups: untreated (P-V-E-), treated with pIL-15 (P+) or backbone plasmid (V+), with or without electroporation (E+ or E-).
  • These results demonstrate the ability of pIL-15 to mediate B16 melanoma regression, with the effect being significantly enhanced by electroporative delivery.
  • This is the first description of the ability of a naked DNA plasmid expressing IL-15 to alone mediate complete regression of B16 melanoma tumors and underscores the potential clinical use of these plasmids for the treatment of malignant tumors when delivered with in vivo electroporation.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Expert Opin Drug Deliv. 2005 Mar;2(2):255-68 [16296752.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3281-4 [11309280.001]
  • [Cites] Mol Ther. 2002 Jun;5(6):668-75 [12027550.001]
  • [Cites] Gene Ther. 2002 Oct;9(19):1321-5 [12224015.001]
  • [Cites] Cytotherapy. 2005;7(1):23-35 [16040381.001]
  • [Cites] Gene Ther. 2004 Oct;11 Suppl 1:S33-42 [15454955.001]
  • [Cites] Cell Immunol. 1995 Oct 15;165(2):289-93 [7553894.001]
  • [Cites] EMBO J. 1996 Sep 16;15(18):4928-39 [8890166.001]
  • [Cites] J Immunol. 2005 Jul 1;175(1):112-23 [15972637.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3392-7 [12626740.001]
  • (PMID = 16763607.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / F32AI054152; United States / NIAID NIH HHS / AI / F32 AI054152; United States / NCI NIH HHS / CA / R01 CA122518-01A2; United States / NCI NIH HHS / CA / R01 CA122518; United States / NCI NIH HHS / CA / CA122518-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-15
  • [Other-IDs] NLM/ NIHMS253299; NLM/ PMC3277848
  •  go-up   go-down


59. McCarthy DO, Graves E: Conjugated linoleic acid preserves muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma. Res Nurs Health; 2006 Apr;29(2):98-104
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conjugated linoleic acid preserves muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma.
  • The B16 melanoma expresses TNFa mRNA, and induced SMW with no change in muscle levels of TNFa type 1 receptor (TNFR1) protein.
  • A diet containing .5% CLA had no effect on SMW or TNFR1 in mice bearing B16 tumors.
  • [MeSH-minor] Analysis of Variance. Animals. Carcinoma, Lewis Lung. Female. Male. Melanoma, Experimental. Mice. Mice, Inbred C57BL. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Tumor Necrosis Factor-alpha / metabolism

  • MedlinePlus Health Information. consumer health - Dietary Fats.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley Periodicals, Inc.
  • (PMID = 16532476.001).
  • [ISSN] 0160-6891
  • [Journal-full-title] Research in nursing & health
  • [ISO-abbreviation] Res Nurs Health
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dietary Fats; 0 / Linoleic Acids, Conjugated; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


60. Ohguchi K, Banno Y, Nakagawa Y, Akao Y, Nozawa Y: Negative regulation of melanogenesis by phospholipase D1 through mTOR/p70 S6 kinase 1 signaling in mouse B16 melanoma cells. J Cell Physiol; 2005 Dec;205(3):444-51
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Negative regulation of melanogenesis by phospholipase D1 through mTOR/p70 S6 kinase 1 signaling in mouse B16 melanoma cells.
  • Melanogenesis is a principal parameter of differentiation in melanocytes and melanoma cells.
  • To investigate the role of PLD1, we examined the effect of knockdown of endogenous PLD1 by small interference RNA (siRNA) on melanogenesis in B16 melanoma cells.
  • [MeSH-major] Melanins / antagonists & inhibitors. Melanins / biosynthesis. Melanoma / metabolism. Phospholipase D / physiology. Protein Kinases / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / physiology

  • MedlinePlus Health Information. consumer health - Melanoma.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15895362.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Melanins; 0 / RNA, Small Interfering; 0 / protein kinase modulator; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.1 / ribosomal protein S6 kinase, 70kD, polypeptide 1; EC 3.1.4.4 / Phospholipase D; EC 3.1.4.4 / phospholipase D1; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


61. Itoh T, Furuichi Y: Hot-water extracts from adzuki beans (Vigna angularis) stimulate not only melanogenesis in cultured mouse B16 melanoma cells but also pigmentation of hair color in C3H mice. Biosci Biotechnol Biochem; 2005 May;69(5):873-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hot-water extracts from adzuki beans (Vigna angularis) stimulate not only melanogenesis in cultured mouse B16 melanoma cells but also pigmentation of hair color in C3H mice.
  • Its distilled water fraction (WEx) was found to stimulate tyrosinase activity in cultured mouse B16 melanoma cells and hair color pigmentation in C3H mice.
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Melanoma, Experimental / metabolism. Mice. Mice, Inbred C3H. Plant Extracts / chemistry. Plant Extracts / pharmacology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15914904.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Melanins; 0 / Plant Extracts
  •  go-up   go-down


62. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


63. Graves E, Ramsay E, McCarthy DO: Inhibitors of COX activity preserve muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma. Res Nurs Health; 2006 Apr;29(2):87-97
Hazardous Substances Data Bank. INDOMETHACIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitors of COX activity preserve muscle mass in mice bearing the Lewis lung carcinoma, but not the B16 melanoma.
  • We report that indomethacin, a nonspecific inhibitor of COX, and NS398, a specific inhibitor of COX2, preserved muscle mass and reduced type 1 TNF receptors in muscles of mice bearing the Lewis lung carcinoma, but not in mice bearing the B16 melanoma.
  • [MeSH-minor] Analysis of Variance. Animals. Carcinoma, Lewis Lung. Female. Interleukin-6 / metabolism. Melanoma, Experimental. Mice. Mice, Inbred C57BL. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley Periodicals, Inc.
  • (PMID = 16532483.001).
  • [ISSN] 0160-6891
  • [Journal-full-title] Research in nursing & health
  • [ISO-abbreviation] Res Nurs Health
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Interleukin-6; 0 / Nitrobenzenes; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Sulfonamides; 0 / Tumor Necrosis Factor-alpha; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; XXE1CET956 / Indomethacin
  •  go-up   go-down


64. Wu SP, Lee I, Ghoroghchian PP, Frail PR, Zheng G, Glickson JD, Therien MJ: Near-infrared optical imaging of B16 melanoma cells via low-density lipoprotein-mediated uptake and delivery of high emission dipole strength tris[(porphinato)zinc(II)] fluorophores. Bioconjug Chem; 2005 May-Jun;16(3):542-50
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Near-infrared optical imaging of B16 melanoma cells via low-density lipoprotein-mediated uptake and delivery of high emission dipole strength tris[(porphinato)zinc(II)] fluorophores.
  • The reconstituted LDL(PZn(3)) proteins can be used to deliver rapidly hundreds of copies of PZn(3) to a given murine B16 melanoma cell via LDL receptor-mediated endocytosis.
  • Confocal NIR fluorescence microscopy evinces that B16 cells can be imaged at very low doses (approximately nM) of NIRF.
  • The highly attractive photophysical properties of PZn(3) and closely related chromophores, coupled with their lack of toxicity and compatibility with uptake into apo-LDL and subsequent rapid delivery to B16 cells via LDLr-mediated endocytosis, suggest the potential utility of this platform for NIR optical imaging of cancer cells in vivo.
  • [MeSH-major] Fluorescent Dyes / metabolism. Lipoproteins, LDL / metabolism. Melanoma, Experimental / metabolism. Melanoma, Experimental / pathology. Metalloporphyrins / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15898720.001).
  • [ISSN] 1043-1802
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-37199; United States / NCI NIH HHS / CA / P20-CA86255; United States / NCI NIH HHS / CA / R24-CA83105-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Lipoproteins, LDL; 0 / Metalloporphyrins; 0 / tris(porphinato)zinc(II)
  •  go-up   go-down


65. Wu TG, Perdigão JR, Umhoefer TK, Cao J, Ansari DA, Albrecht TB, Knutson EP, Rose WA 2nd, Jorgensen AJ, Ryan LM, Abdalla LE, Fleischmann WR Jr: Heterogeneous interleukin-15 inducibilities in murine B16 melanoma and RM-1 prostate carcinoma by interferon-alpha treatment. J Interferon Cytokine Res; 2009 Nov;29(11):719-28
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heterogeneous interleukin-15 inducibilities in murine B16 melanoma and RM-1 prostate carcinoma by interferon-alpha treatment.
  • Long-term treatment of mouse cancer cells with interferon-alpha (IFN-alpha) converts parental B16 melanoma cells to B16alpha vaccine cells.
  • Inoculation of syngeneic mice with UV-irradiated B16alpha vaccine cells triggers immunity to the parental B16 tumor that is mediated by host macrophages, T cells, and NK cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol. 2008 Feb 15;180(4):2099-106 [18250415.001]
  • [Cites] J Interferon Cytokine Res. 2001 Dec;21(12):1117-27 [11798470.001]
  • [Cites] Int Immunol. 2002 Aug;14(8):917-24 [12147628.001]
  • [Cites] J Virol. 2001 Jul;75(13):5921-9 [11390593.001]
  • [Cites] J Immunol. 2003 May 15;170(10):5018-26 [12734346.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1969-74 [14762166.001]
  • [Cites] J Biol Chem. 2004 Oct 1;279(40):42192-201 [15284244.001]
  • [Cites] Nat New Biol. 1973 Apr 4;242(118):148-9 [4512654.001]
  • [Cites] Can J Microbiol. 1975 Aug;21(8):1247-53 [240500.001]
  • [Cites] J Interferon Res. 1983;3(4):425-35 [6323591.001]
  • [Cites] Science. 1994 May 13;264(5161):965-8 [8178155.001]
  • [Cites] J Exp Med. 1995 Mar 1;181(3):1255-9 [7869044.001]
  • [Cites] J Steroid Biochem Mol Biol. 1995 May;52(5):403-13 [7538321.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2897-902 [8610139.001]
  • [Cites] J Immunol. 1998 May 1;160(9):4418-26 [9574546.001]
  • [Cites] J Interferon Cytokine Res. 1998 Oct;18(10):829-39 [9809618.001]
  • [Cites] Blood. 1999 May 15;93(10):3531-9 [10233906.001]
  • [Cites] J Interferon Cytokine Res. 2007 Jan;27(1):13-22 [17266439.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • (PMID = 19642895.001).
  • [ISSN] 1557-7465
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES10018
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Interferon-alpha; 0 / Interleukin-15; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC3096523
  •  go-up   go-down


66. Jérôme V, Graser A, Müller R, Kontermann RE, Konur A: Cytotoxic T lymphocytes responding to low dose TRP2 antigen are induced against B16 melanoma by liposome-encapsulated TRP2 peptide and CpG DNA adjuvant. J Immunother; 2006 May-Jun;29(3):294-305
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxic T lymphocytes responding to low dose TRP2 antigen are induced against B16 melanoma by liposome-encapsulated TRP2 peptide and CpG DNA adjuvant.
  • Using the poorly immunogenic B16 melanoma model we could demonstrate that vaccination with liposomal TRP2 peptide plus CpG ODNs but not vaccination with free peptide or adjuvant alone resulted in tumor protection in subcutaneous and metastatic tumor models.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Immunotherapy / methods. Liposomes / chemistry. Melanoma, Experimental / metabolism. Membrane Proteins / chemistry. Oligodeoxyribonucleotides / chemistry. Peptide Fragments / chemistry. Peptides / chemistry. T-Lymphocytes, Cytotoxic / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16699372.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, Neoplasm; 0 / CPG-oligonucleotide; 0 / Cancer Vaccines; 0 / Liposomes; 0 / Membrane Proteins; 0 / Oligodeoxyribonucleotides; 0 / Peptide Fragments; 0 / Peptides; 0 / peptide SVYDFFVWL; 9007-49-2 / DNA
  •  go-up   go-down


67. Ehira N, Oshiumi H, Matsumoto M, Kondo T, Asaka M, Seya T: An embryo-specific expressing TGF-β family protein, growth-differentiation factor 3 (GDF3), augments progression of B16 melanoma. J Exp Clin Cancer Res; 2010;29:135
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An embryo-specific expressing TGF-β family protein, growth-differentiation factor 3 (GDF3), augments progression of B16 melanoma.
  • Malignant tumor cells often express embryonic antigens which share the expression with embryonic stem (ES) cells.
  • We examined the expression of ES cell-specific genes in the mouse B16 melanoma cell line to identify the factors promoting tumorigenesis.
  • We found that endogenous growth-differentiation factor 3 (GDF3) expression was induced in implant B16 tumor during tumor progression in syngenic C57BL/6 mice.
  • B16 F10, a subline with a high metastatic potential, continuously expressed GDF3 while low metastatic B16 F1 expressed comparatively decreased levels of GDF3.
  • Overexpression of GDF3 promoted growth of implanted melanoma B16 F1 and F10 in syngenic mice.
  • Such a profile was reported to be characteristic of melanoma stem cell-like cells.
  • Since GDF3-driven CD24 acts as a receptor for endogenous innate immune ligands that modulate cell proliferation, CD24 is an effective determinant of tumorigenesis in malignant cell transformation.
  • Finally, our results support the view that GDF3 has the ability to induce progression of CD24-inducible melanoma in mice.
  • [MeSH-major] Growth Differentiation Factor 3 / metabolism. Melanoma, Experimental / metabolism
  • [MeSH-minor] Animals. Antigens, CD24 / metabolism. Antigens, CD44 / metabolism. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Cell Line, Tumor. Cell Proliferation. Disease Progression. Gene Expression Regulation, Neoplastic. Immunity, Innate. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Time Factors. Transfection. Tumor Burden

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell Mol Immunol. 2007 Dec;4(6):467-72 [18163959.001]
  • [Cites] Cell Oncol. 2006;28(5-6):315-26 [17167184.001]
  • [Cites] Expert Opin Ther Targets. 2008 Aug;12(8):1021-33 [18620523.001]
  • [Cites] Cancer Biol Ther. 2008 May;7(5):777-82 [18376139.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):755-68 [18784658.001]
  • [Cites] Nature. 2008 Dec 4;456(7222):593-8 [19052619.001]
  • [Cites] Science. 2009 Mar 27;323(5922):1722-5 [19264983.001]
  • [Cites] Mod Pathol. 2009 Aug;22(8):1066-74 [19396148.001]
  • [Cites] Clin Cancer Res. 2009 Sep 1;15(17):5518-27 [19706825.001]
  • [Cites] Genes Cells. 2009 Jun;14(6):683-94 [19476507.001]
  • [Cites] Trends Immunol. 2009 Dec;30(12):557-61 [19786366.001]
  • [Cites] Cancer Lett. 2010 Jun 1;292(1):17-23 [19944522.001]
  • [Cites] Nature. 2008 Jan 17;451(7176):345-9 [18202660.001]
  • [Cites] Trends Mol Med. 2002 Apr;8(4):179-86 [11927276.001]
  • [Cites] Histol Histopathol. 2002;17(3):951-9 [12168807.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):779-85 [12576450.001]
  • [Cites] Mol Cell. 2003 Apr;11(4):915-26 [12718878.001]
  • [Cites] Oncogene. 2003 May 29;22(22):3424-30 [12776194.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Aug 22;308(2):251-6 [12901861.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4906-13 [14581365.001]
  • [Cites] Cell. 2003 Oct 31;115(3):281-92 [14636556.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):395-402 [14724568.001]
  • [Cites] Stem Cells. 2004;22(2):169-79 [14990856.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2709-19 [15102675.001]
  • [Cites] Mol Endocrinol. 1992 Nov;6(11):1961-8 [1480182.001]
  • [Cites] J Biol Chem. 1993 Feb 15;268(5):3444-9 [8429021.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Oncogene. 1998 Jan 8;16(1):95-103 [9467948.001]
  • [Cites] J Biochem. 1998 Nov;124(5):1020-5 [9792928.001]
  • [Cites] Oncogene. 2005 Feb 24;24(9):1491-500 [15674344.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2746-54 [15805274.001]
  • [Cites] Cancer. 2005 Nov 15;104(10):2255-65 [16228988.001]
  • [Cites] Development. 2006 Jan;133(2):209-16 [16339188.001]
  • [Cites] Development. 2006 Jan;133(2):319-29 [16368929.001]
  • [Cites] Cell Cycle. 2006 May;5(10):1069-73 [16721050.001]
  • [Cites] Cell. 2006 Aug 25;126(4):663-76 [16904174.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2726-35 [16763212.001]
  • [Cites] Mod Pathol. 2006 Dec;19(12):1585-92 [16998462.001]
  • [ErratumIn] J Exp Clin Cancer Res. 2014;33:22
  • (PMID = 20950440.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD24; 0 / Antigens, CD44; 0 / Cd24a protein, mouse; 0 / Cd44 protein, mouse; 0 / Gdf3 protein, mouse; 0 / Growth Differentiation Factor 3
  • [Other-IDs] NLM/ PMC2972255
  •  go-up   go-down


68. Yu J, Tian R, Xiu B, Yan J, Jia R, Zhang L, Chang AE, Song H, Li Q: Antitumor activity of T cells generated from lymph nodes draining the SEA-expressing murine B16 melanoma and secondarily activated with dendritic cells. Int J Biol Sci; 2009;5(2):135-46
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of T cells generated from lymph nodes draining the SEA-expressing murine B16 melanoma and secondarily activated with dendritic cells.
  • We transferred the bacterial superantigen staphylococcal enterotoxin A (SEA) gene into B16 murine melanoma tumor cells, and used them to induce TDLN (SEA TDLN) in syngeneic hosts.
  • Wild-type (wt) TDLN induced by parental B16 tumor was used as a control.
  • DC-stimulated SEA TDLN cells eliminated nearly 90% of the pulmonary metastasis in mice bearing established B16 melanoma micrometastases.
  • [MeSH-major] Dendritic Cells / physiology. Enterotoxins / metabolism. Immunotherapy, Adoptive / methods. Lymph Nodes / cytology. Melanoma, Experimental / therapy. T-Lymphocytes / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 1999 Feb;5(2):461-9 [10037198.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3675-81 [12839958.001]
  • [Cites] Br J Cancer. 1999 Sep;81(2):359-66 [10496366.001]
  • [Cites] Infect Immun. 2005 Feb;73(2):1044-51 [15664948.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):1063-70 [15705908.001]
  • [Cites] Int J Biochem Cell Biol. 2005 Jun;37(6):1219-31 [15778086.001]
  • [Cites] Cancer. 2005 Apr 1;103(7):1519-28 [15739200.001]
  • [Cites] J Immunol. 2005 Aug 1;175(3):1424-32 [16034078.001]
  • [Cites] J Immunother. 2005 Nov-Dec;28(6):551-9 [16224272.001]
  • [Cites] Clin Immunol. 2007 Jun;123(3):298-310 [17449328.001]
  • [Cites] J Immunother. 2008 May;31(4):345-58 [18391761.001]
  • [Cites] Cancer Res. 2008 Jun 1;68(11):4431-41 [18519706.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):666-75 [12951585.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8466-75 [14679011.001]
  • [Cites] J Immunol. 2004 Feb 1;172(3):1719-26 [14734754.001]
  • [Cites] Cancer Res. 2004 Mar 1;64(5):1867-74 [14996751.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6783-90 [15374997.001]
  • [Cites] Immunology. 1993 Oct;80(2):236-41 [7505257.001]
  • [Cites] J Immunother Emphasis Tumor Immunol. 1995 Jan;17(1):1-11 [7728301.001]
  • [Cites] Cancer Gene Ther. 1996 Jan-Feb;3(1):39-47 [8785710.001]
  • [Cites] J Exp Med. 1996 Mar 1;183(3):791-800 [8642283.001]
  • [Cites] Cancer Immunol Immunother. 1996 May;42(4):237-45 [8665571.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15388-93 [8986821.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):796-807 [9053507.001]
  • [Cites] J Immunol. 1997 Jul 15;159(2):664-73 [9218581.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9482-7 [9689106.001]
  • [Cites] J Immunol. 1998 Sep 15;161(6):3033-41 [9743368.001]
  • [Cites] Clin Immunol. 2000 Jan;94(1):64-72 [10607491.001]
  • [Cites] Hum Gene Ther. 2000 Apr 10;11(6):839-50 [10779161.001]
  • [Cites] Cancer Res. 2000 May 1;60(9):2449-57 [10811123.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6391-5 [11103803.001]
  • [Cites] Nat Med. 2001 Apr;7(4):452-8 [11283672.001]
  • [Cites] Immunol Invest. 2001 Feb;30(1):33-45 [11419910.001]
  • [Cites] J Immunol. 2001 Sep 1;167(5):2929-35 [11509641.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8127-34 [11719441.001]
  • [Cites] J Immunother. 2001 Nov-Dec;24(6):493-501 [11759072.001]
  • [Cites] J Immunol. 2002 Jan 1;168(1):73-80 [11751948.001]
  • [Cites] J Immunother. 2002 Jul-Aug;25(4):304-13 [12142553.001]
  • [Cites] J Immunol. 2002 Sep 15;169(6):3314-20 [12218152.001]
  • [Cites] J Immunol. 2002 Nov 1;169(9):4811-21 [12391191.001]
  • [Cites] Science. 2002 Oct 25;298(5594):850-4 [12242449.001]
  • [Cites] J Immunol. 2003 Jan 1;170(1):99-106 [12496388.001]
  • [Cites] J Clin Oncol. 2003 Mar 1;21(5):884-90 [12610189.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2546-52 [12750278.001]
  • [Cites] J Immunother. 2003 May-Jun;26(3):222-33 [12806276.001]
  • [Cites] Clin Immunol. 1999 Jun;91(3):345-53 [10370381.001]
  • (PMID = 19173035.001).
  • [ISSN] 1449-2288
  • [Journal-full-title] International journal of biological sciences
  • [ISO-abbreviation] Int. J. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Enterotoxins; 37337-57-8 / enterotoxin A, Staphylococcal
  • [Other-IDs] NLM/ PMC2631223
  • [Keywords] NOTNLM ; Adoptive therapy / B16 melanoma / Staphylococcal enterotoxin A (SEA) / T lymphocyte / dendritic cells (DC)
  •  go-up   go-down


69. Zhao KJ, Cheng H, Zhu KJ, Xu Y, Chen ML, Zhang X, Song T, Ye J, Wang Q, Chen DF: Recombined DNA vaccines encoding calreticulin linked to HPV6bE7 enhance immune response and inhibit angiogenic activity in B16 melanoma mouse model expressing HPV 6bE7 antigen. Arch Dermatol Res; 2006 Jul;298(2):64-72
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recombined DNA vaccines encoding calreticulin linked to HPV6bE7 enhance immune response and inhibit angiogenic activity in B16 melanoma mouse model expressing HPV 6bE7 antigen.
  • Therefore, we constructed DNA vaccines by employing different lengths of CRT chimerically linked to a model antigen HPV6bE7 and investigated the immunological and antiangiogenic effects of these vaccines in a B16 melanoma model that express HPV6bE7 antigen.
  • Vaccination with CRT180/HPV6bE7 generated the best protective effect of delaying tumor formation and reduction of tumor size in tumor growth inhibition experiment among all DNA constructs.
  • [MeSH-major] Human papillomavirus 6 / genetics. Human papillomavirus 6 / immunology. Melanoma, Experimental / immunology. Melanoma, Experimental / therapy. Oncogene Proteins, Viral / genetics. Oncogene Proteins, Viral / immunology. S100 Calcium Binding Protein G / genetics. S100 Calcium Binding Protein G / immunology. Vaccines, DNA / pharmacology. Viral Vaccines / pharmacology

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16710741.001).
  • [ISSN] 0340-3696
  • [Journal-full-title] Archives of dermatological research
  • [ISO-abbreviation] Arch. Dermatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Calbindin 2; 0 / DNA Primers; 0 / E7 protein, Human papillomavirus 6b; 0 / Interleukin-2; 0 / Oncogene Proteins, Viral; 0 / S100 Calcium Binding Protein G; 0 / Vaccines, DNA; 0 / Viral Vaccines; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


70. Seo WG, Hwang JC, Kang SK, Jin UH, Suh SJ, Moon SK, Kim CH: Suppressive effect of Zedoariae rhizoma on pulmonary metastasis of B16 melanoma cells. J Ethnopharmacol; 2005 Oct 3;101(1-3):249-57
Hazardous Substances Data Bank. NITRIC OXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppressive effect of Zedoariae rhizoma on pulmonary metastasis of B16 melanoma cells.
  • The inhibitory effect of Curcuma zedoaria Roscoe (WE-CZ) on experimental pulmonary metastasis of B16 melanoma cells was investigated.
  • When the duration of WE-CZ intake was examined, survival time was not affected by pre-intake before B16 melanoma cell inoculation and was slightly extended by post-intake after B16 melanoma cell inoculation, although the life span was prolonged by intake throughout the experiment.
  • The elevated NO was found to serve as a cytotoxic mediator against B16 melanoma cells in co-culture with macrophages.
  • On the contrary, B16 melanoma-conditioned medium reduced NO production by macrophages.
  • These findings indicate that WE-CZ possesses anti-migratory effects on B16 melanoma cells and that the macrophage function-modulating activity by WE-CZ appears to underlie its anti-metastatic activity, which leads to a decrease in the number of lung metastatic surface nodules and the extension of life span.
  • [MeSH-major] Curcuma. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Melanoma, Experimental / drug therapy. Phytotherapy. Plant Extracts / therapeutic use

  • MedlinePlus Health Information. consumer health - Herbal Medicine.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16023317.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Plant Extracts; 31C4KY9ESH / Nitric Oxide
  •  go-up   go-down


71. Vandercappellen J, Liekens S, Bronckaers A, Noppen S, Ronsse I, Dillen C, Belleri M, Mitola S, Proost P, Presta M, Struyf S, Van Damme J: The COOH-terminal peptide of platelet factor-4 variant (CXCL4L1/PF-4var47-70) strongly inhibits angiogenesis and suppresses B16 melanoma growth in vivo. Mol Cancer Res; 2010 Mar;8(3):322-34
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The COOH-terminal peptide of platelet factor-4 variant (CXCL4L1/PF-4var47-70) strongly inhibits angiogenesis and suppresses B16 melanoma growth in vivo.
  • In addition, low (7 microg total) doses of intratumoral CXCL4L1/PF-4var(47-70) inhibited B16 melanoma growth in mice more extensively than CXCL4/PF-4(47-70).
  • This antitumoral activity was predominantly mediated through inhibition of angiogenesis (without affecting blood vessel stability) and induction of apoptosis, as evidenced by immunohistochemical and fluorescent staining of B16 tumor tissue.
  • [MeSH-major] Angiostatic Proteins / pharmacology. Antineoplastic Agents / pharmacology. Melanoma, Experimental / drug therapy. Neovascularization, Pathologic / drug therapy. Peptide Fragments / pharmacology. Platelet Factor 4 / pharmacology
  • [MeSH-minor] Animals. Biological Assay. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Cell Proliferation / drug effects. Cells, Cultured. Chick Embryo. Disease Models, Animal. Humans. Mice. Mice, Inbred C57BL. Mice, Nude

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


72. Yang J, Zhang W, Shi P, Chen J, Han X, Wang Y: Effects of exopolysaccharide fraction (EPSF) from a cultivated Cordyceps sinensis fungus on c-Myc, c-Fos, and VEGF expression in B16 melanoma-bearing mice. Pathol Res Pract; 2005;201(11):745-50
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of exopolysaccharide fraction (EPSF) from a cultivated Cordyceps sinensis fungus on c-Myc, c-Fos, and VEGF expression in B16 melanoma-bearing mice.
  • The mice (C57BL/6) were administered three different doses of EPSF peritoneally every 2 days, starting from the day of implantation of B16 melanoma cells through their tail veins for 27 days (14 times).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cordyceps. Melanoma, Experimental / metabolism. Polysaccharides / pharmacology. Proto-Oncogene Proteins c-fos / biosynthesis. Proto-Oncogene Proteins c-myc / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16325517.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Myc protein, mouse; 0 / Polysaccharides; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-myc; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse
  •  go-up   go-down


73. Amarzguioui M, Peng Q, Wiiger MT, Vasovic V, Babaie E, Holen T, Nesland JM, Prydz H: Ex vivo and in vivo delivery of anti-tissue factor short interfering RNA inhibits mouse pulmonary metastasis of B16 melanoma cells. Clin Cancer Res; 2006 Jul 1;12(13):4055-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ex vivo and in vivo delivery of anti-tissue factor short interfering RNA inhibits mouse pulmonary metastasis of B16 melanoma cells.
  • In this study, we explore the effects of ex vivo and in vivo delivery of short interfering RNA (siRNA) targeting tissue factor on B16 melanoma colonization of the lung in a murine model for metastasis.
  • EXPERIMENTAL DESIGN AND RESULTS: C57BL/6 mice were evaluated for pulmonary metastases following tail vein injection of B16 cells transfected with either active or inactive siRNA.
  • The average time point at which the mice started to exhibit tumor-associated stress was also increased significantly from 22 days for the control group to 27 days for the experimental group (P = 0.01).
  • [MeSH-major] Drug Delivery Systems. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Melanoma, Experimental / drug therapy. RNA, Small Interfering / administration & dosage. Thromboplastin / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Female. Injections, Intravenous. Injections, Subcutaneous. Mice. Mice, Inbred C57BL. Neoplasm Transplantation

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16818705.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 9035-58-9 / Thromboplastin
  •  go-up   go-down


74. Curran MA, Montalvo W, Yagita H, Allison JP: PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors. Proc Natl Acad Sci U S A; 2010 Mar 2;107(9):4275-80
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PD-1 and CTLA-4 combination blockade expands infiltrating T cells and reduces regulatory T and myeloid cells within B16 melanoma tumors.
  • Vaccination with irradiated B16 melanoma cells expressing either GM-CSF (Gvax) or Flt3-ligand (Fvax) combined with antibody blockade of the negative T-cell costimulatory receptor cytotoxic T-lymphocyte antigen-4 (CTLA-4) promotes rejection of preimplanted tumors.
  • Here, we show that the combination of CTLA-4 and PD-1 blockade is more than twice as effective as either alone in promoting the rejection of B16 melanomas in conjunction with Fvax.
  • Combination blockade also synergistically increases Teff-to-myeloid-derived suppressor cell ratios within B16 melanomas.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2000 Jun 15;60(12):3239-46 [10866317.001]
  • [Cites] Immunol Rev. 2008 Aug;224:141-65 [18759925.001]
  • [Cites] J Exp Med. 2003 Apr 7;197(7):875-83 [12668647.001]
  • [Cites] J Exp Med. 2004 Jun 7;199(11):1479-89 [15184501.001]
  • [Cites] J Exp Med. 1991 Mar 1;173(3):721-30 [1847722.001]
  • [Cites] Immunity. 1995 Nov;3(5):541-7 [7584144.001]
  • [Cites] J Exp Med. 1999 Aug 2;190(3):355-66 [10430624.001]
  • [Cites] Immunity. 1999 Aug;11(2):141-51 [10485649.001]
  • [Cites] J Immunol. 2005 Aug 1;175(3):1586-92 [16034097.001]
  • [Cites] Mol Cell Biol. 2005 Nov;25(21):9543-53 [16227604.001]
  • [Cites] J Immunol. 2006 Mar 15;176(6):3321-9 [16517699.001]
  • [Cites] J Clin Invest. 2006 Jul;116(7):1935-45 [16778987.001]
  • [Cites] J Clin Invest. 2007 Jul;117(7):1902-13 [17557120.001]
  • [Cites] Int Immunol. 2007 Jul;19(7):813-24 [17606980.001]
  • [Cites] Immunity. 2007 Jul;27(1):111-22 [17629517.001]
  • [Cites] Scand J Immunol. 2007 Oct;66(4):435-40 [17850588.001]
  • [Cites] Eur J Immunol. 2007 Dec;37(12):3445-54 [18034419.001]
  • [Cites] Nat Rev Immunol. 2008 Feb;8(2):153-60 [18219311.001]
  • [Cites] Clin Cancer Res. 2008 May 15;14(10):3044-51 [18483370.001]
  • [Cites] Cancer Immunol Immunother. 2009 May;58(5):687-97 [18828017.001]
  • [Cites] Nat Rev Immunol. 2009 Mar;9(3):162-74 [19197294.001]
  • [Cites] PLoS Pathog. 2009 Feb;5(2):e1000313 [19247441.001]
  • [Cites] Clin Cancer Res. 2009 Mar 1;15(5):1623-34 [19208793.001]
  • [Cites] J Exp Med. 2009 Aug 3;206(8):1717-25 [19581407.001]
  • [Cites] Int Immunol. 2009 Sep;21(9):1065-77 [19651643.001]
  • [Cites] Cancer Res. 2009 Oct 1;69(19):7747-55 [19738077.001]
  • [Cites] Nat Immunol. 2009 Nov;10(11):1185-92 [19783989.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12293-7 [12218188.001]
  • (PMID = 20160101.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Cancer Vaccines; 0 / Pdcd1 protein, mouse; 0 / Programmed Cell Death 1 Receptor; 82115-62-6 / Interferon-gamma; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse
  • [Other-IDs] NLM/ PMC2840093
  •  go-up   go-down


75. Benlloch M, Mena S, Ferrer P, Obrador E, Asensi M, Pellicer JA, Carretero J, Ortega A, Estrela JM: Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor necrosis factor-alpha and chemotherapy. J Biol Chem; 2006 Jan 6;281(1):69-79
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor necrosis factor-alpha and chemotherapy.
  • Mitochondrial glutathione (mtGSH) depletion increases sensitivity of Bcl-2-overexpressing B16 melanoma (B16M)-F10 cells (high metastatic potential) to tumor necrosis factor-alpha (TNF-alpha)-induced oxidative stress and death in vitro.
  • [MeSH-major] Glutamine / pharmacology. Melanoma / drug therapy. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics. Soft Tissue Neoplasms / drug therapy. Superoxide Dismutase / genetics. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animal Feed. Animals. Antineoplastic Agents / pharmacology. Combined Modality Therapy. Disease Models, Animal. Drug Resistance, Neoplasm. Genetic Therapy. Glutathione / metabolism. Male. Mice. Mice, Inbred C57BL. Mitochondria / metabolism. Neoplasm Transplantation. Oxidative Stress

  • MedlinePlus Health Information. consumer health - Melanoma.
  • Hazardous Substances Data Bank. Glutamine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16263711.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Necrosis Factor-alpha; 0RH81L854J / Glutamine; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione
  •  go-up   go-down


76. Sitdikova SM, Amandzholov BS, Kiselevskii MV, Donenko FV: Specificity of relapses and metastases of experimental transplanted Ehrlich carcinoma and B16 melanoma. Bull Exp Biol Med; 2007 Jan;143(1):80-2

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18019019.001).
  • [ISSN] 0007-4888
  • [Journal-full-title] Bulletin of experimental biology and medicine
  • [ISO-abbreviation] Bull. Exp. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


77. Ohguchi K, Akao Y, Nozawa Y: Stimulation of melanogenesis by the citrus flavonoid naringenin in mouse B16 melanoma cells. Biosci Biotechnol Biochem; 2006 Jun;70(6):1499-501
MedlinePlus Health Information. consumer health - Melanoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stimulation of melanogenesis by the citrus flavonoid naringenin in mouse B16 melanoma cells.
  • In this study, we examined the effect of naringenin on melanogenesis in mouse B16 melanoma cells.
  • [MeSH-major] Citrus / chemistry. Flavanones / pharmacology. Melanins / metabolism. Melanoma / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16794334.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Flavanones; 0 / Melanins; HN5425SBF2 / naringenin
  •  go-up   go-down


78. 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
Hazardous Substances Data Bank. (Z)-9-OCTADECENAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Animals. Disease Progression. Humans. Male. Mice. Mice, Inbred C57BL

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


79. Maeda M, Murakami M, Takegami T, Ota T: Promotion or suppression of experimental metastasis of B16 melanoma cells after oral administration of lapachol. Toxicol Appl Pharmacol; 2008 Jun 1;229(2):232-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promotion or suppression of experimental metastasis of B16 melanoma cells after oral administration of lapachol.
  • The effect of lapachol on the experimental metastasis of murine B16BL6 melanoma cells was examined.
  • [MeSH-major] Melanoma, Experimental / pathology. Naphthoquinones / pharmacology. Neoplasm Metastasis / prevention & control

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18294668.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Naphthoquinones; 12001-79-5 / Vitamin K; B221938VB6 / lapachol
  •  go-up   go-down


80. 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
MedlinePlus Health Information. consumer health - Immunization.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The formation of a pseudocapsule, peripheral node addresin expression in small venules, and the recruitment of a wide variety of cellular populations, including macrophages, polymorphonuclear lymphocytes, and CD8+ and CD4+ T lymphocytes found in association with DC, evidenced the formation of tertiary lymphoid tissue in the vaccination site in our experimental system.
  • [MeSH-major] Cancer Vaccines / immunology. Dendritic Cells / immunology. Lymphoid Tissue / physiology. Melanoma, Experimental / immunology. Melanoma, Experimental / prevention & control. Vaccination / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


81. Murakami T, Sato A, Chun NA, Hara M, Naito Y, Kobayashi Y, Kano Y, Ohtsuki M, Furukawa Y, Kobayashi E: Transcriptional modulation using HDACi depsipeptide promotes immune cell-mediated tumor destruction of murine B16 melanoma. J Invest Dermatol; 2008 Jun;128(6):1506-16
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional modulation using HDACi depsipeptide promotes immune cell-mediated tumor destruction of murine B16 melanoma.
  • With melanoma, as with many other malignancies, aberrant transcriptional repression is a hallmark of refractory cancer.
  • Herein, we demonstrate that depsipeptide promotes tumor-specific T-cell-mediated killing of B16/F10 murine melanoma cells.
  • Second, the sublethal dose of depsipeptide treatment with either a recombinant Fas ligand or tumor-specific T cells synergistically enhanced apoptotic cell death in B16/F10 cells in vitro.
  • Finally, in vivo metastatic growth of B16/F10 in the lung was significantly inhibited by a combination of depsipeptide treatment and immune cell adoptive transfer from immunized mice using irradiated B16 cells and gp100-specific (Pmel-1) TCR transgenic mice (P<0.05, vs cell transfer alone).
  • Consequently, employment of a transcriptional modulation strategy using HDACis might prove to be a useful pretreatment for human melanoma immunotherapy.
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacology. Antigens, CD95 / metabolism. Caspase 3 / metabolism. Caspase 7 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Depsipeptides / pharmacology. Histone Deacetylases / metabolism. Melanoma / pathology. Melanoma, Experimental. Mice. Mice, Transgenic. Oligonucleotide Array Sequence Analysis

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18185535.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antigens, CD95; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Depsipeptides; CX3T89XQBK / romidepsin; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


82. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


83. Wang T, Yang M, Chen J, Watkins T, Xiuyun C: Inhibition of B16 melanoma growth in vivo by retroviral vector-mediated human ribonuclease inhibitor. Angiogenesis; 2005;8(1):73-81
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of B16 melanoma growth in vivo by retroviral vector-mediated human ribonuclease inhibitor.
  • To study the links between hRI, angiogenesis, and melanoma growth, the hRI gene was intravenously administered to mice in a recombinant retroviral vector, and expression of the hRI gene was induced to block melanoma angiogenesis.
  • More hRI expression in vimentin-positive cells of the tumor than in melanoma cells suggested that mesenchymal cells in the fibrous envelope of the tumor play important roles in this gene therapy.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Melanoma, Experimental / blood supply. Placental Hormones / therapeutic use. Ribonucleases / antagonists & inhibitors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16132620.001).
  • [ISSN] 0969-6970
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Placental Hormones; 120178-77-0 / placental ribonuclease inhibitor; EC 3.1.- / Ribonucleases
  •  go-up   go-down


84. Gong W, Zhang GM, Liu Y, Lei Z, Li D, Yuan Y, Huang B, Feng ZH: IFN-gamma withdrawal after immunotherapy potentiates B16 melanoma invasion and metastasis by intensifying tumor integrin alphavbeta3 signaling. Int J Cancer; 2008 Aug 1;123(3):702-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IFN-gamma withdrawal after immunotherapy potentiates B16 melanoma invasion and metastasis by intensifying tumor integrin alphavbeta3 signaling.
  • Here, we report that the termination of immunotherapy strikingly increases the metastatic potential of remnant melanoma.
  • The relief of IFN-gamma stress led to the increase of alphavbeta3 integrin expression in B16 cells, which increased the adhesion of B16 cells to fibrinogen, fibronectin and laminin.
  • Through alphavbeta3 signaling, the activation of FAK, upregulation of cdc2, production of active MMP-2 and MMP-9 and actin polymerization were intensified in B16 cells stimulated with ECM molecules 24 h after the withdrawal of IFN-gamma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Fibronectins / pharmacology. Immunotherapy. Integrin alphaVbeta3 / metabolism. Interferon-gamma / administration & dosage. Melanoma, Experimental / immunology. Melanoma, Experimental / pathology. Recombinant Proteins / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18470915.001).
  • [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 / CH50 recombinant polypeptide; 0 / Fibronectins; 0 / Integrin alphaVbeta3; 0 / Recombinant Proteins; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


85. Banciu M, Fens MH, Storm G, Schiffelers RM: Antitumor activity and tumor localization of liposomal glucocorticoids in B16 melanoma-bearing mice. J Control Release; 2008 Apr 21;127(2):131-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity and tumor localization of liposomal glucocorticoids in B16 melanoma-bearing mice.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Budesonide / pharmacology. Dexamethasone / analogs & derivatives. Liposomes / pharmacology. Melanoma, Experimental / drug therapy. Methylprednisolone / analogs & derivatives. Prednisolone / analogs & derivatives

  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. METHYLPREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18291548.001).
  • [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 / Liposomes; 312-93-6 / dexamethasone 21-phosphate; 51333-22-3 / Budesonide; 6089CVN95V / methylprednisolone sodium phosphate; 752SY38R6C / prednisolone phosphate; 7S5I7G3JQL / Dexamethasone; 9PHQ9Y1OLM / Prednisolone; X4W7ZR7023 / Methylprednisolone
  •  go-up   go-down


86. Ren T, Chen Q, Tian Z, Wei H: Down-regulation of surface fractalkine by RNA interference in B16 melanoma reduced tumor growth in mice. Biochem Biophys Res Commun; 2007 Dec 28;364(4):978-84
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down-regulation of surface fractalkine by RNA interference in B16 melanoma reduced tumor growth in mice.
  • Here, we show that CX3CL1/fractalkine was expressed on both mouse and human solid tumors, and small interfering RNA-mediated knock down of fractalkine gene inhibited melanoma B16-F0 cells growth in vivo, which was correlated to the decreased angiogenesis around the tumor.
  • [MeSH-major] Chemokine CX3CL1 / metabolism. Genetic Therapy / methods. Melanoma / genetics. Melanoma / therapy. RNA Interference


87. Bellei B, Flori E, Izzo E, Maresca V, Picardo M: GSK3beta inhibition promotes melanogenesis in mouse B16 melanoma cells and normal human melanocytes. Cell Signal; 2008 Oct;20(10):1750-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GSK3beta inhibition promotes melanogenesis in mouse B16 melanoma cells and normal human melanocytes.
  • Exposure of the murine melanoma cell line B16 and normal human melanocytes to GSK3beta specific inhibitors (SB216763, SB415286, BIO, and LiCl) resulted in a dose-dependent accumulation of beta-catenin.
  • Moreover, treatment of B16 cells with a siRNA targeted against beta-catenin completely abolished the promelanogenic effect of GSK3beta inhibition, however, the overexpression of a constitutively active mutant form of beta-catenin (pCS2beta-cat-mut) only slightly increased the degree of pigmentation.
  • [MeSH-major] Glycogen Synthase Kinase 3 / antagonists & inhibitors. Melanins / biosynthesis. Melanocytes / enzymology. Melanoma, Experimental / enzymology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18602000.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Melanins; 0 / Microphthalmia-Associated Transcription Factor; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 0 / beta Catenin; EC 1.14.18.1 / Monophenol Monooxygenase; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  •  go-up   go-down


88. Ohguchi K, Akao Y, Nozawa Y: Involvement of calpain in melanogenesis of mouse B16 melanoma cells. Mol Cell Biochem; 2005 Jul;275(1-2):103-7

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16335789.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Cysteine Proteinase Inhibitors; 0 / Hormones; 0 / Indolequinones; 0 / Leupeptins; 0 / Melanins; 0 / RNA, Messenger; 110044-82-1 / acetylleucyl-leucyl-norleucinal; 3571-34-4 / dopachrome; 581-05-5 / alpha-MSH; 79079-11-1 / calpastatin; EC 1.14.18.1 / Monophenol Monooxygenase; EC 3.4.22.- / Calpain
  •  go-up   go-down


89. Lee YS, Kim HK, Lee KJ, Jeon HW, Cui S, Lee YM, Moon BJ, Kim YH, Lee YS: Inhibitory effect of glyceollin isolated from soybean against melanogenesis in B16 melanoma cells. BMB Rep; 2010 Jul;43(7):461-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effect of glyceollin isolated from soybean against melanogenesis in B16 melanoma cells.
  • Here, we investigated the effect of glyceollin produced to induce disease resistance responses of soybean to specific races of an incompatible pathogen, phytophthora sojae, on melanogenesis and discussed their mechanisms in melanin biosynthesis.
  • We found that glyceollin inhibits melanin synthesis and tyrosinase activity in B16 melanoma cells without cytotoxicity.
  • Additionally, glyceollin effectively inhibited intracellular cAMP levels in B16 melanoma cells stimulated by alpha-melanocyte stimulating hormone (alpha-MSH).
  • These results suggest that the whitening activity of glyceollin may be due to the inhibition of cAMP involved in the signal pathway of alpha-MSH in B16 melanoma cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclic AMP / metabolism. Intramolecular Oxidoreductases / antagonists & inhibitors. Intramolecular Oxidoreductases / metabolism. Melanoma, Experimental / enzymology. Melanoma, Experimental / metabolism. Monophenol Monooxygenase / antagonists & inhibitors. Monophenol Monooxygenase / metabolism. Oxidoreductases / antagonists & inhibitors. Oxidoreductases / metabolism. Signal Transduction. alpha-MSH / metabolism

  • MedlinePlus Health Information. consumer health - Cosmetics.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20663406.001).
  • [ISSN] 1976-670X
  • [Journal-full-title] BMB reports
  • [ISO-abbreviation] BMB Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Cosmetics; 0 / Melanins; 0 / Pterocarpans; 581-05-5 / alpha-MSH; 6461TV6UCH / glyceollin; E0399OZS9N / Cyclic AMP; EC 1.- / Oxidoreductases; EC 1.14.18.- / tyrosinase-related protein-1; EC 1.14.18.1 / Monophenol Monooxygenase; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.3.12 / dopachrome isomerase
  •  go-up   go-down


90. Yamaoka Y, Ohguchi K, Itoh T, Nozawa Y, Akao Y: Effects of theaflavins on melanin biosynthesis in mouse b16 melanoma cells. Biosci Biotechnol Biochem; 2009 Jun;73(6):1429-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of theaflavins on melanin biosynthesis in mouse b16 melanoma cells.
  • In this study, we examined the effects of theaflavins, polyphenols in black tea, on alpha melanocyte-stimulating hormone (alphaMSH)-induced melanogenesis in mouse B16 melanoma cells.
  • [MeSH-major] Biflavonoids / pharmacology. Catechin / pharmacology. Melanins / biosynthesis. Melanoma, Experimental / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19502752.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biflavonoids; 0 / DNA Primers; 0 / Melanins; 0 / RNA, Messenger; 1IA46M0D13 / theaflavin; 8R1V1STN48 / Catechin; EC 1.14.18.1 / Monophenol Monooxygenase
  •  go-up   go-down


91. Ohguchi K, Ito M, Yokoyama K, Iinuma M, Itoh T, Nozawa Y, Akao Y: Effects of sesquiterpene lactones on melanogenesis in mouse B16 melanoma cells. Biol Pharm Bull; 2009 Feb;32(2):308-10
National BioResource Project. culture/stock collections - NBRP resources .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of sesquiterpene lactones on melanogenesis in mouse B16 melanoma cells.
  • In this study, we examined the effect of sesquiterpene lactones isolated from Calea urticifolia and Tanacetum parthenium (feverfew) on melanogenesis in mouse B16 melanoma cells.
  • In response to 3-isobutyl-1-methylxanthin (IBMX), B16 melanoma cells underwent differentiation characterized by increased melanin biosynthesis.
  • Treatment of B16 cells with 2,3-epoxyjuanislamin elicited significant decreases in tyrosinase protein and mRNA levels.
  • [MeSH-major] Lactones / pharmacology. Melanins / biosynthesis. Melanoma, Experimental / metabolism. Sesquiterpenes / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19182396.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Lactones; 0 / Melanins; 0 / Phosphodiesterase Inhibitors; 0 / Plant Extracts; 0 / Sesquiterpenes; EC 1.14.18.1 / Monophenol Monooxygenase; TBT296U68M / 1-Methyl-3-isobutylxanthine
  •  go-up   go-down


92. Ohguchi K, Koike M, Suwa Y, Koshimizu S, Mizutani Y, Nozawa Y, Akao Y: Inhibitory effects of whisky congeners on melanogenesis in mouse B16 melanoma cells. Biosci Biotechnol Biochem; 2008 Apr;72(4):1107-10

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18391453.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Melanins; 0 / Phenols; 0 / Polyphenols; 581-05-5 / alpha-MSH; EC 1.14.18.1 / Monophenol Monooxygenase
  •  go-up   go-down


93. Matsuda H, Hirata N, Kawaguchi Y, Naruto S, Takata T, Oyama M, Iinuma M, Kubo M: Melanogenesis stimulation in murine B16 melanoma cells by Kava (Piper methysticum) rhizome extract and kavalactones. Biol Pharm Bull; 2006 Apr;29(4):834-7

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16595931.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Lactones; 0 / Melanins; 0 / Plant Extracts
  •  go-up   go-down


94. Triba MN, Starzec A, Bouchemal N, Guenin E, Perret GY, Le Moyec L: Metabolomic profiling with NMR discriminates between biphosphonate and doxorubicin effects on B16 melanoma cells. NMR Biomed; 2010 Nov;23(9):1009-16
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metabolomic profiling with NMR discriminates between biphosphonate and doxorubicin effects on B16 melanoma cells.
  • The metabolomic profiles of B16 melanoma cells were investigated in vitro with high resolution-magic angle spinning proton magnetic resonance spectroscopy and OPLS multivariate statistical analyse.
  • We compared the profiles for untreated melanoma B16-F10 cells and Ca(2+) chelating EGTA, doxorubicin or BP7033 bisphosphonate treated cells.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Bone Density Conservation Agents / therapeutic use. Diphosphonates / therapeutic use. Doxorubicin / therapeutic use. Magnetic Resonance Spectroscopy / methods. Melanoma, Experimental. Metabolomics / methods

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20963798.001).
  • [ISSN] 1099-1492
  • [Journal-full-title] NMR in biomedicine
  • [ISO-abbreviation] NMR Biomed
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 80168379AG / Doxorubicin
  •  go-up   go-down


95. Arung ET, Yoshikawa K, Shimizu K, Kondo R: Isoprenoid-substituted flavonoids from wood of Artocarpus heterophyllus on B16 melanoma cells: cytotoxicity and structural criteria. Fitoterapia; 2010 Mar;81(2):120-3
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isoprenoid-substituted flavonoids from wood of Artocarpus heterophyllus on B16 melanoma cells: cytotoxicity and structural criteria.
  • A structure-activity investigation of the effect of these isolated compounds (1-9) and structurally related compounds on B16 melanoma cells indicated that isoprenoid moiety substitutions in flavonoids enhance their cytotoxicity, and that the position of attachment and the number of isoprenoid-substituent moieties per molecule influence flavonoid cytotoxicity.
  • [MeSH-major] Artocarpus / chemistry. Flavonoids / pharmacology. Melanoma, Experimental / drug therapy. Plant Extracts / pharmacology. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19686821.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Plant Extracts; 0 / Terpenes
  •  go-up   go-down


96. Koo JH, Lee I, Yun SK, Kim HU, Park BH, Park JW: Saponified sunflower and safflower oils inhibit melanogenesis in B16 melanoma cells. Mol Med Rep; 2010 Mar-Apr;3(2):281-5

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


97. Chang TS, Lin JJ: Inhibitory effect of danazol on melanogenesis in mouse B16 melanoma cells. Arch Pharm Res; 2010 Dec;33(12):1959-65
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effect of danazol on melanogenesis in mouse B16 melanoma cells.
  • In the present study, more than 200 generic drugs were screened to verify their applicability as a skin-lightening agent using mouse B16 melanoma cells.
  • Of the numerous agents, danazol was found to inhibit melanogenesis in B16 cells in a dose-dependent manner with an IC(50) value of 9.3 μM.
  • In addition, danazol reduced cellular tyrosinase activity in B16 cells but did not directly inhibit the murine tyrosinase activity in the cell-free system.
  • Western blotting analysis confirmed that danazol downregulated the levels of tyrosinase protein in B16 cells, and reverse-transcription polymerase chain reaction (RT-PCR) analysis revealed that danazol did not downregulate the levels of tyrosinase mRNA in the cells.
  • These results indicate that danazol inhibits melanogenesis in B16 cells via reducing the tyrosinase activity by post-transcriptional regulation.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell-Free System / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Drug Evaluation, Preclinical. High-Throughput Screening Assays. Melanoma, Experimental. Mice. Monophenol Monooxygenase / genetics. Monophenol Monooxygenase / metabolism. RNA, Messenger / metabolism. Transcription, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21191761.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Melanins; 0 / RNA, Messenger; EC 1.14.18.1 / Monophenol Monooxygenase; N29QWW3BUO / Danazol
  •  go-up   go-down


98. Chen J, Peng H, Ou-Yang X, He X: Research on the antitumor effect of ginsenoside Rg3 in B16 melanoma cells. Melanoma Res; 2008 Oct;18(5):322-9
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Research on the antitumor effect of ginsenoside Rg3 in B16 melanoma cells.
  • The experiment demonstrated that it might effectively inhibit proliferation and metastasis of tumor cells.
  • To further explore the antitumor function of Rg3, we investigated the in-vitro and in-vivo activity of Rg3 in the treatment of B16 melanoma cells, derived from C57BL/6 mouse, capable of forming tumor colonies in the lungs following intravenous injection.
  • B16 melanoma-bearing mice were used to evaluate in vivo the antitumor activity of Rg3.
  • This research might supply valuable data for chemotherapy with Rg3 in melanoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Proliferation / drug effects. Ginsenosides / therapeutic use. Lung Neoplasms / drug therapy. Melanoma, Experimental / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18781130.001).
  • [ISSN] 1473-5636
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ginsenosides; 0 / Proto-Oncogene Proteins c-bcl-2; 14197-60-5 / ginsenoside Rg3; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


99. Sun B, Zhang S, Zhang D, Yin X, Wang S, Gu Y, Wang Y: Doxycycline influences microcirculation patterns in B16 melanoma. Exp Biol Med (Maywood); 2007 Nov;232(10):1300-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Doxycycline influences microcirculation patterns in B16 melanoma.
  • To examine the effects of doxycycline on invasion-related protein expression and proliferation of melanoma cells and to evaluate its effect on microcirculation patterns in melanoma, we injected murine melanoma B16 cell suspensions into the groin areas of C57BL/6 mice that were randomly divided into treatment and control groups.
  • Doxycycline treatment partly suppressed the growth of engrafted B16 melanoma, with an inhibition rate of 35.63%.
  • Doxycycline inhibits the growth of engrafted melanoma and results in reduced expression of MMP-2, MMP-9, and VM formations.
  • [MeSH-major] Doxycycline / pharmacology. Melanoma, Experimental / blood supply. Microcirculation / drug effects

  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17959842.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.- / Matrix Metalloproteinases; N12000U13O / Doxycycline
  •  go-up   go-down


100. Kline J, Brown IE, Zha YY, Blank C, Strickler J, Wouters H, Zhang L, Gajewski TF: Homeostatic proliferation plus regulatory T-cell depletion promotes potent rejection of B16 melanoma. Clin Cancer Res; 2008 May 15;14(10):3156-67
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Homeostatic proliferation plus regulatory T-cell depletion promotes potent rejection of B16 melanoma.
  • EXPERIMENTAL DESIGN: B16 melanoma cells were engineered to express the model SIYRYYGL (SIY) antigen to enable immune monitoring.
  • To determine whether Treg depletion could synergize with homeostatic proliferation, RAG2-/- mice received total or CD25-depleted T cells, followed or preceded by B16.SIY challenge.
  • RESULTS: Adoptive transfer of total splenic T cells into RAG2-/- mice moderately affected the growth rate of B16.SIY.
  • Interestingly, transfer of CD25-depleted T cells into RAG2-/- mice resulted in potent rejection of B16 melanoma in both prophylactic and short-term preimplanted tumor settings and was associated with maintained T-cell effector function.
  • [MeSH-major] Cell Proliferation. Homeostasis / immunology. Immunotherapy, Adoptive / methods. Lymphocyte Depletion. Melanoma, Experimental / therapy. T-Lymphocytes, Regulatory / immunology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18483384.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA97296; United States / NCI NIH HHS / CA / R01 CA118153
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down






Advertisement