[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 2777
1. Oh JW, Olman M, Benveniste EN: CXCL12-mediated induction of plasminogen activator inhibitor-1 expression in human CXCR4 positive astroglioma cells. Biol Pharm Bull; 2009 Apr;32(4):573-7
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] CXCL12-mediated induction of plasminogen activator inhibitor-1 expression in human CXCR4 positive astroglioma cells.
  • Glioblastoma is the most malignant and common brain tumor.
  • To promote their growth, these glioma cells secrete a variety of soluble factors including plasminogen activator inhibitor-1 (PAI-1), which functions as an inhibitor of plasminogen activators.
  • We report here with the basis of microarray gene expression analysis that CXCR4 expressing glioma cells are capable of expressing PAI-1 mRNA and protein upon CXCL12 stimulation.
  • Interestingly, CXCL12 showed additive effects with another PAI-1 inducers, tumor necrosis factor (TNF)-alpha and/or tumor growth factor (TGF)-beta1, in increasing PAI-1 expression.
  • These results indicate that CXCL12/CXCR4 signaling in glioma cells may be another mechanism for these cells to express PAI-1, which may be involved in angiogenesis and tumor invasion in brain tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Chemokine CXCL12 / physiology. Plasminogen Activator Inhibitor 1 / biosynthesis. Receptors, CXCR4 / physiology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Extracellular Signal-Regulated MAP Kinases / physiology. GTP-Binding Protein alpha Subunits, Gi-Go / metabolism. GTP-Binding Protein alpha Subunits, Gi-Go / physiology. Humans. In Situ Hybridization. Indicators and Reagents. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / physiology. Nuclease Protection Assays. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. RNA, Complementary / biosynthesis. RNA, Complementary / genetics. Signal Transduction / drug effects. Signal Transduction / physiology. Transforming Growth Factor beta1 / pharmacology. Tumor Necrosis Factor-alpha / pharmacology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 = 19336886.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Enzyme Inhibitors; 0 / Indicators and Reagents; 0 / Plasminogen Activator Inhibitor 1; 0 / RNA, Complementary; 0 / Receptors, CXCR4; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go
  •  go-up   go-down


2. Jung SH, Woo MS, Kim SY, Kim WK, Hyun JW, Kim EJ, Kim DH, Kim HS: Ginseng saponin metabolite suppresses phorbol ester-induced matrix metalloproteinase-9 expression through inhibition of activator protein-1 and mitogen-activated protein kinase signaling pathways in human astroglioma cells. Int J Cancer; 2006 Jan 15;118(2):490-7
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] Ginseng saponin metabolite suppresses phorbol ester-induced matrix metalloproteinase-9 expression through inhibition of activator protein-1 and mitogen-activated protein kinase signaling pathways in human astroglioma cells.
  • Aberrant expression of matrix metalloproteinase-9 (MMP-9) is implicated in the process of invasion and angiogenesis of malignant tumors as well as in inflammatory diseases of the CNS.
  • We investigated the effects of a ginseng saponin metabolite, compound K (20-O-(beta-D-glucopyranosyl)-20(S)-protopanaxadiol), on MMP-9 expression in human astroglioma cells.
  • Finally, compound K inhibited the in vitro invasiveness of glioma cells.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Ginsenosides / pharmacology. Matrix Metalloproteinase 9 / biosynthesis
  • [MeSH-minor] DNA, Neoplasm. Humans. MAP Kinase Signaling System / drug effects. Neoplasm Invasiveness. Neovascularization, Pathologic. Signal Transduction. Transcription Factor AP-1 / drug effects. Transcription Factor AP-1 / physiology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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
  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16049964.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Ginsenosides; 0 / Transcription Factor AP-1; 0 / ginsenoside M1; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


3. Nozell S, Laver T, Patel K, Benveniste EN: Mechanism of IFN-beta-mediated inhibition of IL-8 gene expression in astroglioma cells. J Immunol; 2006 Jul 15;177(2):822-30
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] Mechanism of IFN-beta-mediated inhibition of IL-8 gene expression in astroglioma cells.
  • However, some diseases are characterized by excessive inflammation and high levels of IL-8.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • 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
  • (PMID = 16818736.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI 07051; United States / NINDS NIH HHS / NS / NS 36765; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NIAID NIH HHS / AI / T32 AI 07493; United States / NCI NIH HHS / CA / CA 97247
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Histones; 0 / Interleukin-8; 0 / NCOR2 protein, human; 0 / NF-kappa B; 0 / Nuclear Receptor Co-Repressor 2; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Transcription Factors; 77238-31-4 / Interferon-beta; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


Advertisement
4. Kim SW, Kim JB, Kim JH, Lee JK: Interferon-gamma-induced expressions of heat shock protein 60 and heat shock protein 10 in C6 astroglioma cells: identification of the signal transducers and activators of transcription 3-binding site in bidirectional promoter. Neuroreport; 2007 Mar 5;18(4):385-9
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] Interferon-gamma-induced expressions of heat shock protein 60 and heat shock protein 10 in C6 astroglioma cells: identification of the signal transducers and activators of transcription 3-binding site in bidirectional promoter.
  • Here, we report that the expressions of heat shock protein 60 and heat shock protein 10 were upregulated in interferon-gamma-treated C6 astroglioma cells, and the 582 bp in the bidirectional promoter of the heat shock protein 60 and heat shock protein 10 genes is responsible for interferon-gamma-induced induction.
  • These results suggest that interferon-gamma-induced upregulations of heat shock protein 60 and heat shock protein 10 in C6 astroglioma cells are mediated by the signal transducers and activators of transcription 3-binding site, localized in the bidirectional promoter.
  • [MeSH-minor] Animals. Binding Sites / drug effects. Binding Sites / physiology. Cell Line, Tumor. Glioma / metabolism. Mutation / physiology. Protein Binding / drug effects. Protein Binding / physiology. RNA, Messenger / biosynthesis. Rats. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Time Factors. Transcription, Genetic / drug effects

  • COS Scholar Universe. author profiles.
  • 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 = 17435608.001).
  • [ISSN] 0959-4965
  • [Journal-full-title] Neuroreport
  • [ISO-abbreviation] Neuroreport
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chaperonin 10; 0 / Chaperonin 60; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, rat; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


5. Pérez-Ortiz JM, Tranque P, Burgos M, Vaquero CF, Llopis J: Glitazones induce astroglioma cell death by releasing reactive oxygen species from mitochondria: modulation of cytotoxicity by nitric oxide. Mol Pharmacol; 2007 Aug;72(2):407-17
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] Glitazones induce astroglioma cell death by releasing reactive oxygen species from mitochondria: modulation of cytotoxicity by nitric oxide.
  • We described previously the apoptotic effects of glitazones on astroglioma cells ( J Biol Chem 279: 8976-8985, 2004 ).
  • At certain concentrations, we found a selective lethality on glioma cells versus astrocytes that was dependent on a rapid production of reactive oxygen species (ROS) and seemed unrelated to the receptor peroxisome proliferator activated receptor-gamma.
  • The present study was aimed at characterizing the oxygen derivatives induced by ciglitazone, rosiglitazone, and pioglitazone in C6 glioma cells and to investigate their intracellular source.
  • We examined the interaction of ROS with nitric oxide (NO) and its consequences for glioma cell survival.
  • NO synthase inhibitors revealed that superoxide anion combines with NO to yield peroxynitrite and that the latter contributes to the cytotoxicity of glitazones in astroglioma cells.
  • [MeSH-major] Astrocytoma / drug therapy. Mitochondria / drug effects. Nitric Oxide / physiology. Reactive Oxygen Species / metabolism. Thiazolidinediones / pharmacology
  • [MeSH-minor] Animals. Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology. Cell Line, Tumor. Electron Transport / drug effects. Hydrogen-Ion Concentration. NADPH Oxidase / physiology. NG-Nitroarginine Methyl Ester / pharmacology. Rats. Superoxides / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17504946.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Thiazolidinediones; 11062-77-4 / Superoxides; 31C4KY9ESH / Nitric Oxide; 370-86-5 / Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; 74772-77-3 / ciglitazone; EC 1.6.3.1 / NADPH Oxidase; V55S2QJN2X / NG-Nitroarginine Methyl Ester
  •  go-up   go-down


6. Jin Q, Agrawal L, Vanhorn-Ali Z, Alkhatib G: GLUT-1-independent infection of the glioblastoma/astroglioma U87 cells by the human T cell leukemia virus type 1. Virology; 2006 Sep 15;353(1):99-110
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] GLUT-1-independent infection of the glioblastoma/astroglioma U87 cells by the human T cell leukemia virus type 1.

  • Genetic Alliance. consumer health - Glioblastoma.
  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • 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
  • (PMID = 16781755.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA098095; United States / NCI NIH HHS / CA / 1R21CA98095-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Glucose Transporter Type 1
  •  go-up   go-down


7. Giammarioli AM, Vona R, Gambardella L, Ascione B, Maselli A, Barbati C, Tinari A, Malorni W: Interferon-gamma bolsters CD95/Fas-mediated apoptosis of astroglioma cells. FEBS J; 2009 Oct;276(20):5920-35
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] Interferon-gamma bolsters CD95/Fas-mediated apoptosis of astroglioma cells.
  • In the present study, we investigated the mechanisms of the resistance to CD95-mediated cell death and the effects of interferon-gamma in modulating the susceptibility to CD95-induced apoptosis of human astroglioma cells.
  • Taken together, these findings suggest that interferon-gamma could represent a promising candidate for modulating astroglioma cell apoptotic susceptibility.
  • [MeSH-major] Antigens, CD95 / metabolism. Apoptosis / drug effects. Astrocytoma / metabolism. Interferon-gamma / pharmacology
  • [MeSH-minor] Antiviral Agents / pharmacology. Blotting, Western. Caspase 10 / metabolism. Caspase 8 / metabolism. Caspase 9 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. DNA Fragmentation / drug effects. Flow Cytometry. Humans. Microscopy. Microscopy, Electron, Transmission. Mitochondria / drug effects. Mitochondria / metabolism. Mitochondria / ultrastructure. Proteasome Endopeptidase Complex / drug effects. Proteasome Endopeptidase Complex / 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 = 19740103.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antiviral Agents; 82115-62-6 / Interferon-gamma; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 10; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  •  go-up   go-down


8. Kwon D, Cheong JH, Lee JC, Kwon JH, Kim WK: Lipopolysaccharides-activated human astroglioma cells induce apoptotic death of T-lymphocytes via c-Jun N-terminal kinases-dependent up-regulation of TRAIL. Neurosci Res; 2006 Apr;54(4):338-43
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] Lipopolysaccharides-activated human astroglioma cells induce apoptotic death of T-lymphocytes via c-Jun N-terminal kinases-dependent up-regulation of TRAIL.
  • In the present study, we report that activated human astroglioma cells can injure T-lymphocytes by producing tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL).
  • Treatment with lipopolysaccharides (LPS), a well-known immune stimulator, increased the expression levels of TRAIL mRNA and protein in human astroglioma cells.
  • Activated human astroglioma cells markedly induced the apoptotic death of T-lymphocytes.
  • Pre-treatment with the TRAIL antagonistic protein TRAIL-R2:Fc prevented the death of T-lymphocytes caused by activated human astroglioma cells.
  • The present results suggest that astroglioma cells may down-regulate T-lymphocytes via up-regulation of TRAIL.
  • [MeSH-major] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Astrocytes / physiology. JNK Mitogen-Activated Protein Kinases / physiology. Lipopolysaccharides / pharmacology. Membrane Glycoproteins / biosynthesis. T-Lymphocytes / cytology. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Astrocytoma. Cell Line, Tumor. Humans. Phosphorylation. RNA, Messenger / biosynthesis. TNF-Related Apoptosis-Inducing Ligand. Transcription Factor AP-1 / metabolism. Up-Regulation

  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16442178.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Lipopolysaccharides; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  •  go-up   go-down


9. de Oliveira EF, Guerreiro JR, Silva CA, Benedetti GF, Lebrun I, Ulrich H, Lameu C, Camargo AC: Enhancement of the citrulline-nitric oxide cycle in astroglioma cells by the proline-rich peptide-10c from Bothrops jararaca venom. Brain Res; 2010 Dec 2;1363:11-9
Hazardous Substances Data Bank. (L)-ARGININE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhancement of the citrulline-nitric oxide cycle in astroglioma cells by the proline-rich peptide-10c from Bothrops jararaca venom.
  • Bj-PRO-10c was internalized by C6 astroglioma cells where it induces NO production and upregulation of the citrulline-NO cycle cells in a dose-dependent fashion.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Citrulline / metabolism. Crotalid Venoms / toxicity. Neuroglia / drug effects. Nitric Oxide / metabolism
  • [MeSH-minor] Animals. Arginine / metabolism. Argininosuccinate Lyase / metabolism. Argininosuccinate Synthase / metabolism. Cell Division / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Design. Proline-Rich Protein Domains / physiology. Rats. Up-Regulation / drug effects

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20875803.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Crotalid Venoms; 29VT07BGDA / Citrulline; 31C4KY9ESH / Nitric Oxide; 94ZLA3W45F / Arginine; EC 4.3.2.1 / Argininosuccinate Lyase; EC 6.3.4.5 / Argininosuccinate Synthase
  •  go-up   go-down


10. Kim SY, Kim DH, Han SJ, Hyun JW, Kim HS: Repression of matrix metalloproteinase gene expression by ginsenoside Rh2 in human astroglioma cells. Biochem Pharmacol; 2007 Dec 3;74(11):1642-51
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] Repression of matrix metalloproteinase gene expression by ginsenoside Rh2 in human astroglioma cells.
  • Matrix metalloproteinases (MMPs) play an important role in glioma infiltration, facilitating cell migration and tumor invasion through their ability to degrade the extracellular matrix.
  • This study examined the effect of ginsenoside Rh2 on the expression of MMPs in human astroglioma cells.
  • The molecular mechanism underlying MMP-9 inhibition was further investigated because MMP-9 plays a major role in the invasiveness of glioma.
  • It was found that Rh2 inhibited the secretion and protein expression of MMP-9 induced by PMA in human astroglioma cells.
  • Finally, Rh2 inhibited the in vitro invasiveness of glioma cells, which might be attributed to the broad-spectrum inhibition of MMPs by Rh2.
  • [MeSH-minor] Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / pathology. Binding Sites / genetics. Blotting, Western. Cell Line, Tumor. Cell Movement / drug effects. Cell Survival / drug effects. DNA-Binding Proteins / metabolism. Dose-Response Relationship, Drug. Electrophoretic Mobility Shift Assay. Humans. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 14 / genetics. Matrix Metalloproteinase 14 / metabolism. Matrix Metalloproteinase 3 / genetics. Matrix Metalloproteinase 3 / metabolism. Matrix Metalloproteinase 9 / genetics. Matrix Metalloproteinase 9 / metabolism. Molecular Structure. NF-kappa B / metabolism. Neoplasm Invasiveness. Phosphorylation / drug effects. Protein Binding / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Tetradecanoylphorbol Acetate / pharmacology. Transcription Factor AP-1 / metabolism

  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • 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 = 17880928.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Ginsenosides; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 78214-33-2 / ginsenoside Rh2; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1; EC 3.4.24.80 / Matrix Metalloproteinase 14; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


11. Franceschi E, Tosoni A, Ermani M, Spagnolli F, La Torre L, Galzio RJ, Pozzati E, Talacchi A, Benevento F, Brandes AA: Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas.
  • : e13003 Background: Chromosomes 1p/19q codeletion has been recognized as a prognostic and predictive factor in patients (pts) with grade 3 gliomas.
  • Non-codeleted (intact) anaplastic oligodendroglioma showed a survival comparable to that usually observed in pts with anaplastic astrocytomas; MGMT methylation status, moreover, has been found to be a prognostic factor in glioblastoma and anaplastic gliomas (AG).
  • Histology was anaplastic oligodendroglioma in 17 pts, anaplastic oligoastrocytoma in 20 pts, and anaplastic astrocytoma in 30 pts; all these pts were 1p19q intact and received surgery, RT, and CT.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962754.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Rudnick JD, Phuphanich S, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Black KL, Wheeler C, Yu J: A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma.
  • : 2033 Background: Our prior immunotherapy trials demonstrated efficacy in generating a tumor specific immune response in malignant glioma and the potential for high tumor-specific toxicity and sustained tumoricidal activity.
  • METHODS: We exploited this synergistic effect to maintain a cytotoxic environment around the tumor milieu.
  • Patients with high-grade glioma were eligible after maximal resection with biodegradable carmustine (BCNU) wafer placement.
  • Screening leukapheresis is used to isolate mononuclear cells which are differentiated into dendritic cells, pulsed with tumor lysate, and then 3 intradermal vaccines are administered at 2-week intervals.
  • The histology included 3 newly diagnosed glioblastoma multiforme (GBM), 8 recurrent GBM, 2 newly diagnosed anaplastic astrocytoma (AA), and 2 recurrent AA.
  • A stable disease interval of 13 to 90 weeks was observed for patients who received vaccine.
  • The 3 newly diagnosed GBM patients have stable disease (18 to 71 weeks).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964627.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


13. Potthast L, Chowdhary S, Pan E, Yu D, Zhu W, Brem S: The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab.
  • : 2057 Background: There is no standard of care for recurrent gliomas; however, bevacizumab is often used as a salvage chemotherapy regimen.
  • A diffuse, infiltrative pattern of recurrence, as evidenced by MR imaging, was seen manifesting as multifocal disease or presumed CSF dissemination with subependymal spread.
  • METHODS: We conducted a retrospective analysis of 40 recurrent glioma patients followed at Moffitt Cancer Center from September 2006 through December 2008 treated with bevacizumab alone or in combination with irinotecan.
  • Histologies included glioblastoma (GB), anaplastic astrocytomas (AA), anaplastic oligodendrogliomas (AO), anaplastic oligoastrocytomas (AOA), and low-grade astrocytomas.
  • CONCLUSIONS: There appears to be an increase in a diffuse, infiltrative pattern of recurrence among recurrent glioma patients treated with bevacizumab as a salvage regimen.
  • It is unclear why the disparity among this subset of patients occurs, however, we hypothesize that this may once again highlight the distinct tumor biology among young glioma patients.
  • The impact of this observation on clinical decision making on whether to utilize bevacizumab in young recurrent glioma patients warrants further investigation.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964663.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Ochsenbein AF, Schubert AD, Vassella E, Mariani L: Quantitative analysis of 0<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):2069

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of 0<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas.
  • : 2069 Background: Loss of heterozygosity (LOH) on the chromosomes 1p and 19q is associated with sensitivity to alkylating agents like temozolomide (TMZ) in patients with low-grade gliomas; whether methylation of the MGMT-promoter, a predictive factor in glioblastoma patients, also correlates with tumor response to TMZ in low-grade gliomas is unclear.
  • METHODS: We performed a retrospective analysis of patients with histologically verified low-grade gliomas (WHO Grade II) who were treated with TMZ for tumor progression at our hospital between November 1999 and November 2007.
  • Objective tumor response was assessed by MRI at 6-month intervals.
  • LOH of microsatellite markers on chromosomes 1p and 19q was determined by polymerase chain reaction (PCR) amplification of the matched pairs of blood and tumor DNA.
  • Seven patients had prior surgical resection of the tumor.
  • Histological classification revealed 10 oligodendrogliomas, 7 oligoastrocytomas, and 5 astrocytomas.
  • CONCLUSIONS: Quantitative methylation-specific PCR of the MGMT promoter correlates with radiological response to chemotherapy with temozolomide in WHO grade II gliomas.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964685.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Herndon J 2nd, Vredenburgh J, Reardon D, Desjardins A, Peters K, Gururangan S, Norfleet J, Friedman A, Bigner D, Friedman HS: Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas.
  • : e13016 Background: Recurrent malignant gliomas have a poor prognosis, with a median survival of 6-15 months, with grade 4 glioblastomas more aggressive than grade 3 anaplastic astrocytomas or oligodendrogliomas.
  • Vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) are critically important in glioma biology.
  • We report a phase I trial of vandetanib in combination with oral etoposide for recurrent malignant glioma.
  • METHODS: Patients with histologically documented recurrent grade 3 or grade 4 malignant glioma were eligible.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962830.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Merrell RT, Lachance DH, Anderson SK: Seizures in patients with glioma treated with phenytoin and levetiracetam. J Clin Oncol; 2009 May 20;27(15_suppl):e13020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Seizures in patients with glioma treated with phenytoin and levetiracetam.
  • : e13020 Background: Seizures are common in patients with glioma.
  • We compare seizure outcomes and side effects in patients with glioma treated with phenytoin and levetiracetam monotherapy.
  • METHODS: Retrospective analysis of consecutive patients with glioma.
  • RESULTS: 76 patients (34 female) with pathologically proven glioma and seizures were identified, 25 treated with phenytoin and 51 with levetiracetam.
  • 64% had grade 4 astrocytoma.
  • When adjusting for age, gender, type of seizure, type of glioma, and dosage using univariate and multivariate models there were no differences between the treatment groups and none of these covariates were statistically significant for explaining the second seizure rates between treatment groups (all p values >0.05).
  • CONCLUSIONS: In this study, glioma patients treated with levetiracetam had similar seizure control as patients treated with phenytoin.
  • Levetiracetam is a safe, effective, and preferred alternative for seizure management in patients with glioma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962817.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Lin Y, Jiang T, Li G: MGMT expression in low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MGMT expression in low-grade gliomas.
  • : e13001 Background: To evaluate the expression of MGMT in low-grade gliomas, and explore the relationship between its expression and the histological type of the tumour and the corresponding MRI characteristics.
  • METHODS: We assessed 389 low-grade gliomas (182 astrocytomas, 145 oligoastrocytomas, 61 oligodendrocytomas) with immunohistochemistry staining.
  • We also recorded the preoperational MRI criteria such as tumor volume on T2 image, enhancing volume, tumor location, and relationship with ventricles.
  • RESULTS: The expression of MGMT in astrocytomas, oligoastrocytomas, and oligocytomas were 1.67 ± 0.78, 1.41 ± 0.86,1.44 ± 0.78, respectively.
  • Significant stronger expression of MGMT was observed in astrocytomas than oligoastrocytomas and oligodendrocytomas (t = 3.00, p = 0.03), but no significant difference was observed between the latter two (t = 0.28, p = 0.78).
  • MGMT expression level was significantly correlated with the enhancing volume of the tumor (r = -0.605, p = 0.002), but did not correlate with the total tumor volume (p = 0.504).
  • This suggest that MGMT may contribute to the tumor resistance to radiotherapy and chemotherapy in low-grade gliomas.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962757.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Knizetova P, Darling JL, Bartek J: Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy. J Cell Mol Med; 2008 Jan-Feb;12(1):111-25
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy.
  • Malignant astrogliomas are among the most aggressive, highly vascular and infiltrating tumours bearing a dismal prognosis, mainly due to their resistance to current radiation treatment and chemotherapy.
  • Efforts to identify and target the mechanisms that underlie astroglioma resistance have recently focused on candidate cancer stem cells, their biological properties, interplay with their local microenvironment or 'niche', and their role in tumour progression and recurrence.
  • Both paracrine and autocrine regulation of astroglioma cell behaviour by locally produced cytokines such as the vascular endothelial growth factor (VEGF) are emerging as key factors that determine astroglioma cell fate.
  • Here, we review these recent rapid advances in astroglioma research, with emphasis on the significance of VEGF in astroglioma stem-like cell biology.
  • Furthermore, we highlight the unique DNA damage checkpoint properties of the CD133-marker-positive astroglioma stem-like cells, discuss their potential involvement in astroglioma radioresistance, and consider the implications of this new knowledge for designing combinatorial, more efficient therapeutic strategies.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / therapy. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Neoplastic Stem Cells / metabolism. Vascular Endothelial Growth Factor A / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18031298.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 129
  • [Other-IDs] NLM/ PMC3823475
  •  go-up   go-down


19. Witt H, Korshunov A, Remke M, Janzarik WG, Gnekow A, Scheurlen W, Kulozik AE, Lichter P, Pfister S: DNA methylation pattern of brain stem pilocytic astrocytomas in children. J Clin Oncol; 2009 May 20;27(15_suppl):10021

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation pattern of brain stem pilocytic astrocytomas in children.
  • : 10021 Background: Pilocytic astrocytoma (WHO grade I) comprises the most frequent brain tumor in childhood.
  • METHODS: To identify novel genes involved in astrocytoma pathogenesis, we performed a genome-wide DNA methylation analysis of 78 pilocytic astrocytoma samples from different tumor locations (diencephalic, cerebral, cerebellar, brain stem).
  • Two CpG sites were analyzed for each of a total of 14.000 promoters per sample.
  • Moreover, from 14 tumors clustering together with the brain stem tumors, 5 patients experienced disease recurrence (38%) as opposed to 20% in the remaining group.
  • Genes contained in the signature most interestingly included three homeobox family genes (HOXB1, HOXD3, and HOXD4), and NES, a tumor stem cell marker.
  • CONCLUSIONS: These data suggest that brain stem pilocytic astrocytomas display biologic features different from most tumors of other locations and share a methylation signature with tumors prone to disease recurrence from other locations.
  • We provide first evidence for a role of differentially methylated homeobox family genes in the pathogenesis of pilocytic astrocytoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


20. Chen SH, Gillespie GY, Benveniste EN: Divergent effects of oncostatin M on astroglioma cells: influence on cell proliferation, invasion, and expression of matrix metalloproteinases. Glia; 2006 Jan 15;53(2):191-200
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] Divergent effects of oncostatin M on astroglioma cells: influence on cell proliferation, invasion, and expression of matrix metalloproteinases.
  • Oncostatin M (OSM), a cytokine of the interleukin-6 (IL-6) family, can either promote or inhibit cell growth in various normal and tumor cells.
  • We addressed the effects of exogenous OSM on the proliferation and invasion of human astroglioma cells.
  • We found that OSM inhibited the proliferation of two human astroglioma cell lines (CH235-MG and U87-MG), and that this effect was not due to apoptosis.
  • To extend these findings, we analyzed the effects of OSM on primary tumor cells from glioblastoma patients.
  • Interestingly, OSM did not suppress astroglioma cell invasion.
  • We found that OSM inhibited the constitutive expression of MMP-2, while MMP-9 expression was enhanced in astroglioma cell lines.
  • We conclude that OSM inhibits proliferation of human astroglioma cells and primary glioblastoma cells via the gp130/OSMRbeta receptor complex.
  • However, OSM does not affect the invasive capacity of the astroglioma cells, which may be due to the divergent effects of OSM on MMP-2 and MMP-9 expression.
  • Collectively, these findings suggest a complex role for OSM in astroglioma biology.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Astrocytoma / pathology. Brain Neoplasms / pathology. Matrix Metalloproteinases / biosynthesis. Neoplasm Invasiveness / pathology. Peptides / pharmacology
  • [MeSH-minor] Annexin A5 / metabolism. Apoptosis / drug effects. Astrocytes / metabolism. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Gelatin / metabolism. Humans. Indicators and Reagents. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinase 9 / genetics. Oncostatin M. Reverse Transcriptase Polymerase Chain Reaction. Thymidine / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GELATIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16206166.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-97247; United States / NINDS NIH HHS / NS / NS-39954
  • [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 / Annexin A5; 0 / Antineoplastic Agents; 0 / Indicators and Reagents; 0 / OSM protein, human; 0 / Peptides; 106956-32-5 / Oncostatin M; 9000-70-8 / Gelatin; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; VC2W18DGKR / Thymidine
  •  go-up   go-down


21. Woo MS, Jung SH, Kim SY, Hyun JW, Ko KH, Kim WK, Kim HS: Curcumin suppresses phorbol ester-induced matrix metalloproteinase-9 expression by inhibiting the PKC to MAPK signaling pathways in human astroglioma cells. Biochem Biophys Res Commun; 2005 Oct 7;335(4):1017-25
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] Curcumin suppresses phorbol ester-induced matrix metalloproteinase-9 expression by inhibiting the PKC to MAPK signaling pathways in human astroglioma cells.
  • The aberrant expression of matrix metalloproteinase-9 (MMP-9) is implicated in the invasion and angiogenesis process of brain tumor.
  • This study has investigated the effects of curcumin on MMP-9 expression in human astroglioma cell lines.
  • Therefore, the inhibition of MMP-9 expression by curcumin might have therapeutic potential for controlling the growth and invasiveness of brain tumor.
  • [MeSH-major] Astrocytoma / enzymology. Curcumin / administration & dosage. MAP Kinase Signaling System / drug effects. Matrix Metalloproteinase 9 / metabolism. Mitogen-Activated Protein Kinases / metabolism. Phorbol Esters / administration & dosage. Protein Kinase C / metabolism
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Drug Interactions. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Matrix Metalloproteinase Inhibitors. Signal Transduction / drug effects

  • Hazardous Substances Data Bank. CURCUMIN .
  • 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 = 16102725.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Matrix Metalloproteinase Inhibitors; 0 / Phorbol Esters; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9; IT942ZTH98 / Curcumin
  •  go-up   go-down


22. Ahn BH, Min G, Bae YS, Bae YS, Min DS: Phospholipase D is activated and phosphorylated by casein kinase-II in human U87 astroglioma cells. Exp Mol Med; 2006 Feb 28;38(1):55-62
Hazardous Substances Data Bank. N-BUTYL ALCOHOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phospholipase D is activated and phosphorylated by casein kinase-II in human U87 astroglioma cells.
  • Elevated expression of protein casein kinase II (CKII) stimulated basal phospholipase D (PLD) activity as well as PMA-induced PLD activation in human U87 astroglioma cells.
  • [MeSH-major] Astrocytoma / enzymology. Casein Kinase II / pharmacology. Phospholipase D / metabolism
  • [MeSH-minor] 1-Butanol / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation. Enzyme Inhibitors / pharmacology. Glutathione Transferase / metabolism. Humans. Kinetics. Phosphorylation / drug effects. Precipitin Tests. Recombinant Fusion Proteins / metabolism. Tetradecanoylphorbol Acetate / pharmacology

  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16520553.001).
  • [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 / Enzyme Inhibitors; 0 / Recombinant Fusion Proteins; 8PJ61P6TS3 / 1-Butanol; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.11.1 / Casein Kinase II; EC 3.1.4.4 / Phospholipase D; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


23. Kim SY, Lee EJ, Woo MS, Jung JS, Hyun JW, Min SW, Kim DH, Kim HS: Inhibition of matrix metalloproteinase-9 gene expression by an isoflavone metabolite, irisolidone in U87MG human astroglioma cells. Biochem Biophys Res Commun; 2008 Feb 8;366(2):493-9
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] Inhibition of matrix metalloproteinase-9 gene expression by an isoflavone metabolite, irisolidone in U87MG human astroglioma cells.
  • Matrix metalloproteinase-9 (MMP-9) plays an important role in mediating the invasion and angiogenic process of malignant gliomas.
  • This study was undertaken to determine if an isoflavone metabolite, irisolidone, inhibits MMP-9 expression in human astroglioma cells.
  • Irisolidone was found to inhibit the secretion and protein expression of MMP-9 induced by PMA in U87 MG glioma cells, accompanied by the inhibition of MMP-9 mRNA expression and promoter activity.
  • The Matrigel-invasion assay showed that irisolidone suppresses the in vitro invasiveness of glioma cells.
  • Therefore, the strong inhibition of MMP-9 expression by irisolidone might be a potential therapeutic modality for controlling the growth and invasiveness of gliomas.
  • [MeSH-major] Astrocytoma / metabolism. Flavonoids / administration & dosage. Gene Expression Regulation, Neoplastic / drug effects. Matrix Metalloproteinase 9 / metabolism. NF-kappa B / metabolism. Transcription Factor AP-1 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Isoflavones / administration & dosage. Isoflavones / 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 = 18070596.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Isoflavones; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / irisolidone; 4737-27-3 / isoflavanone; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


24. Desjardins A, Reardon DA, Gururangan S, Peters K, Threatt S, Friedman A, Friedman H, Vredenburgh J: Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG). J Clin Oncol; 2009 May 20;27(15_suppl):e13004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG).
  • METHODS: Eligibility included: adult patients with stable or recurrent MG (GBM, anaplastic astrocytoma [AA], anaplastic oligodendroglioma [AO]) previously treated with radiation therapy (RT) and with or without chemotherapy; interval of at least two weeks between prior RT, or four weeks between prior chemotherapy; Karnofsky ≥ 60%; and adequate hematologic, renal and liver function.
  • Radiographic evaluation reported: 2 partial responses, 14 stable disease for at least 4 cycles, and 11 disease progression after either the first or second cycle.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962751.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


25. Komotar RJ, Carson BS, Rao C, Chaffee S, Goldthwaite PT, Tihan T: Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases. Neurosurgery; 2005 Jan 01;56(1):E206-E210

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28184642.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


26. Uno M, Oba-Shinjo SM, Wakamatsu A, Huang N, Avancini Ferreira Alves V, Rosemberg S, Pires de Aguiar PH, Leite C, Miura F, Marino J R, Scaff M, Nagahashi-Marie SK: Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas. Int J Biol Markers; 2006 Jan - Mar;21(1):50-57

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas.
  • : Clarification of TP53 alterations is important to understand the mechanisms underlying the development of diffuse astrocytomas.
  • The aim of this study was to analyze the possible association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult Brazilian patients with diffuse astrocytomas.
  • We analyzed 56 surgical specimens of diffuse astrocytomas for alterations of TP53, using polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) direct sequencing. p53 and cleaved caspase 3 protein expression were assessed by immunohistochemistry.
  • We concluded that clarification of the TP53 alterations allows a better understanding of the mechanisms involved in the progression of diffuse astrocytomas, and the allele status at codon 72 was not associated with apoptosis in these tumors.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28207094.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  •  go-up   go-down


27. Ahn BH, Park MH, Lee YH, Kwon TK, Min do S: Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells. Biochim Biophys Acta; 2007 Dec;1773(12):1721-31
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] Up-regulation of cyclooxygenase-2 by cobalt chloride-induced hypoxia is mediated by phospholipase D isozymes in human astroglioma cells.
  • Cyclooxygenase-2 (COX-2) is an isoform of prostaglandin H synthase induced by hypoxia and has been implicated in the growth and progression of a variety of human cancers.
  • In the present study, we investigated the role of phospholipase D (PLD) isozymes in cobalt chloride (CoCl(2))-induced hypoxia-driven COX-2 expression in U87 MG human astroglioma cells.
  • Taken together, our results demonstrate for the first time that PLD1 and PLD2 isozymes enhance CoCl(2)-induced COX-2 expression through differential signaling pathways in astroglioma cells.
  • [MeSH-major] Astrocytoma / enzymology. Astrocytoma / genetics. Cobalt / pharmacology. Cyclooxygenase 2 / genetics. Phospholipase D / metabolism. Up-Regulation / drug effects

  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • Hazardous Substances Data Bank. COBALT, ELEMENTAL .
  • Hazardous Substances Data Bank. COBALTOUS CHLORIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17640750.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Lipopolysaccharides; 3G0H8C9362 / Cobalt; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.4.2.31 / Pertussis Toxin; EC 3.1.1.4 / Phospholipases A2; EC 3.1.4.- / Type C Phospholipases; EC 3.1.4.4 / Phospholipase D; EVS87XF13W / cobaltous chloride; K7Q1JQR04M / Dinoprostone; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


28. Karrasch M, Gillespie GY, Braz E, Liechty PG, Nabors LB, Lakeman AD, Palmer CA, Parker JN, Whitley RJ, Markert JM: Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results. J Clin Oncol; 2009 May 20;27(15_suppl):2042

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results.
  • Safety and efficacy of intracerebral inoculations of G207 to patients suffering from recurrent malignant gliomas have been demonstrated in previous clinical trials.
  • METHODS: In this phase I clinical trial, a total of 1 x 10<sup>9</sup> plaque forming units (pfu) G207 were administered by five stereotactic injections of 0.2 mL each into regions of recurrent malignant glioma defined by MRI, followed by focal radiation therapy 24 hours post injection.
  • Included patients suffered from inoperable pathologically proven recurrent glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) which was progressive despite radiotherapy or chemotherapy and failed external beam radiotherapy > 5 Gray prior to study enrolment.
  • The 2 patients with initial PR (1xGBM, 1xAA) were re-treated with G207/Irradiation at time point of tumor recurrence, showing PR one month after re-treatment again.
  • Within persistent areas of tumor, HSV staining was present by using a polyclonal antibody for HSV, indicating intratumoral G207 replication (proof of concept).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964649.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


29. Simonelli M, Banna G, Navarria P, Di Ieva A, Zucali P, De Vincenzo F, Gaetani P, Condorelli R, Rodriguez Y Baena R, Scorsetti M, Santoro A: Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas.
  • : e13037 Background: Anaplastic astrocytoma (AA), oligodendroglioma (AOD), and oligoastrocytoma (AOA) are rare tumors showing variable outcome due to their histological heterogeneity and different chemo- and radio-sensitivity.
  • Currently, the addition of chemotherapy to radiotherapy (RT) for newly diagnosed anaplastic gliomas is not sustained by available data.
  • We evaluated the addition of temozolomide (TMZ) to radiotherapy for newly diagnosed anaplastic gliomas in terms of tolerability, progression-free survival (PFS), and overall survival (OS).
  • METHODS: Since September 2004, following initial surgery, patients (pts) with histologically confirmed anaplastic glioma, Karnofsky Performance Status (KPS) ≥40, adequate organ function, no prior chemotherapy, were treated with RT to limited fields once daily at 2 Gy per fraction, 5 days a week, for a total of 60 Gy with concomitant TMZ (75 mg/m<sup>2</sup> for 7 days a week) followed by 6 cycles of maintenance TMZ at 200 mg/m<sup>2</sup> on days 1-5 every 28 days.
  • Nine pts (32%) underwent tumor complete resection, 10 partial resection (36%), and 9 (32%) tumor biopsy.
  • CONCLUSIONS: The addition of temozolomide to radiation therapy for newly diagnosed anaplastic gliomas is well tolerated and seems active; efficacy needs confirmation in a randomized clinical trial.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962859.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


30. Abacioglu MU, Caglar HB, Yumuk PF, Akgun Z, Atasoy BM, Sengoz M: Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma. J Clin Oncol; 2009 May 20;27(15_suppl):e13018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma.
  • : e13018 Background: The study was aimed to evaluate the efficacy of TMZ on a protracted dose-dense schedule after standard 5-day TMZ regimen in patients with progressive high-grade glioma.
  • METHODS: In this phase II prospective study, patients who had progression on standard 5-day TMZ for recurrence (group 1) or recurrence after concurrent radiotherapy+TMZ and ≥ 2 cycles of adjuvant TMZ (group 2) for high-grade glioma received TMZ 100 mg/m2× 21 q28 days until progression according to MacDonald's criteria.
  • The histopathology was glioblastoma in 18 and grade 3 glioma (anaplastic astrocytoma, anaplastic oligoastrocytoma or anaplastic oligodendroglioma) in 7.
  • The best response during treatment was partial response in 2 (8%), stable disease in 9 (36%), and progression in 9 (36%) out of 20 patients assessed.
  • CONCLUSIONS: Protracted dose-dense TMZ after 5-day schedule for recurrent or progressive disease has modest efficacy with tolerable toxicity.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962826.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


31. Kim SY, Jung SH, Kim HS: Curcumin is a potent broad spectrum inhibitor of matrix metalloproteinase gene expression in human astroglioma cells. Biochem Biophys Res Commun; 2005 Nov 18;337(2):510-6
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] Curcumin is a potent broad spectrum inhibitor of matrix metalloproteinase gene expression in human astroglioma cells.
  • The abnormal expression of matrix metalloproteinases (MMPs) plays an important role in the invasion of malignant gliomas into the surrounding normal brain tissue.
  • This study showed that curcumin has broad-spectrum inhibitory activity against MMP gene expression in human astroglioma cells.
  • Curcumin was also found to significantly repress the in vitro invasion of glioma cells.
  • Therefore, the broad-spectrum inhibition of MMP gene expression by curcumin might provide a novel therapeutic strategy for treating gliomas.
  • [MeSH-major] Astrocytoma / enzymology. Curcumin / pharmacology. Enzyme Inhibitors / pharmacology. Matrix Metalloproteinase Inhibitors. Tissue Inhibitor of Metalloproteinase-3 / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Base Sequence. Brain Neoplasms / pathology. Gene Expression. Glioma / drug therapy. Humans. Matrix Metalloproteinases / genetics. Mitogen-Activated Protein Kinases / metabolism. Ribonucleases / metabolism. Tissue Inhibitor of Metalloproteinase-1 / genetics. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. CURCUMIN .
  • 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 = 16198311.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / Transcription Factor AP-1; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.1.- / Ribonucleases; EC 3.4.24.- / Matrix Metalloproteinases; IT942ZTH98 / Curcumin
  •  go-up   go-down


32. Badisa RB, Darling-Reed SF, Goodman CB: Cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells. Neurochem Res; 2010 Feb;35(2):288-97
Hazardous Substances Data Bank. COCAINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells.
  • The present study was aimed to discern the effect of cocaine on rat astroglioma cells and analyzed qualitatively for morphological features as well as vacuolation by phase contrast microscope, quantitatively for cytotoxicity, mitochondrial membrane potential by rhodamine- 123 fluorometric assay, and cell cycle analysis by flow cytometry.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Pharmacol. 2002 Mar;61(3):486-94 [11854428.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Aug;298(2):744-52 [11454939.001]
  • [Cites] Int Rev Neurobiol. 2002;51:325-76 [12420364.001]
  • [Cites] Phytother Res. 2003 May;17(5):472-6 [12748981.001]
  • [Cites] Life Sci. 2003 Jun 20;73(5):617-26 [12770616.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Jan;53(1):89-90 [14586558.001]
  • [Cites] Acta Neuropathol. 1968 Jun 7;10(4):347-55 [4179085.001]
  • [Cites] Dev Biol. 1984 Nov;106(1):53-60 [6489611.001]
  • [Cites] In Vitro. 1984 Sep;20(9):732-8 [6500611.001]
  • [Cites] Am J Physiol. 1986 Nov;251(5 Pt 1):C748-53 [3535530.001]
  • [Cites] J Cell Biol. 1989 Jan;108(1):141-51 [2910876.001]
  • [Cites] Pharm Res. 1988 Jul;5(7):440-2 [3247314.001]
  • [Cites] Am J Pathol. 1989 Jul;135(1):85-91 [2774060.001]
  • [Cites] Circulation. 1990 Mar;81(3):1012-6 [2306813.001]
  • [Cites] Cancer Commun. 1990;2(2):81-6 [1695520.001]
  • [Cites] Cancer Res. 1990 Oct 15;50(20):6744-56 [2208138.001]
  • [Cites] Toxicology. 1992;72(2):175-87 [1566279.001]
  • [Cites] Exp Neurol. 1993 Apr;120(2):245-63 [8491281.001]
  • [Cites] Neurotoxicology. 1993 Spring;14(1):19-22 [8361674.001]
  • [Cites] Neuroscience. 1993 Nov;57(2):467-72 [7509470.001]
  • [Cites] J Clin Invest. 1994 Mar;93(3):1179-85 [8132758.001]
  • [Cites] J Neurosci. 1994 Oct;14(10):5858-64 [7931548.001]
  • [Cites] J Biol Chem. 1995 Oct 13;270(41):23937-40 [7592587.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 21;92(24):11029-33 [7479930.001]
  • [Cites] Toxicology. 1996 Aug 1;112(1):1-10 [8792843.001]
  • [Cites] J Pharmacol Exp Ther. 1998 Jan;284(1):413-9 [9435205.001]
  • [Cites] Mol Cell. 1997 Dec;1(1):3-11 [9659898.001]
  • [Cites] J Neurovirol. 1998 Dec;4(6):619-26 [10065903.001]
  • [Cites] Carcinogenesis. 1999 Jul;20(7):1193-9 [10383889.001]
  • [Cites] J Biol Chem. 1958 Sep;233(3):637-42 [13575428.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Jan;312(1):112-9 [15365088.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Apr;46(4):1330-8 [15790899.001]
  • [Cites] Neurosurg Focus. 2005 Oct 15;19(4):E1 [16241103.001]
  • [Cites] Ann N Y Acad Sci. 2000 Sep;914:82-91 [11085311.001]
  • [Cites] Neuroscience. 2006 Feb;137(3):905-13 [16298078.001]
  • [Cites] Brain Res. 2006 May 17;1089(1):44-54 [16638611.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Sep;318(3):1280-6 [16766721.001]
  • [Cites] J Biomed Sci. 2008 Mar;15(2):215-26 [17922255.001]
  • [Cites] PLoS Med. 2008 Jun 10;5(6):e117 [18593214.001]
  • [Cites] Anticancer Res. 2009 Aug;29(8):2993-6 [19661306.001]
  • [Cites] J Cell Biol. 1967 Feb;32(2):297-308 [10976223.001]
  • [Cites] Br J Pharmacol. 2001 Mar;132(5):1063-70 [11226137.001]
  • [Cites] Analyst. 2001 Apr;126(4):513-7 [11340990.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Jul;298(1):180-7 [11408540.001]
  • [Cites] Parkinsonism Relat Disord. 2002 Sep;8(6):407-11 [12217628.001]
  • (PMID = 19757036.001).
  • [ISSN] 1573-6903
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR003020-255372; United States / NIGMS NIH HHS / GM / GM08111; United States / NCRR NIH HHS / RR / G12 RR003020; United States / NCRR NIH HHS / RR / RR003020-255372; United States / NCRR NIH HHS / RR / G12 RR003020-25; United States / NIGMS NIH HHS / GM / S06 GM008111; United States / NCRR NIH HHS / RR / RR003020-25; United States / NCRR NIH HHS / RR / G12 RR003020-255370; United States / NCRR NIH HHS / RR / RR003020-255370; United States / NCRR NIH HHS / RR / G12RR03020; United States / PHS HHS / / SD34HP04018
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] I5Y540LHVR / Cocaine
  • [Other-IDs] NLM/ NIHMS204547; NLM/ PMC2885962
  •  go-up   go-down


33. Choi SJ, Kim MH, Lim SW, Gwak MS: Effect of ketamine on apoptosis by energy deprivation in astroglioma cells using flow cytometry system. J Korean Med Sci; 2005 Feb;20(1):113-20
Hazardous Substances Data Bank. KETAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of ketamine on apoptosis by energy deprivation in astroglioma cells using flow cytometry system.
  • Ischemic insults was induced with iodoacetate/ carbonylcyanide m-chlorophenylhydrazone (IAA/CCCP) 1.5 mM/20 microm or 150 microm/2 microm for 1 hr in the HTB-15 and CRL-1690 astrocytoma cells.
  • Ketamine may have a valuable effect on amelioration of early and late apoptosis in the astrocytoma cells, even though the exact mechanism remains to be verified.
  • [MeSH-major] Anesthetics, Dissociative / pharmacology. Astrocytoma / drug therapy. Flow Cytometry / methods. Ketamine / pharmacology
  • [MeSH-minor] Annexin A5 / pharmacology. Apoptosis. Astrocytes / metabolism. Brain / pathology. Carbonyl Cyanide m-Chlorophenyl Hydrazone / pharmacology. Cell Line, Tumor. Cell Size. Cell Survival. Central Nervous System / drug effects. Central Nervous System / pathology. Enzyme Inhibitors / pharmacology. Humans. Indicators and Reagents / pharmacology. Iodoacetates / pharmacology. Ischemia / pathology. Light. Neurons / metabolism. Neurons / pathology. Neutrophils / metabolism. Perfusion. Propidium / pharmacology. Scattering, Radiation. Time Factors. Uncoupling Agents / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biotechniques. 1997 Sep;23(3):525-31 [9298227.001]
  • [Cites] J Neurosci Res. 1997 Jun 15;48(6):563-70 [9210526.001]
  • [Cites] Anesth Analg. 1998 Nov;87(5):1186-93 [9806706.001]
  • [Cites] Histochem Cell Biol. 1998 Nov;110(5):467-76 [9826126.001]
  • [Cites] Kidney Int. 1998 Dec;54(6):1955-66 [9853260.001]
  • [Cites] Histochem Cell Biol. 1998 Dec;110(6):553-8 [9860253.001]
  • [Cites] Brain Res Brain Res Protoc. 1999 Jul;4(2):209-16 [10446416.001]
  • [Cites] Cytometry. 1998 Jan 1;31(1):1-9 [9450519.001]
  • [Cites] Neuroreport. 1997 Dec 22;8(18):3871-5 [9462458.001]
  • [Cites] Exp Neurol. 1998 Jan;149(1):51-63 [9454614.001]
  • [Cites] Annu Rev Physiol. 2001;63:795-813 [11181976.001]
  • [Cites] Glia. 2001 Aug;35(2):121-30 [11460268.001]
  • [Cites] J Neurosci. 2001 Sep 1;21(17):6512-21 [11517240.001]
  • [Cites] Neurochem Int. 2002 May;40(6):511-26 [11850108.001]
  • [Cites] Brain Pathol. 2002 Oct;12(4):475-81 [12408234.001]
  • [Cites] J Cereb Blood Flow Metab. 2003 Feb;23(2):137-49 [12571445.001]
  • [Cites] J Neurosci. 2003 Apr 15;23(8):3364-72 [12716944.001]
  • [Cites] Methods Mol Biol. 2003;228:271-9 [12824560.001]
  • [Cites] Anal Biochem. 2004 Aug 15;331(2):385-94 [15265746.001]
  • [Cites] Neuroscience. 1987 Jun;21(3):673-8 [2819768.001]
  • [Cites] Brain Res. 1989 May 22;487(2):380-3 [2567200.001]
  • [Cites] J Gen Physiol. 1990 May;95(5):837-66 [2163431.001]
  • [Cites] Ann N Y Acad Sci. 1991;625:818-20 [2058937.001]
  • [Cites] Neuroscience. 1991;45(2):461-5 [1837070.001]
  • [Cites] Anesthesiology. 1992 May;76(5):755-62 [1575344.001]
  • [Cites] J Cell Biol. 1992 Nov;119(3):493-501 [1400587.001]
  • [Cites] FEBS Lett. 1994 Feb 14;339(1-2):40-4 [8313978.001]
  • [Cites] J Immunol Methods. 1994 Jun 3;172(1):1-16 [8207258.001]
  • [Cites] Stroke. 1994 Aug;25(8):1637-43 [8042217.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Aug 1;92(16):7162-6 [7638161.001]
  • [Cites] J Exp Med. 1995 Nov 1;182(5):1545-56 [7595224.001]
  • [Cites] Stroke. 1996 Apr;27(4):747-52 [8614942.001]
  • [Cites] J Immunol. 1996 Jul 15;157(2):512-21 [8752896.001]
  • [Cites] Cytometry. 1996 Jun 1;24(2):131-9 [8725662.001]
  • [Cites] Anesthesiology. 1997 Feb;86(2):394-404 [9054257.001]
  • [Cites] Anaesthesist. 1997 Mar;46 Suppl 1:S47-54 [9163279.001]
  • [Cites] J Exp Med. 1997 Apr 21;185(8):1481-6 [9126928.001]
  • [Cites] J Neurochem. 1998 Oct;71(4):1588-96 [9751192.001]
  • (PMID = 15716615.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Anesthetics, Dissociative; 0 / Annexin A5; 0 / Enzyme Inhibitors; 0 / Indicators and Reagents; 0 / Iodoacetates; 0 / Uncoupling Agents; 36015-30-2 / Propidium; 555-60-2 / Carbonyl Cyanide m-Chlorophenyl Hydrazone; 690G0D6V8H / Ketamine
  • [Other-IDs] NLM/ PMC2808556
  •  go-up   go-down


34. Tosoni A, Franceschi E, Ermani M, Bacci A, Volpin L, Lombardo L, Ravenna G, Pinna G, Poggi R, Brandes AA: MGMT methylation status as a prognostic factor in anaplastic astrocytomas. J Clin Oncol; 2009 May 20;27(15_suppl):2052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MGMT methylation status as a prognostic factor in anaplastic astrocytomas.
  • However, further data on the epigenetic feature are needed before its role in rare diseases such as anaplastic astrocytomas (AA) can be established.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964674.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


35. Rüweler M, Gülden M, Maser E, Murias M, Seibert H: Cytotoxic, cytoprotective and antioxidant activities of resveratrol and analogues in C6 astroglioma cells in vitro. Chem Biol Interact; 2009 Dec 10;182(2-3):128-35
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] Cytotoxic, cytoprotective and antioxidant activities of resveratrol and analogues in C6 astroglioma cells in vitro.
  • In the present study cultured C6 glioma cells were used in order to investigate the relationship between the antioxidant, cytoprotective and cytotoxic activities of resveratrol and selected analogues, e.g., 3,3',4',5-trans-tetrahydroxystilbene (piceatannol), 3,3',5,5'-trans-tetrahydroxystilbene (3,3',5,5'-THS) and 3,3',4',5,5'-trans-pentahydroxystilbene (3,3',4',5,5'-PHS).
  • [MeSH-minor] Animals. Astrocytoma / drug therapy. Astrocytoma / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Free Radicals / metabolism. Oxidative Stress / drug effects. Rats. Reactive Oxygen Species / pharmacology

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • Hazardous Substances Data Bank. RESVERATROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19744470.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Free Radicals; 0 / Reactive Oxygen Species; 0 / Stilbenes; Q369O8926L / resveratrol
  •  go-up   go-down


36. Rüweler M, Anker A, Gülden M, Maser E, Seibert H: Inhibition of peroxide-induced radical generation by plant polyphenols in C6 astroglioma cells. Toxicol In Vitro; 2008 Aug;22(5):1377-81
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 peroxide-induced radical generation by plant polyphenols in C6 astroglioma cells.
  • Cumene hydroperoxide (CHP) was used as a model to induce radical generation which was measured by means of a fluorometric 2',7'-dichlorodihydro-fluorescein assay.
  • This ranking is completely different from that obtained by means of a trolox equivalent antioxidant capacity (TEAC) assay in a cell-free system, thus putting the biological relevance of the latter in question.
  • [MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Flavonoids / pharmacology. Free Radical Scavengers / pharmacology. Oxidative Stress / drug effects. Phenols / pharmacology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • Hazardous Substances Data Bank. GENISTEIN .
  • Hazardous Substances Data Bank. RESVERATROL .
  • Hazardous Substances Data Bank. CUMENE HYDROPEROXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18406568.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzene Derivatives; 0 / Flavonoids; 0 / Free Radical Scavengers; 0 / Free Radicals; 0 / Oxidants; 0 / Phenols; 0 / Plant Extracts; 0 / Polyphenols; 0 / Stilbenes; 142FWE6ECS / galangin; DH2M523P0H / Genistein; KUX1ZNC9J2 / Luteolin; PG7JD54X4I / cumene hydroperoxide; Q369O8926L / resveratrol
  •  go-up   go-down


37. French JL, McCullough J, Bachra P, Bedforth NM: Transversus abdominis plane block for analgesia after caesarean section in a patient with an intracranial lesion. Int J Obstet Anesth; 2009 Jan;18(1):52-4
MedlinePlus Health Information. consumer health - Cesarean Section.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We present our management of a 24-year-old primigravida with a recently diagnosed low-grade left temporal astroglioma, who was delivered by elective caesarean section.
  • [MeSH-minor] Astrocytoma / complications. Astrocytoma / diagnosis. Brain Neoplasms / complications. Brain Neoplasms / diagnosis. Female. Humans. Magnetic Resonance Imaging. Pregnancy. Pregnancy Complications, Neoplastic / diagnosis. Ultrasonography, Interventional. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18996002.001).
  • [ISSN] 1532-3374
  • [Journal-full-title] International journal of obstetric anesthesia
  • [ISO-abbreviation] Int J Obstet Anesth
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


38. Kwon D, Choi IH: Hydrogen peroxide upregulates TNF-related apoptosis-inducing ligand (TRAIL) expression in human astroglial cells, and augments apoptosis of T cells. Yonsei Med J; 2006 Aug 31;47(4):551-7
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, the modulation of TNF-related apoptosis-inducing ligand (TRAIL) expression by oxidative stress was shown in LN215 cells, an astroglioma cell line.
  • [MeSH-minor] Allergy and Immunology. Anoxia. Cell Line, Tumor. Cyclosporine / pharmacology. Humans. Immunosuppressive Agents / pharmacology. Oxidative Stress. Ribonucleases / metabolism

  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1994 Nov 11;269(45):28181-6 [7961754.001]
  • [Cites] J Clin Invest. 1994 Sep;94(3):954-64 [7521890.001]
  • [Cites] Immunity. 1995 Dec;3(6):673-82 [8777713.001]
  • [Cites] Am J Physiol. 1995 Dec;269(6 Pt 1):L829-36 [8572244.001]
  • [Cites] Trends Biochem Sci. 1996 Mar;21(3):83-6 [8882579.001]
  • [Cites] Science. 1997 Apr 4;276(5309):111-3 [9082980.001]
  • [Cites] J Cell Biol. 1997 Apr 7;137(1):221-9 [9105050.001]
  • [Cites] Science. 1997 Aug 8;277(5327):815-8 [9242610.001]
  • [Cites] Science. 1997 Aug 8;277(5327):818-21 [9242611.001]
  • [Cites] Mol Cell Biol. 1997 Nov;17(11):6437-47 [9343406.001]
  • [Cites] J Biol Chem. 1997 Nov 7;272(45):28191-3 [9353266.001]
  • [Cites] Curr Biol. 1998 Jan 15;8(2):113-6 [9427646.001]
  • [Cites] J Biol Chem. 1998 Apr 3;273(14):8048-55 [9525905.001]
  • [Cites] Acta Neuropathol. 1998 Mar;95(3):287-90 [9542594.001]
  • [Cites] J Immunol. 1998 Apr 15;160(8):4042-7 [9558114.001]
  • [Cites] FEBS Lett. 1998 Jun 5;429(1):67-72 [9657385.001]
  • [Cites] Acta Neuropathol. 1999 Jan;97(1):1-4 [9930888.001]
  • [Cites] J Immunol. 1999 Feb 15;162(4):1889-95 [9973455.001]
  • [Cites] J Immunol. 1999 Feb 15;162(4):1988-93 [9973469.001]
  • [Cites] J Immunol. 1999 Mar 1;162(5):2639-47 [10072506.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Apr 13;257(2):454-9 [10198234.001]
  • [Cites] Eur J Clin Invest. 1999 Mar;29(3):220-31 [10202379.001]
  • [Cites] Eur J Immunol. 1999 Apr;29(4):1194-201 [10229086.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Sep 24;276(2):466-71 [11027498.001]
  • [Cites] J Mol Cell Cardiol. 2001 Jan;33(1):83-94 [11133225.001]
  • [Cites] J Neuroimmunol. 2001 Feb 1;113(1):1-9 [11137571.001]
  • [Cites] FASEB J. 2001 Feb;15(2):303-5 [11156944.001]
  • [Cites] Neurochem Int. 2001 Apr;38(5):409-15 [11222921.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):14350-8 [11278367.001]
  • [Cites] J Neurochem. 1992 Nov;59(5):1609-23 [1402908.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1212-20 [8353285.001]
  • [Cites] Cancer Chemother Pharmacol. 1995;36(4):341-4 [7628054.001]
  • (PMID = 16941746.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / TNF-Related Apoptosis-Inducing Ligand; 83HN0GTJ6D / Cyclosporine; BBX060AN9V / Hydrogen Peroxide; EC 3.1.- / Ribonucleases
  • [Other-IDs] NLM/ PMC2687737
  •  go-up   go-down


39. Shin JH, Kim SW, Lim CM, Jeong JY, Piao CS, Lee JK: alphaB-crystallin suppresses oxidative stress-induced astrocyte apoptosis by inhibiting caspase-3 activation. Neurosci Res; 2009 Aug;64(4):355-61
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To investigate the functional significance of alphaB-crystallin induction in astrocytes, we generated a stable C6 astroglioma cell line overexpressing alphaB-crystallin.
  • Furthermore, the repression of alphaB-crystallin expression by alphaB-crystallin siRNA transfection suppressed this protective effect, indicating that alphaB-crystallin is responsible for the protection against H2O2-induced apoptosis in C6 astroglioma cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytoprotection / physiology. Down-Regulation / physiology. Hydrogen Peroxide / toxicity. Neurodegenerative Diseases / genetics. Neurodegenerative Diseases / metabolism. Neurodegenerative Diseases / physiopathology. Oxidants / toxicity. Protein Binding / physiology. RNA Interference / physiology. Rats. Transfection

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19379782.001).
  • [ISSN] 1872-8111
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Oxidants; 0 / alpha-Crystallin B Chain; BBX060AN9V / Hydrogen Peroxide; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


40. Cano OD, Neurauter G, Fuchs D, Shearer GM, Boasso A: Differential effect of type I and type II interferons on neopterin production and amino acid metabolism in human astrocyte-derived cells. Neurosci Lett; 2008 Jun 13;438(1):22-5
Hazardous Substances Data Bank. (L)-Tryptophan .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated whether IFN-alpha/beta, IFN-gamma, or human immunodeficiency virus (HIV) induce neopterin production by human astroglioma cells.
  • In contrast, IFN-alpha/beta, but not IFN-gamma, reduced the uptake of three aromatic amino acids in U87MG and U138 astroglioma cells.
  • [MeSH-minor] AIDS Dementia Complex / immunology. AIDS Dementia Complex / metabolism. AIDS Dementia Complex / physiopathology. Brain / immunology. Brain / metabolism. Brain / virology. Cell Line, Tumor. Humans. Indoleamine-Pyrrole 2,3,-Dioxygenase / drug effects. Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism. Tryptophan / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18457922.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Amino Acids, Aromatic; 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 0 / Interferon-alpha; 670-65-5 / Neopterin; 82115-62-6 / Interferon-gamma; 8DUH1N11BX / Tryptophan
  •  go-up   go-down


41. Zhang D, Hu X, Qian L, Wilson B, Lee C, Flood P, Langenbach R, Hong JS: Prostaglandin E2 released from activated microglia enhances astrocyte proliferation in vitro. Toxicol Appl Pharmacol; 2009 Jul 1;238(1):64-70
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Microglial activation has been implicated in many astrogliosis-related pathological conditions including astroglioma; however, the detailed mechanism is not clear.
  • These findings were further supported by the finding that addition of PGE(2) to the media significantly induced astrocyte proliferation.
  • These findings are important in elucidating the role of activated microglia and PGE(2) in astrocyte proliferation and in suggesting a potential avenue in the use of anti-inflammatory agents for the therapy of astroglioma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Prog Lipid Res. 2004 Jan;43(1):3-35 [14636669.001]
  • [Cites] Brain Res Dev Brain Res. 2003 Oct 10;145(1):9-17 [14519489.001]
  • [Cites] Cancer Control. 2004 May-Jun;11(3):152-64 [15153839.001]
  • [Cites] Pharmacol Ther. 2004 Aug;103(2):147-66 [15369681.001]
  • [Cites] J Neuroimmunol. 1990 Dec;30(2-3):239-43 [2229411.001]
  • [Cites] J Neurochem. 1991 Sep;57(3):823-30 [1861153.001]
  • [Cites] Glia. 1993 Jun;8(2):77-86 [8406676.001]
  • [Cites] J Neurosci. 1994 Feb;14(2):846-56 [8301364.001]
  • [Cites] Folia Neuropathol. 1994;32(4):251-2 [7889340.001]
  • [Cites] Presse Med. 1995 Mar 11;24(10):491-6 [7746807.001]
  • [Cites] J Neurochem. 1995 Dec;65(6):2716-24 [7595570.001]
  • [Cites] J Neurosci. 1996 May 1;16(9):2945-55 [8622125.001]
  • [Cites] Med Res Rev. 1996 Mar;16(2):181-206 [8656779.001]
  • [Cites] Trends Neurosci. 1996 Jan;19(1):13-8 [8787135.001]
  • [Cites] Brain Pathol. 1996 Jul;6(3):289-302 [8864285.001]
  • [Cites] Brain Behav Immun. 1995 Dec;9(4):345-54 [8903851.001]
  • [Cites] Br J Pharmacol. 1997 Sep;122(2):217-24 [9313928.001]
  • [Cites] Trends Neurosci. 1997 Dec;20(12):570-7 [9416670.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):193-209 [9440020.001]
  • [Cites] Ann N Y Acad Sci. 1998 May 1;840:269-81 [9629255.001]
  • [Cites] Biochem Pharmacol. 1999 Oct 15;58(8):1237-46 [10487525.001]
  • [Cites] Brain Res Brain Res Rev. 2004 Dec;47(1-3):263-74 [15572176.001]
  • [Cites] J Endocrinol Invest. 2004 Sep;27(8):742-6 [15636427.001]
  • [Cites] Expert Opin Drug Saf. 2005 May;4(3):433-42 [15934851.001]
  • [Cites] Eur J Neurosci. 2005 Jun;21(11):3189-94 [15978027.001]
  • [Cites] Eur J Neurosci. 2005 Jul;22(2):317-30 [16045485.001]
  • [Cites] J Neurosci Res. 2005 Aug 1;81(3):447-55 [15959903.001]
  • [Cites] Cell Cycle. 2005 Sep;4(9):1286-93 [16082214.001]
  • [Cites] Glia. 2006 Mar;53(4):382-91 [16288481.001]
  • [Cites] J Neurosci. 2006 Apr 19;26(16):4383-93 [16624958.001]
  • [Cites] Clin Immunol. 2006 Jun;119(3):229-40 [16540375.001]
  • [Cites] Acta Physiol (Oxf). 2006 Jul;187(3):419-30 [16776667.001]
  • [Cites] Neurodegener Dis. 2005;2(3-4):139-46 [16909019.001]
  • [Cites] Brain Res. 2007 Jan 19;1129(1):43-52 [17169340.001]
  • [Cites] Brain Res. 2007 Jun 18;1154:206-14 [17482149.001]
  • [Cites] Neurochem Int. 2007 Jul-Sep;51(2-4):112-20 [17629358.001]
  • [Cites] J Neuroimmunol. 2007 Sep;189(1-2):23-30 [17628702.001]
  • [Cites] Expert Rev Anticancer Ther. 2007 Dec;7(12 Suppl):S29-36 [18076315.001]
  • [Cites] Rev Recent Clin Trials. 2006 Sep;1(3):265-81 [18473979.001]
  • [Cites] J Neuroinflammation. 2008;5:21 [18507839.001]
  • [Cites] Neurochem Res. 2008 Oct;33(10):2044-53 [18368483.001]
  • [Cites] J Neurosci Res. 2008 Nov 1;86(14):3212-20 [18615640.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4926-31 [10987308.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Oct;60(10):961-71 [11589427.001]
  • [Cites] Curr Neurol Neurosci Rep. 2001 May;1(3):217-24 [11898521.001]
  • [Cites] Acta Neuropathol. 2002 Jun;103(6):575-82 [12012089.001]
  • [Cites] J Neurooncol. 2002 Apr;57(2):147-50 [12125976.001]
  • [Cites] Exp Neurol. 2002 Aug;176(2):308-21 [12359172.001]
  • [Cites] Glia. 2002 Nov;40(2):252-9 [12379912.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Apr;305(1):212-8 [12649371.001]
  • [Cites] Ann N Y Acad Sci. 2003 Jun;991:214-28 [12846989.001]
  • [Cites] Brain Res. 2003 Sep 19;985(1):89-97 [12957371.001]
  • [Cites] Am J Ther. 2004 Mar-Apr;11(2):141-3 [14999366.001]
  • (PMID = 19397918.001).
  • [ISSN] 1096-0333
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES090082-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Lipopolysaccharides; 0 / Prostaglandin Antagonists; 0 / Thiophenes; 0 / Xanthones; 33458-93-4 / 6-isopropoxy-9-oxoxanthene-2-carboxylic acid; 88149-94-4 / DuP 697; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ NIHMS113622; NLM/ PMC2699578
  •  go-up   go-down


42. Stoevring B, Vang O, Christiansen M: (alpha)B-crystallin in cerebrospinal fluid of patients with multiple sclerosis. Clin Chim Acta; 2005 Jun;356(1-2):95-101
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.
  • Possibly posttranslationally modified aggregates of (alpha)B-crystallin were found in human astroglioma U373 cells.
  • Furthermore, (alpha)B-crystallin in CSF and human astroglioma cell line U373 is found in aggregates.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Astrocytoma / enzymology. Blotting, Western. Cell Line, Tumor. Chickens. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Multiple Sclerosis.
  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878466.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / alpha-Crystallin B Chain
  •  go-up   go-down


43. Fanélus I, Desrosiers RR: Reactive oxygen species generated by thiol-modifying phenylarsine oxide stimulate the expression of protein L-isoaspartyl methyltransferase. Biochem Biophys Res Commun; 2008 Jun 27;371(2):203-8
Hazardous Substances Data Bank. CYSTEINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we report that PIMT was rapidly up-regulated by PAO in U-87 human astroglioma cells.
  • [MeSH-minor] Arsenicals / pharmacology. Cell Line, Tumor. Cysteine / drug effects. Down-Regulation. Enzyme Inhibitors / pharmacology. Humans. RNA, Small Interfering / pharmacology. Up-Regulation

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18407833.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0HUR2WY345 / oxophenylarsine; EC 2.1.1.77 / Protein D-Aspartate-L-Isoaspartate Methyltransferase; K848JZ4886 / Cysteine
  •  go-up   go-down


44. Carroll-Anzinger D, Al-Harthi L: Gamma interferon primes productive human immunodeficiency virus infection in astrocytes. J Virol; 2006 Jan;80(1):541-4
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We evaluated the impact of three cytokines critical to the development of HIV neuropathogenesis, gamma interferon (IFN-gamma), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha, on priming astrocytes for HIV infection.
  • We demonstrate that IFN-gamma was the most potent in its ability to facilitate substantial productive HIV infection of an astroglioma cell line (U87MG) and human fetal astrocytes (HFA).

  • MedlinePlus Health Information. consumer health - HIV/AIDS.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurovirol. 2000 May;6 Suppl 1:S24-32 [10871762.001]
  • [Cites] J Virol. 2005 Aug;79(15):9618-24 [16014924.001]
  • [Cites] Ann Neurol. 2001 Jun;49(6):745-52 [11409426.001]
  • [Cites] Nat Neurosci. 2001 Jul;4(7):702-10 [11426226.001]
  • [Cites] AIDS Res Hum Retroviruses. 2001 Aug 10;17(12):1133-42 [11522183.001]
  • [Cites] AIDS. 2002 Feb 15;16(3):413-20 [11834953.001]
  • [Cites] Blood. 2002 May 1;99(9):3310-8 [11964298.001]
  • [Cites] Nucl Med Commun. 2003 Feb;24(2):209-21 [12548046.001]
  • [Cites] Glia. 2003 Mar;41(4):354-70 [12555203.001]
  • [Cites] Brain Pathol. 2003 Apr;13(2):144-54 [12744468.001]
  • [Cites] J Virol. 2004 Apr;78(8):4120-33 [15047828.001]
  • [Cites] Biol Cell. 2004 May;96(4):279-90 [15145532.001]
  • [Cites] J Virol. 2004 Jul;78(14):7319-28 [15220405.001]
  • [Cites] Brain Res Dev Brain Res. 2004 Sep 17;152(2):159-69 [15351504.001]
  • [Cites] J Biol Chem. 1988 Feb 25;263(6):2632-7 [2963815.001]
  • [Cites] J Virol. 1991 Nov;65(11):6094-100 [1920627.001]
  • [Cites] J Virol. 1994 Jan;68(1):93-102 [8254781.001]
  • [Cites] Am J Pathol. 1994 Apr;144(4):659-66 [8160767.001]
  • [Cites] J Virol. 1995 Apr;69(4):2159-67 [7884864.001]
  • [Cites] J Biol Chem. 1996 Jun 28;271(26):15303-6 [8663435.001]
  • [Cites] Ir J Med Sci. 1996 Apr-Jun;165(2):133-8 [8698561.001]
  • [Cites] Brain Behav Immun. 1995 Dec;9(4):378-88 [8903854.001]
  • [Cites] Mol Med. 1997 Aug;3(8):553-64 [9307983.001]
  • [Cites] Curr Eye Res. 1997 Oct;16(10):1064-8 [9330861.001]
  • [Cites] J Clin Immunol. 1998 Mar;18(2):124-31 [9533656.001]
  • [Cites] Glia. 1998 Aug;23(4):304-15 [9671961.001]
  • [Cites] J Neurovirol. 1998 Aug;4(4):377-86 [9718129.001]
  • [Cites] J Virol. 1999 Jan;73(1):352-61 [9847339.001]
  • [Cites] Glia. 1999 Jan;25(1):44-55 [9888297.001]
  • [Cites] Mol Cell Neurosci. 2004 Nov;27(3):296-305 [15519244.001]
  • [Cites] J Neurochem. 2005 Mar;92(5):997-1009 [15715651.001]
  • [Cites] J Immunol. 2005 Mar 15;174(6):3719-26 [15749911.001]
  • [Cites] Glia. 2001 May;34(3):165-77 [11329179.001]
  • (PMID = 16352578.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1317538
  •  go-up   go-down


45. Le Calvé B, Rynkowski M, Le Mercier M, Bruyère C, Lonez C, Gras T, Haibe-Kains B, Bontempi G, Decaestecker C, Ruysschaert JM, Kiss R, Lefranc F: Long-term in vitro treatment of human glioblastoma cells with temozolomide increases resistance in vivo through up-regulation of GLUT transporter and aldo-keto reductase enzyme AKR1C expression. Neoplasia; 2010 Sep;12(9):727-39
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Glioblastoma (GBM) is the most frequent malignant glioma.
  • The present study aims to identify genes implicated in the acquired resistance of two human GBM cells of astrocytic origin, T98G and U373, to TMZ.
  • Our data show that long-term treatment of human astroglioma cells with TMZ induces increased expression of facilitative glucose transporter/solute carrier GLUT/SLC2A family members, mainly GLUT-3, and of the AKR1C family of proteins.
  • GLUT-3 has been previously suggested to exert roles in GBM neovascularization processes, and TMZ was found to exert antiangiogenic effects in experimental gliomas.
  • Selective targeting of GLUT-3 in GBM and/or AKR1C proteins (by means of jasmonates, for example) could thus delay the acquisition of resistance to TMZ of astroglioma cells in the context of prolonged treatment with this drug.
  • [MeSH-major] Alcohol Oxidoreductases / genetics. Brain Neoplasms / genetics. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Glioblastoma / genetics. Glucose Transport Proteins, Facilitative / genetics
  • [MeSH-minor] Aldehyde Reductase. Animals. Antineoplastic Agents, Alkylating / pharmacology. Antineoplastic Agents, Alkylating / therapeutic use. Cell Culture Techniques. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. HT29 Cells. Humans. Mice. Mice, Nude. Time Factors. Up-Regulation / drug effects. Up-Regulation / genetics. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DACARBAZINE .
  • 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
  • [Cites] Mol Cell Endocrinol. 2004 Feb 27;215(1-2):63-72 [15026176.001]
  • [Cites] Pflugers Arch. 2004 Feb;447(5):480-9 [12750891.001]
  • [Cites] Cancer Res. 1990 Oct 1;50(19):6119-29 [2205376.001]
  • [Cites] Am J Clin Pathol. 1992 Jun;97(6):776-86 [1375804.001]
  • [Cites] Cancer Res. 1992 Jul 15;52(14):3972-9 [1617673.001]
  • [Cites] Hum Pathol. 1993 Aug;24(8):912-20 [8375861.001]
  • [Cites] J Neurochem. 1993 Dec;61(6):2048-53 [8245960.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Sep 30;203(3):1622-8 [7945312.001]
  • [Cites] Brain Res Mol Brain Res. 1994 Nov;27(1):51-7 [7877454.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2933-6 [9230204.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Aug;57(8):791-802 [9720494.001]
  • [Cites] Am J Kidney Dis. 1999 Jul;34(1):189-202 [10401038.001]
  • [Cites] Nat Rev Cancer. 2004 Nov;4(11):891-9 [15516961.001]
  • [Cites] Science. 1956 Feb 24;123(3191):309-14 [13298683.001]
  • [Cites] J Cell Physiol. 2005 Mar;202(3):654-62 [15389572.001]
  • [Cites] Drug News Perspect. 2004 Nov;17(9):563-78 [15645014.001]
  • [Cites] Oncologist. 2007 Dec;12(12):1395-403 [18165616.001]
  • [Cites] Neurosurgery. 2008 Jan;62(1):211-21; discussion 221-2 [18300910.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3015-24 [18565887.001]
  • [Cites] Cancer Res. 2008 Jul 15;68(14):5706-15 [18632623.001]
  • [Cites] Eur J Pharm Biopharm. 2008 Aug;69(3):817-23 [18407478.001]
  • [Cites] Exp Cell Res. 2008 Oct 1;314(16):2985-98 [18598694.001]
  • [Cites] Neoplasia. 2008 Dec;10(12):1383-92 [19048117.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):8205-12 [19088037.001]
  • [Cites] Acta Neurochir (Wien). 2009 Feb;151(2):109-12 [19194651.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):459-66 [19269895.001]
  • [Cites] Neoplasia. 2009 May;11(5):485-96 [19412433.001]
  • [Cites] Cancer Res. 2009 Jun 1;69(11):4769-75 [19487289.001]
  • [Cites] Clin Cancer Res. 2009 Jul 15;15(14):4622-9 [19584161.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Oct;64(5):1053-8 [19597728.001]
  • [Cites] Carcinogenesis. 2009 Oct;30(10):1813-20 [19696165.001]
  • [Cites] Eur J Cancer. 2009 Nov;45(16):2893-905 [19679463.001]
  • [Cites] Neoplasia. 2010 Jan;12(1):69-79 [20072655.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2411-22 [15800333.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6394-400 [16024643.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Lab Invest. 2005 Dec;85(12):1457-70 [16170333.001]
  • [Cites] Nat Genet. 2006 Apr;38(4):452-7 [16550171.001]
  • [Cites] Autophagy. 2006 Jan-Mar;2(1):58-60 [16874033.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4738-46 [16899625.001]
  • [Cites] Mol Cancer Ther. 2006 Sep;5(9):2182-92 [16985051.001]
  • [Cites] J Neurochem. 2006 Nov;99(4):1049-61 [16899068.001]
  • [Cites] Mol Cancer. 2006;5:67 [17140455.001]
  • [Cites] Oncogene. 2007 Jan 11;26(2):186-97 [16819506.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):580-4 [17234766.001]
  • [Cites] Cell Death Differ. 2007 Mar;14(3):548-58 [16946731.001]
  • [Cites] Int J Cancer. 2007 May 1;120(9):2019-27 [17266043.001]
  • [Cites] Am J Pathol. 2007 May;170(5):1445-53 [17456751.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4467-73 [17483362.001]
  • [Cites] Neuropsychopharmacology. 2007 Jun;32(6):1251-60 [17119541.001]
  • [Cites] Chemotherapy. 2007;53(4):233-56 [17595539.001]
  • [Cites] Expert Rev Anticancer Ther. 2007 Nov;7(11):1581-90 [18020926.001]
  • [Cites] Annu Rev Pathol. 2006;1:97-117 [18039109.001]
  • [Cites] Biochem Pharmacol. 2008 Jan 15;75(2):414-26 [17945194.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):448-57 [14713959.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2744-50 [11289157.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Sep;60(9):863-71 [11556543.001]
  • [Cites] Glia. 2001 Dec;36(3):375-90 [11746774.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1915-9 [11912174.001]
  • [Cites] Cancer. 2002 Aug 1;95(3):641-55 [12209758.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1207-13 [12649178.001]
  • [ErratumIn] Neoplasia. 2011 Sep;13(9):5 p following 886
  • (PMID = 20824049.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Glucose Transport Proteins, Facilitative; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.184 / carbonyl reductase (NADPH); EC 1.1.1.21 / Aldehyde Reductase
  • [Other-IDs] NLM/ PMC2933693
  •  go-up   go-down


46. Kim YA, Lim SY, Rhee SH, Park KY, Kim CH, Choi BT, Lee SJ, Park YM, Choi YH: Resveratrol inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in beta-amyloid-treated C6 glioma cells. Int J Mol Med; 2006 Jun;17(6):1069-75
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] Resveratrol inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in beta-amyloid-treated C6 glioma cells.
  • Resveratrol has been reported to exert a variety of important pharmacological effects including anti-inflammatory, cardioprotective and cancer chemopreventive properties; however, its mechanisms of action are not completely under-stood. beta-amyloid protein is considered to be responsible for the formation of senile plaques that accumulate in the brains of patients with Alzheimer disease.
  • In the present study, we investigated the protective effect of resveratrol on beta-amyloid-induced cytoxicity in cultured rat astroglioma C6 cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Dinoprostone / biosynthesis. Down-Regulation. Glioma. NF-kappa B / metabolism. Protein Transport / drug effects. Rats. Transcriptional Activation / drug effects

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • Hazardous Substances Data Bank. RESVERATROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16685418.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Antioxidants; 0 / NF-kappa B; 0 / Neuroprotective Agents; 0 / Stilbenes; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone; Q369O8926L / resveratrol
  •  go-up   go-down


47. Lassman AB, Oligodendroglioma Study Group: Retrospective analysis of outcomes among more than 1,000 patients with newly diagnosed anaplastic oligodendroglial tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2014

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We retrospectively identified adults with newly diagnosed anaplastic oligodendroglioma (AO) or oligo-astrocytoma (AOA) seen at 17 medical centers from 1981-2007 exclusive of phase III or bone marrow transplant trials.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27964586.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


48. Payner T, Leaver HA, Knapp B, Whittle IR, Trifan OC, Miller S, Rizzo MT: Microsomal prostaglandin E synthase-1 regulates human glioma cell growth via prostaglandin E(2)-dependent activation of type II protein kinase A. Mol Cancer Ther; 2006 Jul;5(7):1817-26
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] Microsomal prostaglandin E synthase-1 regulates human glioma cell growth via prostaglandin E(2)-dependent activation of type II protein kinase A.
  • In human gliomas, overexpression of cyclooxygenase-2 has been linked to increased aggressiveness and poor prognosis.
  • In contrast, the role of prostaglandin E synthase in influencing the biological behavior of human gliomas has not been established.
  • We report that constitutive expression of the microsomal prostaglandin E synthase-1 (mPGES-1) is associated with increased prostaglandin E(2) (PGE(2)) production and stimulation of growth in the human astroglioma cell line U87-MG compared with human primary astrocytes.
  • The EP2/EP4 subtype PGE(2) receptors, which are linked to stimulation of adenylate cyclase, were expressed in U87-MG cells to a greater extent than in human astrocytes.
  • Taken together, these results are consistent with the hypothesis that mPGES-1 plays a critical role in promoting astroglioma cell growth via PGE(2)-dependent activation of type II PKA.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinases / metabolism. Dinoprostone / metabolism. Glioma / enzymology. Intramolecular Oxidoreductases / metabolism
  • [MeSH-minor] Astrocytes / drug effects. Astrocytes / enzymology. Cell Proliferation / drug effects. Cyclic AMP-Dependent Protein Kinase Type II. Humans. Microsomes / enzymology. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Glioma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16891468.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinase Type II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.3 / prostaglandin-E synthase; K7Q1JQR04M / Dinoprostone
  •  go-up   go-down


49. Song HY, Ryu J, Ju SM, Park LJ, Lee JA, Choi SY, Park J: Extracellular HIV-1 Tat enhances monocyte adhesion by up-regulation of ICAM-1 and VCAM-1 gene expression via ROS-dependent NF-kappaB activation in astrocytes. Exp Mol Med; 2007 Feb 28;39(1):27-37
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.
  • In this study, we examined the effect of HIV-1 Tat on the expression of adhesion molecules, generation of reactive oxygen species (ROS) and NF-kappaB activation in CRT-MG human astroglioma cells.

  • Genetic Alliance. consumer health - HIV.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17334226.001).
  • [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 / Gene Products, tat; 0 / NF-kappa B; 0 / Reactive Oxygen Species; 0 / Vascular Cell Adhesion Molecule-1; 0 / tat Gene Products, Human Immunodeficiency Virus; 126547-89-5 / Intercellular Adhesion Molecule-1
  •  go-up   go-down


50. Cheng Y, Feng Z, Zhang QZ, Zhang JT: Beneficial effects of melatonin in experimental models of Alzheimer disease. Acta Pharmacol Sin; 2006 Feb;27(2):129-39
Hazardous Substances Data Bank. MELATONIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beneficial effects of melatonin in experimental models of Alzheimer disease.
  • Alzheimer's disease (AD), a progressive degenerative disorder, is characterized by the presence of amyloid deposits, neurofibrillary tangles and neuron loss.
  • These findings led us to study amyloid precursor protein transgenic mice, ovariectomized rats, and pheochromocytoma and astroglioma cell lines, to observe whether melatonin had any effect on Alzheimer's symptoms or pathological changes.
  • [MeSH-major] Alzheimer Disease. Amyloid beta-Peptides / metabolism. Apoptosis / drug effects. Cognition / drug effects. Melatonin / pharmacology

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16412260.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Antioxidants; 0 / Free Radical Scavengers; 0 / tau Proteins; JL5DK93RCL / Melatonin
  • [Number-of-references] 94
  •  go-up   go-down


51. Kim YA, Kim GY, Park KY, Choi YH: Resveratrol inhibits nitric oxide and prostaglandin E2 production by lipopolysaccharide-activated C6 microglia. J Med Food; 2007 Jun;10(2):218-24
Hazardous Substances Data Bank. RESVERATROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Exposure of cultured rat C6 astroglioma cells to LPS increased their release of NO and PGE2 and their inducible expression of NO synthase and cyclooxygenase-2, all of which were significantly inhibited by resveratrol pretreatment.
  • These results demonstrate a potent suppressive effect of resveratrol on pro-inflammatory responses of microglia by modulation of NF-kappaB activity, suggesting a therapeutic potential for this compound in neurodegenerative diseases accompanied by microglial activation.
  • [MeSH-minor] Animals. Astrocytoma. Cell Division / drug effects. Cell Line, Tumor. Cell Nucleus / metabolism. Cyclooxygenase 2 / genetics. Gene Expression / drug effects. NF-kappa B / metabolism. Nitric Oxide Synthase Type II / genetics. Rats

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17651055.001).
  • [ISSN] 1096-620X
  • [Journal-full-title] Journal of medicinal food
  • [ISO-abbreviation] J Med Food
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Stilbenes; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone; Q369O8926L / resveratrol
  •  go-up   go-down


52. Jin JK, Ahn BH, Na YJ, Kim JI, Kim YS, Choi EK, Ko YG, Chung KC, Kozlowski PB, Min do S: Phospholipase D1 is associated with amyloid precursor protein in Alzheimer's disease. Neurobiol Aging; 2007 Jul;28(7):1015-27
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] Phospholipase D1 is associated with amyloid precursor protein in Alzheimer's disease.
  • Amyloid precursor protein (APP) is a widely expressed transmembrane protein of unknown function that is involved in the pathogenesis of Alzheimer's disease (AD).
  • Elevated expression of APP stimulated PLD activity in human astroglioma cells.
  • [MeSH-major] Alzheimer Disease / metabolism. Amyloid beta-Protein Precursor / metabolism. Brain / metabolism. Phospholipase D / metabolism
  • [MeSH-minor] Aged. Animals. Astrocytoma. Blood Proteins / chemistry. Blood Proteins / metabolism. Caveolin 3 / metabolism. Cell Line. Cercopithecus aethiops. Female. Humans. Immunoprecipitation / methods. Mutagenesis / physiology. Phosphoproteins / chemistry. Phosphoproteins / metabolism. Postmortem Changes. Transfection / methods. Up-Regulation / drug effects. Up-Regulation / physiology

  • MedlinePlus Health Information. consumer health - Alzheimer's Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16797788.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Blood Proteins; 0 / Caveolin 3; 0 / Phosphoproteins; 0 / platelet protein P47; EC 3.1.4.4 / Phospholipase D; EC 3.1.4.4 / phospholipase D1
  •  go-up   go-down


53. Lai JP, Douglas SD, Wang YJ, Ho WZ: Real-time reverse transcription-PCR quantitation of substance P receptor (NK-1R) mRNA. Clin Diagn Lab Immunol; 2005 Apr;12(4):537-41
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We applied a newly developed real-time reverse transcription (RT)-PCR assay to quantify NK-1R mRNA in human neuronal cell line (NT-2N), a human B-cell line (IM9), monocyte-derived macrophages (MDM), peripheral blood lymphocytes (PBL), and human astroglioma cells (U87 MG).
  • These data indicate that the NK-1R real-time RT-PCR has potential for a wide application in investigation of NK-1R expression at the mRNA level under physiological and pathological conditions in both the central nervous system and the immune system.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neuroimmunol. 2000 Jan 24;102(2):163-71 [10636485.001]
  • [Cites] J Neuroimmunol. 1998 Nov 2;91(1-2):121-8 [9846828.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):3970-5 [11274418.001]
  • [Cites] J Neuroimmunol. 2001 Dec 3;121(1-2):67-75 [11730941.001]
  • [Cites] Clin Diagn Lab Immunol. 2002 Jan;9(1):138-43 [11777843.001]
  • [Cites] FASEB J. 2002 Apr;16(6):616-8 [11919172.001]
  • [Cites] Methods Mol Biol. 2002;193:129-47 [12325504.001]
  • [Cites] J Neurosci Res. 2003 Feb 15;71(4):559-66 [12548712.001]
  • [Cites] Clin Diagn Lab Immunol. 2003 Nov;10(6):1123-8 [14607877.001]
  • [Cites] Glia. 2004 Nov 15;48(3):259-66 [15390113.001]
  • [Cites] Pharmacol Rev. 1983 Jun;35(2):85-141 [6196797.001]
  • [Cites] J Immunol. 1985 Aug;135(2):1331-7 [2409146.001]
  • [Cites] J Immunol Methods. 1986 Dec 24;95(2):273-6 [3794346.001]
  • [Cites] J Immunol. 1987 Aug 1;139(3):749-54 [2439591.001]
  • [Cites] Physiol Rev. 1987 Oct;67(4):1117-42 [2446341.001]
  • [Cites] Biochem Biophys Res Commun. 1987 Nov 13;148(3):1440-5 [2446611.001]
  • [Cites] Science. 1988 Sep 2;241(4870):1218-21 [2457950.001]
  • [Cites] Experientia. 1989 Feb 15;45(2):121-5 [2465912.001]
  • [Cites] Peptides. 1989 Sep-Oct;10(5):957-62 [2481848.001]
  • [Cites] Scand J Immunol. 1990 Apr;31(4):529-33 [1692157.001]
  • [Cites] J Immunol Methods. 1990 Jul 3;130(2):283-5 [2373869.001]
  • [Cites] Immunology. 1990 Sep;71(1):52-6 [1698717.001]
  • [Cites] Endocrinology. 1991 May;128(5):2441-8 [1708336.001]
  • [Cites] Brain Behav Immun. 1991 Mar;5(1):73-83 [1712653.001]
  • [Cites] J Neurosci. 1992 May;12(5):1802-15 [1578271.001]
  • [Cites] Reg Immunol. 1992 Mar-Apr;4(2):105-12 [1380279.001]
  • [Cites] Anal Biochem. 1993 Nov 1;214(2):582-5 [8109752.001]
  • [Cites] Clin Diagn Lab Immunol. 1994 May;1(3):330-5 [7496971.001]
  • [Cites] Genome Res. 1996 Oct;6(10):986-94 [8908518.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2334-9 [9036982.001]
  • [Cites] J Immunol. 1997 Nov 15;159(10):4952-8 [9366421.001]
  • [Cites] Nat Biotechnol. 1998 Jan;16(1):49-53 [9447593.001]
  • [Cites] J Immunol. 1997 Dec 1;159(11):5654-60 [9548509.001]
  • [Cites] J Clin Invest. 1998 Apr 15;101(8):1547-50 [9541482.001]
  • [Cites] Neuropeptides. 1997 Dec;31(6):537-63 [9574822.001]
  • [Cites] J Neuroimmunol. 1998 Jun 1;86(1):80-6 [9655475.001]
  • [Cites] Neuroscience. 2000;101(4):1137-44 [11113362.001]
  • (PMID = 15817763.001).
  • [ISSN] 1071-412X
  • [Journal-full-title] Clinical and diagnostic laboratory immunology
  • [ISO-abbreviation] Clin. Diagn. Lab. Immunol.
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH049981; United States / NIDA NIH HHS / DA / NIH-DA112815; United States / NIMH NIH HHS / MH / NIH-MH 49981
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Neurokinin-1
  • [Other-IDs] NLM/ PMC1074379
  •  go-up   go-down


54. Freese C, Garratt AN, Fahrenholz F, Endres K: The effects of alpha-secretase ADAM10 on the proteolysis of neuregulin-1. FEBS J; 2009 Mar;276(6):1568-80
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.
  • Thus, therapeutical approaches for the prevention of Alzheimer's disease by upregulation of this metalloproteinase may have severe side effects.
  • Studies with beta- and gamma-secretase inhibitors, as well as with the metalloproteinase inhibitor GM6001, revealed an inhibition of neuregulin-1 processing in human astroglioma cell line U373; however, specific RNA interference-induced knockdown of ADAM10 remained without effect.
  • Adverse reactions of an ADAM10-based therapy of Alzheimer's disease due to neuregulin-1 cleavage are therefore unlikely.
  • [MeSH-minor] Amino Acid Sequence. Animals. Astrocytoma. Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Humans. Hydrolysis. Mice. Mice, Transgenic. Molecular Sequence Data. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Sequence Homology, Amino Acid

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19220854.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Membrane Proteins; 0 / Neuregulin-1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / Adam10 protein, mouse
  •  go-up   go-down


55. Hynd MR, Frampton JP, Dowell-Mesfin N, Turner JN, Shain W: Directed cell growth on protein-functionalized hydrogel surfaces. J Neurosci Methods; 2007 May 15;162(1-2):255-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • As a biological assay, we plated LRM55 astroglioma and primary rat hippocampal neurons on patterned hydrogels.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biomaterials. 1999 Dec;20(23-24):2363-76 [10614942.001]
  • [Cites] J Biomed Mater Res A. 2007 May;81(2):347-54 [17120223.001]
  • [Cites] Mol Cell Neurosci. 2002 May;20(1):140-53 [12056845.001]
  • [Cites] Chem Rev. 2002 Sep;102(9):3067-84 [12222982.001]
  • [Cites] Drug Dev Ind Pharm. 2002 Sep;28(8):957-74 [12378965.001]
  • [Cites] Methods. 2004 Aug;33(4):287-94 [15183177.001]
  • [Cites] Biomaterials. 2005 Mar;26(8):883-9 [15353199.001]
  • [Cites] J Am Chem Soc. 2004 Oct 6;126(39):12204-5 [15453719.001]
  • [Cites] J Biol Chem. 1979 Aug 10;254(15):7076-84 [457670.001]
  • [Cites] Science. 1992 Jan 10;255(5041):200-3 [1553547.001]
  • [Cites] J Neurosci Res. 1993 Aug 1;35(5):567-76 [8377226.001]
  • [Cites] Science. 1994 Apr 29;264(5159):696-8 [8171320.001]
  • [Cites] J Biomed Mater Res. 1995 Feb;29(2):207-15 [7738068.001]
  • [Cites] J Neurosci. 1996 Jun 15;16(12):3960-7 [8656290.001]
  • [Cites] Exp Cell Res. 1997 Sep 15;235(2):305-13 [9299154.001]
  • [Cites] Med Biol Eng Comput. 1998 Jan;36(1):135-41 [9614762.001]
  • [Cites] Biomaterials. 1998 Jul;19(14):1287-94 [9720892.001]
  • [Cites] Biochim Biophys Acta. 1998 Dec 9;1415(1):135-46 [9858712.001]
  • [Cites] Biosens Bioelectron. 2004 Nov 1;20(4):753-64 [15522590.001]
  • [Cites] Langmuir. 2004 Dec 7;20(25):11123-6 [15568866.001]
  • [Cites] Crit Rev Ther Drug Carrier Syst. 2005;22(2):107-49 [15862110.001]
  • [Cites] Nat Methods. 2005 Feb;2(2):119-25 [15782209.001]
  • [Cites] Expert Rev Med Devices. 2005 Jul;2(4):493-500 [16293087.001]
  • [Cites] Adv Exp Med Biol. 2005;561:21-37 [16438286.001]
  • [Cites] Biomaterials. 2006 Aug;27(22):4132-40 [16584769.001]
  • [Cites] J Neurosci Methods. 2007 Mar 15;160(2):317-26 [17049614.001]
  • [Cites] Wound Repair Regen. 2001 Nov-Dec;9(6):513-21 [11896994.001]
  • (PMID = 17368788.001).
  • [ISSN] 0165-0270
  • [Journal-full-title] Journal of neuroscience methods
  • [ISO-abbreviation] J. Neurosci. Methods
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / EB007782-01; United States / NIBIB NIH HHS / EB / EB007782-02; United States / NIBIB NIH HHS / EB / R21 EB007782-01; United States / NIBIB NIH HHS / EB / R21 EB007782-02
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / FM1 43; 0 / Fibronectins; 0 / Hydrogels; 0 / Laminin; 0 / Proteins; 0 / Pyridinium Compounds; 0 / Quaternary Ammonium Compounds
  • [Other-IDs] NLM/ NIHMS22066; NLM/ PMC2729282
  •  go-up   go-down


56. Holden LJ, Coleman MD: Further preliminary assessment of three human glioma cell lines as models of human astrocytic toxicity in vitro. Environ Toxicol Pharmacol; 2008 Nov;26(3):290-6
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] Further preliminary assessment of three human glioma cell lines as models of human astrocytic toxicity in vitro.
  • Three human astroglioma lines U251-MG, U373-MG and CCF-STTG1 have been evaluated further as possible models for astrocytotoxicity (GFAP and IL-6 release).
  • It is possible that batteries of astrocytic human glioma cell lines may be applicable to the sensitive evaluation of toxicants on astrogliotic expression markers such as GFAP and IL-6.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2008 Elsevier B.V. All rights reserved.
  • (PMID = 21791377.001).
  • [ISSN] 1382-6689
  • [Journal-full-title] Environmental toxicology and pharmacology
  • [ISO-abbreviation] Environ. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


57. Slesina M, Inman EM, Rome LH, Volknandt W: Nuclear localization of the major vault protein in U373 cells. Cell Tissue Res; 2005 Jul;321(1):97-104
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The major vault protein (MVP) is the predominant member of a large ribonucleoprotein particle, named vault.
  • Cryo-electron microscopy of human astroglioma U373 cells reveals clusters of immunogold particles at nuclear pores and in the nucleoplasm suggesting that nuclear MVP is associated with particulate structures.
  • [MeSH-major] Astrocytoma / chemistry. Brain Neoplasms / chemistry. Cell Nucleus / metabolism. Vault Ribonucleoprotein Particles / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cryoelectron Microscopy. Cytosol / metabolism. Humans. Immunohistochemistry. Microscopy, Confocal. Microscopy, Immunoelectron. Nuclear Pore / metabolism. Nuclear Pore / ultrastructure. Transfection

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15902504.001).
  • [ISSN] 0302-766X
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
  •  go-up   go-down


58. Röhl C, Armbrust E, Herbst E, Jess A, Gülden M, Maser E, Rimbach G, Bösch-Saadatmandi C: Mechanisms involved in the modulation of astroglial resistance to oxidative stress induced by activated microglia: antioxidative systems, peroxide elimination, radical generation, lipid peroxidation. Neurotox Res; 2010 May;17(4):317-31
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • For C6 astroglioma cells a protective effect of microglia-derived factors could not be observed, underlining the difference of primary cells and cell lines concerning their mechanisms of oxidative stress resistance.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19763738.001).
  • [ISSN] 1476-3524
  • [Journal-full-title] Neurotoxicity research
  • [ISO-abbreviation] Neurotox Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 16,17-cyclohexane-5H-pregnan-3,20-dione; 0 / Antigens, CD11b; 0 / Culture Media, Conditioned; 0 / Lipopolysaccharides; 0 / Peroxides; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 31C4KY9ESH / Nitric Oxide; BBX060AN9V / Hydrogen Peroxide; BXO86P3XXW / Pregnanolone; EC 1.14.99.3 / Heme Oxygenase-1; EC 1.15.1.1 / Superoxide Dismutase; EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione
  •  go-up   go-down


59. Ju SM, Song HY, Lee JA, Lee SJ, Choi SY, Park J: Extracellular HIV-1 Tat up-regulates expression of matrix metalloproteinase-9 via a MAPK-NF-kappaB dependent pathway in human astrocytes. Exp Mol Med; 2009 Feb 28;41(2):86-93
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.
  • In this study, we examined the effect of HIV-1 Tat on the expression of MMP-9 in CRT-MG human astroglioma cells.
  • [MeSH-minor] Humans. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation / drug effects

  • Genetic Alliance. consumer health - HIV.
  • MedlinePlus Health Information. consumer health - HIV/AIDS.
  • 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
  • [Cites] J Neurovirol. 2000 Apr;6(2):145-55 [10822328.001]
  • [Cites] Trends Mol Med. 2007 Nov;13(11):449-59 [18029231.001]
  • [Cites] J Virol. 2000 Oct;74(19):9214-21 [10982368.001]
  • [Cites] Ann Neurol. 2001 Feb;49(2):230-41 [11220743.001]
  • [Cites] J Immunol. 2001 Nov 1;167(9):5150-9 [11673527.001]
  • [Cites] Crit Rev Biochem Mol Biol. 2002 Dec;37(6):375-536 [12540195.001]
  • [Cites] Glia. 2003 Oct;44(1):47-56 [12951656.001]
  • [Cites] Mol Cell Biochem. 2003 Nov;253(1-2):269-85 [14619979.001]
  • [Cites] J Neurovirol. 2004 Feb;10(1):21-8 [14982725.001]
  • [Cites] Microbes Infect. 2004 Feb;6(2):157-63 [14998513.001]
  • [Cites] J Virol. 1993 Jan;67(1):277-87 [8416373.001]
  • [Cites] Neurology. 1994 Mar;44(3 Pt 1):481-7 [8145919.001]
  • [Cites] J Immunol. 1996 Feb 15;156(4):1638-45 [8568270.001]
  • [Cites] J Virol. 1996 Mar;70(3):1384-9 [8627654.001]
  • [Cites] Ann Neurol. 1996 Jun;39(6):705-11 [8651642.001]
  • [Cites] AIDS. 1996 Jul;10(8):843-7 [8828741.001]
  • [Cites] J Immunol. 1997 Oct 15;159(8):4077-83 [9378998.001]
  • [Cites] Trends Neurosci. 1998 Feb;21(2):75-80 [9498303.001]
  • [Cites] J Infect Dis. 1998 Sep;178(3):854-7 [9728558.001]
  • [Cites] J Leukoc Biol. 1999 Apr;65(4):458-65 [10204574.001]
  • [Cites] J Biol Chem. 1999 Jun 11;274(24):17098-102 [10358063.001]
  • [Cites] Ann Neurol. 1999 Sep;46(3):391-8 [10482270.001]
  • [Cites] J Biosci. 2005 Jun;30(3):391-405 [16052077.001]
  • [Cites] Curr Pharm Des. 2006;12(9):1023-44 [16515484.001]
  • [Cites] FASEB J. 2006 Aug;20(10):1736-8 [16807369.001]
  • [Cites] Biochem Pharmacol. 2006 Nov 30;72(11):1493-505 [16723122.001]
  • [Cites] Exp Mol Med. 2007 Feb 28;39(1):27-37 [17334226.001]
  • [Cites] J Cell Physiol. 2007 Nov;213(2):355-64 [17654499.001]
  • [Cites] Semin Cell Dev Biol. 2008 Feb;19(1):42-51 [17646116.001]
  • [Cites] Exp Mol Med. 2007 Dec 31;39(6):778-86 [18160848.001]
  • [Cites] J Neurovirol. 2000 Apr;6(2):156-63 [10822329.001]
  • (PMID = 19287189.001).
  • [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 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 0 / tat Gene Products, Human Immunodeficiency Virus; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2679334
  •  go-up   go-down


60. Smith M, Omidi Y, Gumbleton M: Primary porcine brain microvascular endothelial cells: biochemical and functional characterisation as a model for drug transport and targeting. J Drug Target; 2007 May;15(4):253-68
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Co-cultures of PBMVECs with astrocytes (C6 astroglioma) resulted in trans-endothelial electrical resistance of up to approximately 900Omega cm2 and marked discrimination between the para- and trans- cellular markers sucrose and propranolol.

  • MedlinePlus Health Information. consumer health - Medicines.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Drug Target. 2007 Jul;15(6):454
  • (PMID = 17487694.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Culture Media, Conditioned; 0 / Pharmaceutical Preparations; EC 3.1.3.1 / Alkaline Phosphatase
  •  go-up   go-down


61. Lee EJ, Kim SY, Hyun JW, Min SW, Kim DH, Kim HS: Glycitein inhibits glioma cell invasion through down-regulation of MMP-3 and MMP-9 gene expression. Chem Biol Interact; 2010 Apr 15;185(1):18-24
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] Glycitein inhibits glioma cell invasion through down-regulation of MMP-3 and MMP-9 gene expression.
  • Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that play a pivotal role in invasion and angiogenesis of malignant glioma cells.
  • In the present study, we found that glycitein, a bacterial metabolite of the isoflavone glycitin, inhibits the expression of MMP-3 and MMP-9 at promoter, mRNA, and protein levels in PMA-stimulated U87MG human astroglioma cells.
  • A subsequent Matrigel invasion assay revealed that glycitein suppresses the in vitro invasiveness of glioma cells, which may be at least partly due to the glycitein-mediated inhibition of MMP-3 and MMP-9.
  • In support of this, treatment of MMP-3- or MMP-9-specific inhibitor significantly suppressed PMA-induced invasion of glioma cells.
  • Furthermore, glycitein suppresses PMA-induced phosphorylation of three types of MAP kinases, which are upstream signaling molecules in MMP gene expressions and NF-kappaB and AP-1 activities in glioma cells.
  • Therefore, the inhibition of MMP-3 and MMP-9 expression by glycitein may have therapeutic potential for controlling invasiveness of malignant gliomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / pathology. Glioma / pathology. Isoflavones / pharmacology. Matrix Metalloproteinase 3 / genetics. Matrix Metalloproteinase 9 / genetics. Neoplasm Invasiveness / prevention & control
  • [MeSH-minor] Cell Line, Tumor. DNA / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mitogen-Activated Protein Kinases / metabolism. NF-kappa B / genetics. NF-kappa B / metabolism. Neuroglia / cytology. Promoter Regions, Genetic / drug effects. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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
  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20188714.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Isoflavones; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 9007-49-2 / DNA; 92M5F28TVF / glycitein; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


62. Poenisch M, Burger N, Staeheli P, Bauer G, Schneider U: Protein X of Borna disease virus inhibits apoptosis and promotes viral persistence in the central nervous systems of newborn-infected rats. J Virol; 2009 May;83(9):4297-307
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] Protein X of Borna disease virus inhibits apoptosis and promotes viral persistence in the central nervous systems of newborn-infected rats.
  • Borna disease virus (BDV) is a neurotropic member of the order Mononegavirales with noncytolytic replication and obligatory persistence in cultured cells and animals.
  • Rat C6 astroglioma cells persistently infected with wild-type BDV were significantly more resistant to death receptor-dependent and -independent apoptotic stimuli than uninfected cells or cells infected with a BDV mutant expressing reduced amounts of X.
  • [MeSH-major] Apoptosis. Borna Disease / metabolism. Borna Disease / virology. Borna disease virus / metabolism. Central Nervous System / metabolism. Central Nervous System / virology. Trans-Activators / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell. 2000 Jul;6(1):53-63 [10949027.001]
  • [Cites] J Infect Dis. 2002 Dec 1;186 Suppl 2:S241-7 [12424704.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 May;2(5):339-49 [11331908.001]
  • [Cites] Adv Virus Res. 2001;56:557-82 [11450312.001]
  • [Cites] Methods Mol Biol. 2001;177:211-8 [11530608.001]
  • [Cites] Curr Biol. 2003 Jan 21;13(2):R71-3 [12546810.001]
  • [Cites] J Virol. 2003 Mar;77(6):3371-83 [12610112.001]
  • [Cites] J Neurovirol. 2003 Apr;9(2):259-73 [12707857.001]
  • [Cites] Biochem Biophys Res Commun. 2003 May 9;304(3):433-5 [12729576.001]
  • [Cites] J Virol. 2003 Jul;77(13):7214-24 [12805420.001]
  • [Cites] J Virol. 2003 Nov;77(21):11781-9 [14557662.001]
  • [Cites] J Virol. 2003 Dec;77(23):12886-90 [14610210.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 25;101(21):7988-93 [15148411.001]
  • [Cites] J Gen Virol. 2004 Jul;85(Pt 7):1895-8 [15218174.001]
  • [Cites] J Gen Virol. 2004 Aug;85(Pt 8):2379-87 [15269380.001]
  • [Cites] Cell. 1991 Jun 28;65(7):1107-15 [1648447.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11486-9 [1454837.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8479-83 [8397406.001]
  • [Cites] J Exp Med. 1994 Oct 1;180(4):1547-52 [7523573.001]
  • [Cites] J Virol. 1999 Jun;73(6):5181-5 [10233985.001]
  • [Cites] Arch Virol. 1999;144(6):1209-16 [10446654.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 12;96(21):12102-7 [10518583.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3441-6 [15728364.001]
  • [Cites] Annu Rev Microbiol. 1999;53:577-628 [10547702.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):33-46 [10620603.001]
  • [Cites] J Gen Virol. 2000 Apr;81(Pt 4):939-47 [10725419.001]
  • [Cites] J Exp Med. 2000 May 1;191(9):1487-98 [10790424.001]
  • [Cites] Curr Opin Cell Biol. 2000 Aug;12(4):414-9 [10873816.001]
  • [Cites] Virus Res. 2005 Aug;111(2):148-60 [15992626.001]
  • [Cites] J Virol. 2005 Sep;79(18):11716-23 [16140749.001]
  • [Cites] Virology. 2006 Jan 5;344(1):119-30 [16364743.001]
  • [Cites] J Virol. 2006 Apr;80(7):3369-77 [16537604.001]
  • [Cites] J Virol. 2006 May;80(9):4372-9 [16611896.001]
  • [Cites] J Virol. 2006 Jun;80(11):5644-50 [16699046.001]
  • [Cites] J Virol. 2006 Jun;80(12):5708-15 [16731909.001]
  • [Cites] J Gen Virol. 2006 Jul;87(Pt 7):1935-45 [16760395.001]
  • [Cites] J Virol. 2006 Sep;80(17):8613-26 [16912310.001]
  • [Cites] Cell Mol Life Sci. 2007 May;64(9):1038-42 [17372677.001]
  • [Cites] J Virol. 2007 Jul;81(13):7297-9 [17428855.001]
  • [Cites] J Virol. 2007 Aug;81(15):7933-40 [17522214.001]
  • [Cites] Curr Pharm Des. 2008;14(3):198-220 [18220831.001]
  • [Cites] J Virol. 2008 May;82(10):4774-84 [18321977.001]
  • [Cites] J Gen Virol. 2008 Jun;89(Pt 6):1442-5 [18474560.001]
  • [Cites] Nat Rev Immunol. 2008 Aug;8(8):644-54 [18654572.001]
  • [Cites] J Virol. 2008 Oct;82(19):9537-45 [18653450.001]
  • [Cites] Clin Microbiol Rev. 2008 Jan;21(1):13-25 [18202435.001]
  • [Cites] Nat Med. 2001 Dec;7(12):1306-12 [11726970.001]
  • [Cites] Front Biosci. 2002 Feb 1;7:d569-79 [11815302.001]
  • [Cites] J Biol Chem. 2002 Apr 5;277(14):12151-7 [11796712.001]
  • [Cites] Anticancer Res. 2002 Mar-Apr;22(2A):841-56 [12014661.001]
  • [Cites] J Gen Virol. 2002 Jul;83(Pt 7):1547-64 [12075073.001]
  • [Cites] Nat Immunol. 2002 Nov;3(11):1013-8 [12407409.001]
  • [Cites] Rev Med Virol. 2001 Jan-Feb;11(1):37-57 [11241801.001]
  • (PMID = 19211764.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Trans-Activators
  • [Other-IDs] NLM/ PMC2668499
  •  go-up   go-down


63. Song HY, Ju SM, Lee JA, Kwon HJ, Eum WS, Jang SH, Choi SY, Park J: Suppression of HIV-1 Tat-induced monocyte adhesiveness by a cell-permeable superoxide dismutase in astrocytes. Exp Mol Med; 2007 Dec 31;39(6):778-86
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.
  • This study was performed to determine the regulatory function of superoxide dismutase (SOD) on the HIV-1 Tat-induced signaling pathways leading to NF-kappaB activation, expression of adhesion molecules, and monocyte adhesion in CRT-MG human astroglioma cells by using cell-permeable SOD.
  • These data indicate that SOD has a regulatory function for HIV-1 Tat-induced NF-kappaB activation in astrocytes and suggest that cell-permeable SOD can be used as a feasible therapeutic agent for regulation of ROS-related neurological diseases.

  • Genetic Alliance. consumer health - HIV.
  • 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 = 18160848.001).
  • [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 / Gene Products, tat; EC 1.15.1.1 / Superoxide Dismutase
  •  go-up   go-down


64. Casoli C, Pilotti E, Perno CF, Balestra E, Polverini E, Cassone A, Conti S, Magliani W, Polonelli L: A killer mimotope with therapeutic activity against AIDS-related opportunistic micro-organisms inhibits ex-vivo HIV-1 replication. AIDS; 2006 Apr 24;20(7):975-80
Hazardous Substances Data Bank. ZIDOVUDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To verify whether a synthetic therapeutic killer decapeptide (KP), a functional mimotope of a yeast killer toxin with wide-spectrum microbicidal activity, inclusive of AIDS-related opportunistic micro-organisms, through interaction with beta-glucan receptors, which has been found to possess sequence homology with critical segments in gp160 V1/V2 and V3 loops, may also be inhibiting HIV-1 replication.
  • The binding affinity of KP to CD4, CCR5 and CXCR4 was evaluated on CD4-CCR5 or CD4-CXCR4 transfected astroglioma cell lines.
  • RESULTS: KP was shown to be devoid of cytotoxicity on PBMCs and to inhibit HIV-1 replication in PBMCs of a patient in the acute phase of infection.

  • Genetic Alliance. consumer health - AIDS-HIV.
  • Genetic Alliance. consumer health - HIV.
  • MedlinePlus Health Information. consumer health - HIV/AIDS.
  • MedlinePlus Health Information. consumer health - HIV/AIDS and Infections.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16603848.001).
  • [ISSN] 0269-9370
  • [Journal-full-title] AIDS (London, England)
  • [ISO-abbreviation] AIDS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / HIV Envelope Protein gp160; 0 / Peptides; 0 / RNA, Viral; 0 / Receptors, CCR5; 0 / Receptors, CXCR4; 4B9XT59T7S / Zidovudine
  •  go-up   go-down


65. Wei LC, Shi M, Cao R, Chen LW, Chan YS: Nestin small interfering RNA (siRNA) reduces cell growth in cultured astrocytoma cells. Brain Res; 2008 Feb 27;1196:103-12
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] Nestin small interfering RNA (siRNA) reduces cell growth in cultured astrocytoma cells.
  • Growing evidence has shown that abundant expression of nestin also occurs in both pathological glial-derived tumor cells and reactive astrocytes in various CNS injuries, implying that nestin may play a crucial role in cell growth or proliferation of astrocyte-derived tumor cells.
  • In the present study, we have investigated the possible role of nestin expression in cell growth or survival of CNS tumor cells by using novel small interfering RNA (siRNA) method in cell culture of rat astrocytoma C6 cell line.
  • The nestin expression and cell growth of the cultured astrocytoma cells were examined after nestin siRNA duplex was delivered by cell transfection for 6 h and cell culture was maintained for 48 h.
  • It revealed an effective suppression influence of nestin siRNA on cell growth of cultured astrocytoma cells in a dose-dependent manner.
  • This study has provided in vitro evidence that nestin siRNA can effectively block nestin expression and reduce cell growth of the cultured C6 astrocytoma cells, strongly suggesting that nestin siRNA-induced suppression of tumor cell growth may provide a potential novel clinical therapy against CNS astroglioma events.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / physiopathology. Intermediate Filament Proteins / genetics. Nerve Tissue Proteins / genetics. RNA, Small Interfering / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Cell Count. Cell Line, Tumor. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Glial Fibrillary Acidic Protein / metabolism. Nestin. Rats

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18234160.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / RNA, Small Interfering
  •  go-up   go-down


66. Choi WH, Ji KA, Jeon SB, Yang MS, Kim H, Min KJ, Shong M, Jou I, Joe EH: Anti-inflammatory roles of retinoic acid in rat brain astrocytes: Suppression of interferon-gamma-induced JAK/STAT phosphorylation. Biochem Biophys Res Commun; 2005 Apr 1;329(1):125-31
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In primary cultured rat brain astrocytes and C6 astroglioma cells, both cRA and tRA decreased IFN-gamma-induced expression of interferon regulatory factor-1.
  • Furthermore, the effect of pre-treated RA was abolished in the presence of cycloheximide, indicating a requirement for de novo protein synthesis.

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. CYCLOHEXIMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15721283.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Protein Synthesis Inhibitors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / Socs1 protein, rat; 0 / Socs3 protein, rat; 0 / Stat1 protein, rat; 0 / Stat3 protein, rat; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 5688UTC01R / Tretinoin; 82115-62-6 / Interferon-gamma; 98600C0908 / Cycloheximide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak1 protein, rat; EC 2.7.10.2 / Jak2 protein, rat; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 2
  •  go-up   go-down


67. Regan EM, Uney JB, Dick AD, Zhang Y, Nunez-Yanez J, McGeehan JP, Claeyssens F, Kelly S: Differential patterning of neuronal, glial and neural progenitor cells on phosphorus-doped and UV irradiated diamond-like carbon. Biomaterials; 2010 Jan;31(2):207-15
Hazardous Substances Data Bank. PHOSPHORUS, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the present study we complement and extend these findings by exploring patterning of dorsal root ganglion (DRG) explants, human neural progenitor cells (hNPC) and U-87 astroglioma cells on P:DLC.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19833386.001).
  • [ISSN] 1878-5905
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 27YLU75U4W / Phosphorus; 7782-40-3 / Diamond
  •  go-up   go-down


68. Kim SW, Lee JK: NO-induced downregulation of HSP10 and HSP60 expression in the postischemic brain. J Neurosci Res; 2007 May 1;85(6):1252-9
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.
  • The downregulation of HSP60 and HSP10 by NO were confirmed in vitro, wherein HSP10 and SHP60 expressions were increased by treatment of LPS and IFN gamma (LPS/INF gamma) in C6 astroglioma cells and further upregulated by NMMA, another iNOS inhibitor.
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Interactions. Electrophoretic Mobility Shift Assay / methods. Enzyme Inhibitors / pharmacology. Glioma / pathology. Interferon-gamma / pharmacology. Lipopolysaccharides / pharmacology. Male. Protein Binding / drug effects. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction / methods. STAT Transcription Factors / metabolism. Time Factors. Transfection / methods

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17348040.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chaperonin 10; 0 / Chaperonin 60; 0 / Enzyme Inhibitors; 0 / Lipopolysaccharides; 0 / STAT Transcription Factors; 31C4KY9ESH / Nitric Oxide; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


69. Kalluri SR, Illes Z, Srivastava R, Cree B, Menge T, Bennett JL, Berthele A, Hemmer B: Quantification and functional characterization of antibodies to native aquaporin 4 in neuromyelitis optica. Arch Neurol; 2010 Oct;67(10):1201-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Antibodies targeting membrane proteins play an important role in various autoimmune diseases of the nervous system.
  • DESIGN, SETTING, AND PARTICIPANTS: We developed a novel bioassay for quantification and characterization of human anti-AQP4 antibodies based on high-level expression of native AQP4 (nAQP4) protein on the surface of human astroglioma cells.
  • The test was validated in 2 independent cohorts of patients with NMO spectrum disease.
  • RESULTS: We detected anti-nAQP4-IgG with a sensitivity of 57.9% and specificity of 100% in patients with NMO spectrum diseases, suggesting that our bioassay is at least as sensitive and specific as the gold-standard NMO-IgG assay.
  • Our findings demonstrate the potential of bioassays to characterize biologically relevant antibodies in human autoimmune diseases.
  • [MeSH-minor] Adult. Aged. Biological Assay / methods. Cell Line, Tumor. Cohort Studies. Cytotoxicity Tests, Immunologic / methods. Female. Flow Cytometry / methods. Gene Expression Regulation, Neoplastic / physiology. Glioma / pathology. Humans. Male. Middle Aged. Transfection / methods. Young Adult

  • Genetic Alliance. consumer health - Devic Disease.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20937947.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AQP4 protein, human; 0 / Aquaporin 4; 0 / Immunoglobulin G
  •  go-up   go-down


70. Gardner J, Borgmann K, Deshpande MS, Dhar A, Wu L, Persidsky R, Ghorpade A: Potential mechanisms for astrocyte-TIMP-1 downregulation in chronic inflammatory diseases. J Neurosci Res; 2006 May 15;83(7):1281-92
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] Potential mechanisms for astrocyte-TIMP-1 downregulation in chronic inflammatory diseases.
  • In the context of disease, TIMP-1 has emerged as an important multifunctional protein capable of regulating inflammation.
  • TIMP-1 mRNA stability was measured in astrocytes and U87 astroglioma cells by real-time PCR, and TIMP-1 promoter activation was studied using TIMP-1-luciferase reporter constructs in transfected astrocytes.
  • These data are important for unraveling the mechanisms underlying astrocyte responses during chronic neuroinflammation and have broader implications in other inflammatory diseases that involve MMP/TIMP imbalance.
  • [MeSH-minor] Antigens, CD95 / drug effects. Antigens, CD95 / metabolism. Cell Line, Tumor. Cells, Cultured. Humans. Interleukin-1 / metabolism. Interleukin-1 / pharmacology. Promoter Regions, Genetic / drug effects. Promoter Regions, Genetic / physiology. Protein Binding / drug effects. Protein Binding / physiology. RNA Stability / physiology. RNA, Messenger / metabolism. Receptors, Interleukin-1 / metabolism. Regulatory Elements, Transcriptional / drug effects. Regulatory Elements, Transcriptional / genetics. Transcriptional Activation / drug effects. Transcriptional Activation / physiology

  • MedlinePlus Health Information. consumer health - Encephalitis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16555295.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS43113; United States / NINDS NIH HHS / NS / R01 NS48837
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Interleukin-1; 0 / RNA, Messenger; 0 / Receptors, Interleukin-1; 0 / Tissue Inhibitor of Metalloproteinase-1
  •  go-up   go-down


71. Mishra MK, Kumawat KL, Basu A: Japanese encephalitis virus differentially modulates the induction of multiple pro-inflammatory mediators in human astrocytoma and astroglioma cell-lines. Cell Biol Int; 2008 Dec;32(12):1506-13
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] Japanese encephalitis virus differentially modulates the induction of multiple pro-inflammatory mediators in human astrocytoma and astroglioma cell-lines.
  • We have shown that Japanese encephalitis virus (JEV) infection causes morphological and functional changes in astrocytic cell-lines.
  • [MeSH-minor] Animals. Animals, Newborn. Astrocytoma / immunology. Brain Neoplasms / immunology. Cell Line, Transformed. Cell Line, Tumor. Ceruloplasmin / immunology. Ceruloplasmin / metabolism. Chemokines / immunology. Chemokines / metabolism. Cytokines / immunology. Cytokines / metabolism. Encephalitis Virus, Japanese / immunology. Humans. Mice. Mice, Inbred BALB C. Reactive Oxygen Species / immunology. Reactive Oxygen Species / metabolism. Thioredoxins / immunology. Thioredoxins / metabolism. Vesicular Glutamate Transport Proteins / immunology. Vesicular Glutamate Transport Proteins / metabolism

  • Genetic Alliance. consumer health - Japanese encephalitis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18801452.001).
  • [ISSN] 1095-8355
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Cytokines; 0 / Reactive Oxygen Species; 0 / Vesicular Glutamate Transport Proteins; 52500-60-4 / Thioredoxins; EC 1.16.3.1 / Ceruloplasmin
  •  go-up   go-down


72. Brard L, Singh RK, Kim KK, Lange TS, Sholler GL: Induction of cytotoxicity, apoptosis and cell cycle arrest by 1-t-butyl carbamoyl, 7-methyl-indole-3-ethyl isothiocyanate (NB7M) in nervous system cancer cells. Drug Des Devel Ther; 2009 Feb 06;2:61-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the NCI 60 cell screen 1-dose assay, NB7M (10 microM) reduced the growth (-89 to -27 % growth) of CNS cancer cell lines SF-268, SF-295, SNB-75 (glioblastoma), SF-539 (gliosarcoma), and U251 (astroglioma) while SNB-19 glioblastoma cells were relatively resistant (19% growth).

  • COS Scholar Universe. author profiles.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1270-9 [12649187.001]
  • [Cites] J Biol Chem. 2003 May 23;278(21):19245-56 [12637505.001]
  • [Cites] Pharm Res. 2002 Oct;19(10):1509-15 [12425469.001]
  • [Cites] Cell Signal. 2002 May;14(5):381-95 [11882383.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(1):18-26 [10623689.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Bioorg Med Chem Lett. 2007 Nov 1;17(21):5846-52 [17855093.001]
  • [Cites] Br J Cancer. 2007 Sep 3;97(5):628-36 [17637678.001]
  • [Cites] Cancer Lett. 2007 Jun 18;251(1):1-16 [17125914.001]
  • [Cites] Trends Mol Med. 2007 Jan;13(1):4-11 [17118707.001]
  • [Cites] Vascul Pharmacol. 2007 Feb;46(2):77-84 [16938492.001]
  • [Cites] J Exp Ther Oncol. 2006;5(4):287-300 [17024969.001]
  • [Cites] Gynecol Oncol. 2006 Oct;103(1):261-70 [16624391.001]
  • [Cites] J Agric Food Chem. 2006 Mar 8;54(5):1656-62 [16506816.001]
  • [Cites] Anticancer Res. 2005 Sep-Oct;25(5):3375-86 [16101152.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 26;102(17):5998-6003 [15837920.001]
  • [Cites] J Biol Chem. 2005 Mar 11;280(10):8756-64 [15611077.001]
  • [Cites] N Engl J Med. 1999 Oct 14;341(16):1165-73 [10519894.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):8208-16 [10075725.001]
  • [Cites] Cytometry. 1996 Jun 1;24(2):131-9 [8725662.001]
  • [Cites] J Nutr. 2004 Sep;134(9):2229-36 [15333709.001]
  • [Cites] Int J Cancer. 2004 Dec 20;112(6):974-85 [15386344.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2774-84 [15077141.001]
  • [Cites] Curr Cancer Drug Targets. 2004 Feb;4(1):65-75 [14965268.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6836-48 [12972603.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):241-50 [12414812.001]
  • (PMID = 19920894.001).
  • [ISSN] 1177-8881
  • [Journal-full-title] Drug design, development and therapy
  • [ISO-abbreviation] Drug Des Devel Ther
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD043447-05; United States / NICHD NIH HHS / HD / K12 HD043447; United States / NCRR NIH HHS / RR / P20 RR018728; United States / NICHD NIH HHS / HD / K12 HD043447-05
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2761180
  • [Keywords] NOTNLM ; MAPK / apoptosis / cell cycle analysis / cytotoxicity
  •  go-up   go-down


73. Linden A, Gülden M, Martin HJ, Maser E, Seibert H: Peroxide-induced cell death and lipid peroxidation in C6 glioma cells. Toxicol In Vitro; 2008 Aug;22(5):1371-6
Hazardous Substances Data Bank. CUMENE HYDROPEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peroxide-induced cell death and lipid peroxidation in C6 glioma cells.
  • To this end (i) the ability to induce lipid peroxidation in C6 rat astroglioma cells of hydrogen peroxide (H2O2), cumene hydroperoxide (CHP) and t-butyl hydroperoxide (t-BuOOH) (ii) the relation between peroxide-induced lipid peroxidation and cell death in terms of time and concentration dependency and (iii) the capability of the lipid peroxidation chain breaking alpha-tocopherol to prevent peroxide-induced lipid peroxidation and/or cell death were investigated.
  • [MeSH-major] Glioma / drug therapy. Oxidants / toxicity. Oxidative Stress / drug effects. Peroxides / toxicity
  • [MeSH-minor] Aldehydes / metabolism. Animals. Antioxidants / pharmacology. Benzene Derivatives / toxicity. Cell Death / drug effects. Cell Line, Tumor. Chromatography, High Pressure Liquid. Dose-Response Relationship, Drug. Drug Combinations. Hydrogen Peroxide / toxicity. Lipid Peroxidation / drug effects. Malondialdehyde / metabolism. Rats. Thiobarbituric Acid Reactive Substances / metabolism. alpha-Tocopherol / pharmacology. tert-Butylhydroperoxide / toxicity

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MALONALDEHYDE .
  • Hazardous Substances Data Bank. VITAMIN E .
  • Hazardous Substances Data Bank. HEXALDEHYDE .
  • Hazardous Substances Data Bank. TERT-BUTYL HYDROPEROXIDE .
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18346863.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antioxidants; 0 / Benzene Derivatives; 0 / Drug Combinations; 0 / Oxidants; 0 / Peroxides; 0 / Thiobarbituric Acid Reactive Substances; 29343-52-0 / 4-hydroxy-2-nonenal; 4Y8F71G49Q / Malondialdehyde; 955VYL842B / tert-Butylhydroperoxide; 9DC2K31JJQ / n-hexanal; BBX060AN9V / Hydrogen Peroxide; H4N855PNZ1 / alpha-Tocopherol; PG7JD54X4I / cumene hydroperoxide
  •  go-up   go-down


74. Björklund O, Shang M, Tonazzini I, Daré E, Fredholm BB: Adenosine A1 and A3 receptors protect astrocytes from hypoxic damage. Eur J Pharmacol; 2008 Oct 31;596(1-3):6-13
Hazardous Substances Data Bank. COBALTOUS CHLORIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypoxia caused ATP breakdown and purine release, whereas CoCl(2) (0.8 mM) mainly reduced ATP by causing cell death in human D384 astrocytoma cells.
  • Genetic deletion of A(2A) receptor resulted in less prominent effects.
  • It also reduced apoptosis in human astroglioma D384 cells after oxygen deprivation.

  • Hazardous Substances Data Bank. Adenosine .
  • Hazardous Substances Data Bank. COBALT, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18727925.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenosine A1 Receptor Agonists; 0 / Adenosine A3 Receptor Agonists; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Purines; 0 / Receptor, Adenosine A1; 0 / Receptor, Adenosine A2A; 0 / Receptor, Adenosine A3; 3G0H8C9362 / Cobalt; 8L70Q75FXE / Adenosine Triphosphate; EVS87XF13W / cobaltous chloride; K72T3FS567 / Adenosine
  •  go-up   go-down


75. Esposito G, Iuvone T, Savani C, Scuderi C, De Filippis D, Papa M, Di Marzo V, Steardo L: Opposing control of cannabinoid receptor stimulation on amyloid-beta-induced reactive gliosis: in vitro and in vivo evidence. J Pharmacol Exp Ther; 2007 Sep;322(3):1144-52
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.
  • Beside cytotoxic mechanisms impacting on neurons, amyloid beta (A beta)-induced astroglial activation is operative in Alzheimer's disease brain, suggesting that persistent inflammatory response may have a role in the illness and that positive results may be achieved by curbing the astroglial reaction.
  • C6 rat astroglioma cells were challenged with 1 microg/ml A beta 1-42 in the presence or absence of selective agonists and antagonists of cannabinoid (CB)1 and CB2 receptors.
  • Furthermore, rats were inoculated into the frontal cortex with 30 ng of A beta 1-42 and were i.p. administered with 5 mg/kg of the same substances.
  • Finally, to our knowledge, the current study is the first showing that interactions at cannabinoid receptors result in a dual regulation of A beta-induced reactive astrogliosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17545311.001).
  • [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 / Amyloid beta-Peptides; 0 / Arachidonic Acids; 0 / Endocannabinoids; 0 / Polyunsaturated Alkamides; 0 / Receptor, Cannabinoid, CB1; 0 / Receptor, Cannabinoid, CB2; 94421-68-8 / anandamide
  •  go-up   go-down


76. Ibeas E, Fuentes L, Martín R, Hernández M, Nieto ML: Inflammatory protein sPLA(2)-IIA abrogates TNFalpha-induced apoptosis in human astroglioma cells: Crucial role of ERK. Biochim Biophys Acta; 2009 Dec;1793(12):1837-47

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammatory protein sPLA(2)-IIA abrogates TNFalpha-induced apoptosis in human astroglioma cells: Crucial role of ERK.
  • Brain injury induces the expression of well-known cytokines, such as tumor necrosis factor-alpha (TNFalpha), and other, which functions are less understood, as secreted phospholipase A(2) group IIA (sPLA(2)-IIA).
  • Since in pathological processes, cytokines function coordinately in networks, to further explore the actions of sPLA(2)-IIA in tumorigenesis, we investigated the effect of sPLA(2)-IIA in the presence of TNFalpha in human 1321N1 astrocytoma cells.
  • These findings thus indicate that sPLA(2)-IIA and TNFalpha transduction pathways interact to modulate inflammatory responses and provide additional insights about the capacity of sPLA(2)-IIA to promote apoptosis resistance in astrocytoma cells.
  • [MeSH-major] Apoptosis. Astrocytoma / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Group II Phospholipases A2 / metabolism. Inflammation Mediators / metabolism. MAP Kinase Signaling System. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cyclooxygenase 2 / biosynthesis. Cyclooxygenase 2 / genetics. Enzyme Induction / drug effects. Enzyme Induction / genetics. Humans. Inflammation / genetics. Inflammation / metabolism. Phosphorylation / drug effects. Phosphorylation / genetics. Protein Structure, Tertiary / genetics. Receptors, Tumor Necrosis Factor, Type I / genetics. Receptors, Tumor Necrosis Factor, Type I / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19850087.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.1.4 / Group II Phospholipases A2
  •  go-up   go-down


77. Stathopoulos A, Melas C, Attali B, Blum D, Levivier M, Brotchi J, Velu T, Tenenbaum L: Overexpression of mouse IsK protein fused to green fluorescent protein induces apoptosis of human astroglioma cells. Neurol Res; 2007 Sep;29(6):628-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of mouse IsK protein fused to green fluorescent protein induces apoptosis of human astroglioma cells.
  • [MeSH-major] Apoptosis / physiology. Astrocytoma / pathology. Gene Expression / physiology. Green Fluorescent Proteins / metabolism. Potassium Channels, Voltage-Gated / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Time Factors. Transfection / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17535562.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Kcne1 protein, mouse; 0 / Potassium Channels, Voltage-Gated; 147336-22-9 / Green Fluorescent Proteins
  •  go-up   go-down


78. Ritch PS, Carroll SL, Sontheimer H: Neuregulin-1 enhances survival of human astrocytic glioma cells. Glia; 2005 Aug 15;51(3):217-28
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] Neuregulin-1 enhances survival of human astrocytic glioma cells.
  • Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.
  • In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.
  • Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.
  • We then verify receptor expression in a panel of human glioma cell lines.
  • Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.
  • Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.
  • Moreover, Nrg-1beta activates an inhibitor of apoptosis, Akt, implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas.
  • This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 .
  • 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
  • [Cites] Oncogene. 1992 Sep;7(9):1859-66 [1354348.001]
  • [Cites] Neurosurgery. 1993 Jul;33(1):106-15 [7689190.001]
  • [Cites] Mol Cell Biol. 1994 Jan;14(1):492-500 [8264617.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 1;91(3):1064-8 [8302832.001]
  • [Cites] Mol Cell Biol. 1994 Mar;14(3):1909-19 [7509448.001]
  • [Cites] Mol Cell Biol. 1994 Jun;14(6):3550-8 [7515147.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9387-91 [7937775.001]
  • [Cites] Biochim Biophys Acta. 1994 Dec 30;1198(2-3):165-84 [7819273.001]
  • [Cites] Oncogene. 1995 Apr 6;10(7):1403-11 [7731691.001]
  • [Cites] J Cell Biol. 1995 Jul;130(1):127-35 [7540614.001]
  • [Cites] J Biol Chem. 1995 Aug 11;270(32):19188-96 [7642587.001]
  • [Cites] Neuron. 1996 Aug;17(2):229-43 [8780647.001]
  • [Cites] Mol Cell Neurosci. 1996 Apr;7(4):247-62 [8793861.001]
  • [Cites] EMBO J. 1997 Apr 1;16(7):1647-55 [9130710.001]
  • [Cites] Nature. 1997 May 29;387(6632):509-12 [9168114.001]
  • [Cites] Nature. 1997 May 29;387(6632):512-6 [9168115.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):4007-14 [9199335.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9562-7 [9275162.001]
  • [Cites] J Neurochem. 1997 Nov;69(5):1859-63 [9349528.001]
  • [Cites] J Neurosci Res. 1997 Dec 1;50(5):755-68 [9418963.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):193-209 [9440020.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):223-48 [9440022.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):335-46 [9440030.001]
  • [Cites] Genes Dev. 1998 Jun 15;12(12):1825-36 [9637684.001]
  • [Cites] Biochem J. 1998 Aug 1;333 ( Pt 3):757-63 [9677338.001]
  • [Cites] Biochem J. 1998 Oct 1;335 ( Pt 1):1-13 [9742206.001]
  • [Cites] Can J Neurol Sci. 1998 Nov;25(4):267-81 [9827227.001]
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3675-85 [9851974.001]
  • [Cites] Eur J Neurosci. 1999 Mar;11(3):769-80 [10103071.001]
  • [Cites] Mol Cell Neurosci. 1999 Feb;13(2):79-94 [10192767.001]
  • [Cites] Oncogene. 1999 Apr 29;18(17):2681-9 [10348342.001]
  • [Cites] EMBO J. 1994 Jun 15;13(12):2831-41 [8026468.001]
  • [Cites] Adv Cancer Res. 2000;77:25-79 [10549355.001]
  • [Cites] Glia. 2000 Jan 15;29(2):104-11 [10625327.001]
  • [Cites] Toxicol Pathol. 2000 Jan-Feb;28(1):171-7 [10669005.001]
  • [Cites] Biochem J. 2000 Mar 15;346 Pt 3:561-76 [10698680.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3159-67 [10880430.001]
  • [Cites] J Neurosci. 2000 Oct 15;20(20):7622-30 [11027222.001]
  • [Cites] Bioessays. 2000 Nov;22(11):987-96 [11056475.001]
  • [Cites] Brain Res Dev Brain Res. 2000 Nov 30;124(1-2):93-9 [11113516.001]
  • [Cites] Annu Rev Neurosci. 2001;24:385-428 [11283316.001]
  • [Cites] Neuro Oncol. 2000 Apr;2(2):96-102 [11303626.001]
  • [Cites] Mol Cell Neurosci. 2001 Apr;17(4):761-7 [11312610.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2841-51 [11042203.001]
  • [Cites] J Biol Chem. 2001 Mar 9;276(10):7320-6 [11058599.001]
  • [Cites] Curr Opin Neurobiol. 2001 Jun;11(3):287-96 [11399426.001]
  • [Cites] J Neurooncol. 2001 Feb;51(3):245-64 [11407596.001]
  • [Cites] J Neurosci. 2001 Jul 1;21(13):4740-51 [11425901.001]
  • [Cites] Genes Dev. 2001 Aug 1;15(15):1913-25 [11485986.001]
  • [Cites] Curr Opin Neurol. 2001 Dec;14(6):683-8 [11723374.001]
  • [Cites] Fed Proc. 1983 Jun;42(9):2627-9 [6852276.001]
  • [Cites] Nature. 1985 Jan 10-18;313(5998):144-7 [2981413.001]
  • [Cites] Cell. 1985 Jul;41(3):697-706 [2860972.001]
  • [Cites] Science. 1985 Dec 6;230(4730):1132-9 [2999974.001]
  • [Cites] Cell. 1986 Jun 6;45(5):649-57 [2871941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903 [3477813.001]
  • [Cites] Cancer Res. 1988 Jul 15;48(14):3910-8 [2454731.001]
  • [Cites] Science. 1989 May 12;244(4905):707-12 [2470152.001]
  • [Cites] Neurosurgery. 1989 Nov;25(5):681-94 [2685640.001]
  • [Cites] J Neurosurg. 1991 Aug;75(2):284-93 [1649272.001]
  • [Cites] Ann N Y Acad Sci. 1991;633:35-47 [1789559.001]
  • [Cites] Cell. 1992 Apr 3;69(1):205-16 [1348215.001]
  • [Cites] J Neurosci Res. 1992 Jan;31(1):175-87 [1377283.001]
  • (PMID = 15812817.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247-010003; United States / NINDS NIH HHS / NS / R01 NS036692-05A1; United States / NCI NIH HHS / CA / CA097247-010003; United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50CA97247; United States / NINDS NIH HHS / NS / NS036692-05A1; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01-NS36692; United States / NINDS NIH HHS / NS / R01 NS036692-06; United States / NINDS NIH HHS / NS / NS036692-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuregulin-1; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS25075; NLM/ PMC2548407
  •  go-up   go-down


79. Shostak KO, Dmitrenko VV, Vudmaska MI, Naidenov VG, Beletskii AV, Malisheva TA, Semenova VM, Zozulya YP, Demotes-Mainard J, Kavsan VM: Patterns of expression of TSC-22 protein in astrocytic gliomas. Exp Oncol; 2005 Dec;27(4):314-8
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of expression of TSC-22 protein in astrocytic gliomas.
  • AIM: To evaluate expression patterns of protein product of putative tumor suppressor gene TSC-22 in human astrocytic tumors by immunohistochemical approach.
  • Immunohistochemical analysis of TSC-22 and GFAP expression with the use of anti-human-TSC-22- and anti-human-GFAP-antibodies was performed on histological slides of astrocytic tumors.
  • RESULTS: Immunohistochemical analysis has shown that the number of cells expressing TSC-22 was significantly lower in glioblastoma tissues than that in diffuse astrocytoma.
  • Double immunohistochemical staining of astrocytic tumors using anti-human-TSC-2- and anti-human-GFAP-antibodies showed that both TSC-22 and GFAP expression is co-localized in astrocytes.
  • In more aggressive forms of astrocytic tumors decreased expression of TSC-22 mRNA correlates with its lowered expression on protein level.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Repressor Proteins / biosynthesis
  • [MeSH-minor] Amino Acid Sequence. Astrocytes / metabolism. Base Sequence. Biomarkers, Tumor / analysis. Gene Expression Profiling. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Microglia / metabolism. Molecular Sequence Data. Recombinant Proteins / biosynthesis. Recombinant Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16404353.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / TSC22D1 protein, human
  •  go-up   go-down


80. Khan MA, Hashmi S: Low-grade astrocytoma causing calvarial scalloping. Pediatr Neurosurg; 2007;43(2):155-7
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-grade astrocytoma causing calvarial scalloping.
  • Gliomas are tumors of the white matter.
  • Only 1 case of low-grade astrocytoma causing calvarial erosion has been reported in the literature of the CT era.
  • We report the first case of a low-grade astrocytoma causing calvarial erosion in an adolescent.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / surgery. Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Osteolysis / pathology. Osteolysis / surgery. Parietal Lobe / pathology. Parietal Lobe / surgery. Skull / pathology. Skull / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 17337932.001).
  • [ISSN] 1016-2291
  • [Journal-full-title] Pediatric neurosurgery
  • [ISO-abbreviation] Pediatr Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


81. Arjona D, Bello MJ, Alonso ME, Aminoso C, Isla A, De Campos JM, Sarasa JL, Gutierrez M, Villalobo A, Rey JA: Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations. Neuropathol Appl Neurobiol; 2005 Aug;31(4):384-94
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] Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations.
  • This report investigates the presence of mutations, amplification and/or over-expression of the EGFR gene in 86 glial tumours including 44 glioblastomas, 21 anaplastic astrocytomas, and 21 WHO grade II astrocytomas, using polymerase chain reaction/single-strand conformation polymorphism, semiquantitative reverse-transcription-polymerase chain reaction (RT-PCR) and Southern Blot techniques.
  • These findings corroborate that EGFR is non-randomly involved in malignant glioma development and that different mutant forms participate in aberrant activation of tyrosine kinase pathways.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Epidermal Growth Factor / genetics. Gene Amplification

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 = 16008822.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 62229-50-9 / Epidermal Growth Factor
  •  go-up   go-down


82. Kwon CH, Zhao D, Chen J, Alcantara S, Li Y, Burns DK, Mason RP, Lee EY, Wu H, Parada LF: Pten haploinsufficiency accelerates formation of high-grade astrocytomas. Cancer Res; 2008 May 1;68(9):3286-94
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] Pten haploinsufficiency accelerates formation of high-grade astrocytomas.
  • We previously reported that central nervous system (CNS) inactivation of Nf1 and p53 tumor suppressor genes in mice results in the development of low-grade to high-grade progressive astrocytomas.
  • When the tumors achieve high grade, they are frequently accompanied by Akt activation, reminiscent of the frequent association of PTEN mutations in human high-grade glioma.
  • In the present study, we introduced CNS heterozygosity of Pten into the Nf1/p53 astrocytoma model.
  • Resulting mice had accelerated morbidity, shortened survival, and full penetrance of high-grade astrocytomas.
  • Haploinsufficiency of Pten accelerated formation of grade 3 astrocytomas, whereas loss of Pten heterozygosity and Akt activation coincided with progression into grade 4 tumors.
  • These data suggest that successive loss of each Pten allele may contribute to de novo formation of high-grade astrocytoma and progression into glioblastoma, respectively, thus providing insight into the etiology of primary glioblastoma.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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
  • [Cites] Brain Res Mol Brain Res. 1997 Apr;45(1):90-8 [9105674.001]
  • [Cites] J Biol Chem. 1997 Jan 31;272(5):2927-35 [9006938.001]
  • [Cites] Lab Invest. 1998 Feb;78(2):165-74 [9484714.001]
  • [Cites] J Biol Chem. 1998 May 29;273(22):13375-8 [9593664.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):348-55 [9697695.001]
  • [Cites] Cell. 1998 Oct 2;95(1):29-39 [9778245.001]
  • [Cites] Curr Biol. 1998 Oct 22;8(21):1169-78 [9799734.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1563-8 [9990064.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4240-5 [10200246.001]
  • [Cites] Cell. 1999 Jun 11;97(6):703-16 [10380923.001]
  • [Cites] Neuron. 1999 Jun;23(2):257-71 [10399933.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7773-9 [15520182.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2065-9 [15781613.001]
  • [Cites] J Neurosci. 2005 Apr 13;25(15):3774-86 [15829629.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5172-80 [15958561.001]
  • [Cites] Neoplasia. 2005 Apr;7(4):356-68 [15967113.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Jun;64(6):479-89 [15977639.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):1929-39 [16488991.001]
  • [Cites] Genesis. 2006 Mar;44(3):130-5 [16496331.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]
  • [Cites] Neuron. 2006 May 4;50(3):377-88 [16675393.001]
  • [Cites] J Neurosci. 2006 Jul 26;26(30):7907-18 [16870736.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7429-37 [16885338.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7473-81 [16885344.001]
  • [Cites] J Natl Cancer Inst. 1999 Nov 17;91(22):1922-32 [10564676.001]
  • [Cites] Science. 2000 Feb 25;287(5457):1433-8 [10688783.001]
  • [Cites] Nat Genet. 2000 May;25(1):55-7 [10802656.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):109-13 [10973261.001]
  • [Cites] Exp Cell Res. 2001 Mar 10;264(1):19-28 [11237520.001]
  • [Cites] Nat Rev Neurosci. 2001 Apr;2(4):287-93 [11283751.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3826-36 [11325859.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1311-33 [11390353.001]
  • [Cites] Genesis. 2001 Oct;31(2):85-94 [11668683.001]
  • [Cites] Science. 2001 Dec 7;294(5549):2186-9 [11691952.001]
  • [Cites] Cell. 2002 Apr 5;109(1):75-86 [11955448.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):157-68 [12086874.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):616-26 [12154354.001]
  • [Cites] Glia. 2002 Sep;39(3):193-206 [12203386.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5551-8 [12359767.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):117-30 [12620407.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5821-8 [14522905.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3525-32 [15150107.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178.001]
  • [Cites] Hum Mol Genet. 1993 Oct;2(10):1687-90 [8268922.001]
  • [Cites] Curr Biol. 1994 Jan 1;4(1):1-7 [7922305.001]
  • [Cites] Science. 1997 May 2;276(5313):791-4 [9115203.001]
  • (PMID = 18451155.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P41 RR002584; United States / NINDS NIH HHS / NS / R37 NS033199-10; United States / NINDS NIH HHS / NS / P50 NS052606-05; None / None / / U24 CA126608-01; United States / NCI NIH HHS / CA / U24CA126608; United States / NINDS NIH HHS / NS / NS033199-10; United States / NINDS NIH HHS / NS / NS052606-05; United States / NCRR NIH HHS / RR / P41-RR02584; United States / NINDS NIH HHS / NS / R37NS33199; United States / NCI NIH HHS / CA / U24 CA126608; United States / NINDS NIH HHS / NS / R37 NS033199; United States / NINDS NIH HHS / NS / P50 NS052606; United States / NCI NIH HHS / CA / U24 CA126608-01
  • [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] EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ NIHMS149010; NLM/ PMC2760841
  •  go-up   go-down


83. Mohyeldin A, Dalgard CL, Lu H, Mcfate T, Tait AS, Patel VC, Wong K, Rushing E, Roy S, Acs G, Verma A: Survival and invasiveness of astrocytomas promoted by erythropoietin. J Neurosurg; 2007 Feb;106(2):338-50
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival and invasiveness of astrocytomas promoted by erythropoietin.
  • Since hypoxia has been implicated in the malignant progression of some human cancers, the authors investigated whether EPO signaling influenced the malignant properties of human astrocytoma cells.
  • Expression of both EPO and EPOR was observed in the hypoxic regions and invasive margins of glioma specimens obtained at biopsy, and expression of EPOR correlated with the stage of the tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Erythropoietin / physiology. Glioma / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Hypoxia / physiology. Cell Line, Tumor. Cisplatin / therapeutic use. Epoetin Alfa. Hematinics / therapeutic use. Humans. Neoplasm Invasiveness. Rats. Rats, Wistar. Receptors, Erythropoietin / metabolism. Recombinant Proteins. Signal Transduction / physiology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. EPOETIN ALFA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Neurosurg. 2007 Feb;106(2):337; discussion 337 [17410720.001]
  • (PMID = 17410721.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS37814
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hematinics; 0 / Receptors, Erythropoietin; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 64FS3BFH5W / Epoetin Alfa; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


84. Andrychowski J, Taraszewska A, Czernicki Z, Jurkiewicz J, Netczuk T, Dabrowski P: Ten years observation and treatment of multifocal pilocytic astrocytoma. Folia Neuropathol; 2009;47(4):362-70
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ten years observation and treatment of multifocal pilocytic astrocytoma.
  • Pilocytic astrocytoma (PA) usually occurs in younger patients.
  • It is a benign, generally well-delineated, WHO grade I tumour with favorable prognosis, which makes it different from diffuse astrocytomas, classified as higher grades of malignancy.
  • The initial symptom of the disease was epileptic seizure at the age of 16.
  • Initially, the histopathological diagnosis of ganglioglioma was suggested for primary tumour, finally the diagnosis of pilocytic astrocytoma for both recurrent and primary tumour was established.
  • Histopathological examinations of the excised foci from spinal canal revealed neoplasm consistent with WHO grade I pilocytic astrocytoma.
  • It is a rare clinical manifestation of a disease ever described in the literature.

  • Genetic Alliance. consumer health - Pilocytic astrocytoma.
  • Genetic Alliance. consumer health - TEN.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20054789.001).
  • [ISSN] 1509-572X
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


85. Watanabe T, Vital A, Nobusawa S, Kleihues P, Ohgaki H: Selective acquisition of IDH1 R132C mutations in astrocytomas associated with Li-Fraumeni syndrome. Acta Neuropathol; 2009 Jun;117(6):653-6
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] Selective acquisition of IDH1 R132C mutations in astrocytomas associated with Li-Fraumeni syndrome.
  • Mutations of the IDH1 gene are frequent in gliomas, with R132H (CGT-->CAT) being the most common (>85%).
  • In astrocytomas, IDH1 mutations are typically co-present with, or precede, TP53 mutations.
  • We identified IDH1 mutations in five astrocytomas that developed in carriers of a TP53 germline mutation.
  • Without exception, all were R132C (CGT-->TGT), which in sporadic astrocytomas accounts for <5% of IDH1 mutations.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, p53. Isocitrate Dehydrogenase / genetics. Li-Fraumeni Syndrome / genetics

  • Genetic Alliance. consumer health - Li Fraumeni syndrome.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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
  • (PMID = 19340432.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
  •  go-up   go-down


86. Kim JH, Choi C, Benveniste EN, Kwon D: TRAIL induces MMP-9 expression via ERK activation in human astrocytoma cells. Biochem Biophys Res Commun; 2008 Dec 5;377(1):195-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TRAIL induces MMP-9 expression via ERK activation in human astrocytoma cells.
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as the death ligand, which induces preferential apoptosis of transformed tumor cells.
  • We demonstrated that TRAIL induces MMP-9 expression in human astrocytoma cells, which is preceded by activation of extracellular signal-regulated protein kinase (ERK).
  • These findings indicate that TRAIL treatment in human astrocytoma cells leads to the activation of NF-kappaB and subsequent expression of MMP-9, which are dependent on ERK activation.
  • Collectively, these results suggest that TRAIL has alternative biological functions in addition to its role in inducing apoptosis in human malignant astrocytoma cells.
  • [MeSH-major] Astrocytoma / enzymology. Extracellular Signal-Regulated MAP Kinases / metabolism. Matrix Metalloproteinase 9 / biosynthesis. TNF-Related Apoptosis-Inducing Ligand / physiology
  • [MeSH-minor] Butadienes / pharmacology. Cell Line, Tumor. Enzyme Activation. Humans. NF-kappa B / metabolism. Nitriles / pharmacology. Protein Kinase Inhibitors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18834856.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butadienes; 0 / NF-kappa B; 0 / Nitriles; 0 / Protein Kinase Inhibitors; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / U 0126; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


87. Kawai H, Ishikawa T, Moroi J, Hanyu N, Sawada M, Kobayashi N, Mutou T, Hikichi K, Suzuki A, Yasui N, Yoshida Y: [Elderly patient with cerebellar malignant astrocytoma]. No Shinkei Geka; 2008 Sep;36(9):799-805
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] [Elderly patient with cerebellar malignant astrocytoma].
  • Malignant cerebellar astrocytoma is very rare and the prognosis is extremely poor.
  • We report herein the case of an elderly patient with malignant cerebellar astrocytoma.
  • Metastatic cerebellar tumor was diagnosed on first admission, based on a past history of colon cancer treated by surgery and magnetic resonance imaging (MRI) findings supporting the diagnosis of metastasis.
  • The tumor represented malignant astrocytoma.
  • [MeSH-major] Astrocytoma / surgery. Cerebellar Neoplasms / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18800635.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 19
  •  go-up   go-down


88. Hwang SL, Lin CL, Lieu AS, Hwang YF, Howng SL, Hong YR, Chang DS, Lee KS: The expression of thyroid hormone receptor isoforms in human astrocytomas. Surg Neurol; 2008 Dec;70 Suppl 1:S1:4-8; discussion S1:8
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of thyroid hormone receptor isoforms in human astrocytomas.
  • However, little was studied about the expression of TR isoforms in human astrocytomas.
  • METHODS: In this study, RT-PCR was used to examine the expression of human TR isoforms in 34 human astrocytoma samples.
  • However, the frequency of TRbeta1 expression significantly increased with the grades of malignancy astrocytomas (P=.017).
  • CONCLUSIONS: Our study demonstrated for the first time that TR isoforms are indeed expressed in human astrocytomas.
  • The expression of TR isoforms is correlated to the malignancy grading of astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Receptors, Thyroid Hormone / biosynthesis

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18617237.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Thyroid Hormone; 0 / Thyroid Hormone Receptors alpha; 0 / Thyroid Hormone Receptors beta; 63231-63-0 / RNA
  •  go-up   go-down


89. Christensen K, Schrøder HD, Kristensen BW: CD133 identifies perivascular niches in grade II-IV astrocytomas. J Neurooncol; 2008 Nov;90(2):157-70
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD133 identifies perivascular niches in grade II-IV astrocytomas.
  • The aim of the present study was to investigate the localization and distribution of the putative brain tumour stem cell marker CD133 in formalin fixed paraffin embedded astrocytomas.
  • A retrospective analysis of 114 grade II, III and IV astrocytomas was undertaken.
  • However, the volume fraction of CD133(+) blood vessels increased significantly from 0.4% in diffuse astrocytomas to 2.2% in glioblastomas.
  • In conclusion, a CD133(+) perivascular stem cell-like entity exists in astrocytomas.
  • [MeSH-major] Antigens, CD / metabolism. Astrocytoma / pathology. Brain Neoplasms / pathology. Endothelium, Vascular / metabolism. Glycoproteins / metabolism. Peptides / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18612800.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Indoles; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Peptides; 47165-04-8 / DAPI; EC 6.3.2.19 / MIB1 ligase, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


90. Arrieta O, Pineda-Olvera B, Guevara-Salazar P, Hernández-Pedro N, Morales-Espinosa D, Cerón-Lizarraga TL, González-De la Rosa CH, Rembao D, Segura-Pacheco B, Sotelo J: Expression of AT1 and AT2 angiotensin receptors in astrocytomas is associated with poor prognosis. Br J Cancer; 2008 Jul 8;99(1):160-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of AT1 and AT2 angiotensin receptors in astrocytomas is associated with poor prognosis.
  • Astrocytomas develop intense vascular proliferation, essential for tumour growth and invasiveness.
  • We studied 133 tumours from patients with diagnosis of astrocytoma who underwent surgery from 1997 to 2002.
  • Ten per cent of low-grade astrocytomas were positive for AT1, whereas grade III and IV astrocytomas were positive in 67% (P<0.001).
  • AT2 receptors were positive in 17% of low-grade astrocytomas and in 53% of high-grade astrocytomas (P=0.01).
  • These findings suggest that ANGII receptors might be potential therapeutic targets for high-grade astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Receptor, Angiotensin, Type 1 / biosynthesis. Receptor, Angiotensin, Type 2 / biosynthesis

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Cancer. 2001 Nov 2;85(9):1396-9 [11720480.001]
  • [Cites] Lab Invest. 2007 Feb;87(2):189-98 [17318197.001]
  • [Cites] Diabetologia. 2002 Jun;45(6):890-8 [12107734.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3210-8 [12115353.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4176-9 [12154013.001]
  • [Cites] Glia. 2002 Sep;39(3):304-13 [12203396.001]
  • [Cites] Braz J Med Biol Res. 2002 Sep;35(9):1001-15 [12219172.001]
  • [Cites] J Mol Cell Cardiol. 2002 Nov;34(11):1525-37 [12431451.001]
  • [Cites] Can J Physiol Pharmacol. 2003 Feb;81(2):142-9 [12710528.001]
  • [Cites] J Clin Invest. 2003 Jul;112(1):67-75 [12840060.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Aug;88(8):3973-82 [12915695.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6613-25 [14583454.001]
  • [Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):228-33 [14734474.001]
  • [Cites] J Biol Chem. 2004 Feb 27;279(9):7901-8 [14645236.001]
  • [Cites] Br J Cancer. 2004 Mar 8;90(5):1059-68 [14997208.001]
  • [Cites] Curr Vasc Pharmacol. 2004 Oct;2(4):385-99 [15320819.001]
  • [Cites] Annu Rev Physiol. 1984;46:17-31 [6324655.001]
  • [Cites] J Lab Clin Med. 1985 Feb;105(2):141-5 [2579174.001]
  • [Cites] Am J Clin Pathol. 1988 Oct;90(4):437-41 [2459955.001]
  • [Cites] Eur J Pharmacol. 1991 Mar 26;195(2):305-6 [1874278.001]
  • [Cites] Adv Exp Med Biol. 1995;377:435-40 [7484446.001]
  • [Cites] Int J Microcirc Clin Exp. 1996 Nov-Dec;16(6):302-7 [9049708.001]
  • [Cites] Annu Rev Physiol. 1997;59:395-412 [9074770.001]
  • [Cites] Endocrinology. 1998 Jan;139(1):365-75 [9421435.001]
  • [Cites] Circ Res. 1998 Mar 23;82(5):619-28 [9529167.001]
  • [Cites] Biochim Biophys Acta. 1998 Feb 4;1401(2):187-94 [9531974.001]
  • [Cites] Int J Cancer. 1999 Feb 19;84(1):10-8 [9988225.001]
  • [Cites] Int J Mol Med. 1999 May;3(5):531-6 [10202187.001]
  • [Cites] Hypertension. 1999 Jul;34(1):126-31 [10406835.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2045-52 [15284177.001]
  • [Cites] Carcinogenesis. 2005 Feb;26(2):271-9 [15637093.001]
  • [Cites] Br J Cancer. 2005 Apr 11;92(7):1247-52 [15785746.001]
  • [Cites] Trends Endocrinol Metab. 2005 Sep;16(7):293-9 [16061390.001]
  • [Cites] Hypertension. 1999 Nov;34(5):1053-9 [10567181.001]
  • [Cites] Surg Neurol. 2000 Feb;53(2):157-62 [10713194.001]
  • [Cites] Mol Cell Biochem. 2000 Sep;212(1-2):183-6 [11108150.001]
  • [Cites] Mol Biol Cell. 2001 Feb;12(2):449-62 [11179427.001]
  • [Cites] Diabetes. 2001 Apr;50(4):867-75 [11289054.001]
  • [Cites] FEBS Lett. 2001 Apr 27;495(3):197-200 [11334891.001]
  • [Cites] Am J Pathol. 2001 May;158(5):1633-7 [11337361.001]
  • [Cites] Acta Neurochir (Wien). 2001;143(2):159-66 [11459088.001]
  • [Cites] Glia. 2001 Aug;35(2):131-46 [11460269.001]
  • [Cites] Am J Cardiol. 2001 Nov 8;88(9A):1L-20L [11694220.001]
  • [Cites] Endocrinology. 1992 Jun;130(6):3641-9 [1597161.001]
  • [Cites] J Clin Invest. 1994 Jun;93(6):2431-7 [8200978.001]
  • [Cites] Eur J Pharmacol. 1994 Sep 15;269(1):115-9 [7828653.001]
  • [Cites] J Clin Invest. 1995 Feb;95(2):651-7 [7860748.001]
  • [Cites] Trends Pharmacol Sci. 1995 Jul;16(7):223-5 [7667895.001]
  • [Cites] J Neurosurg. 1995 Oct;83(4):682-9 [7674019.001]
  • [Cites] Mol Cancer Ther. 2005 Nov;4(11):1699-709 [16275991.001]
  • [Cites] Br J Cancer. 2006 Feb 27;94(4):552-60 [16434990.001]
  • [Cites] Int J Cancer. 2006 May 1;118(9):2182-9 [16331629.001]
  • [Cites] Ann Intern Med. 2006 Mar 7;144(5):337-43 [16520474.001]
  • [Cites] J Clin Oncol. 2006 Mar 10;24(8):1253-65 [16525180.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2563-9 [16735709.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Sep;59(3):181-93 [16860996.001]
  • [Cites] Lab Invest. 2002 Jun;82(6):747-56 [12065685.001]
  • (PMID = 18594540.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptor, Angiotensin, Type 1; 0 / Receptor, Angiotensin, Type 2
  • [Other-IDs] NLM/ PMC2453037
  •  go-up   go-down


91. Shimizu H, Mori O, Ohaki Y, Kamoi S, Kobayashi S, Okada S, Maeda S, Naito Z: Cytological interface of diffusely infiltrating astrocytoma and its marginal tissue. Brain Tumor Pathol; 2005;22(2):59-74
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytological interface of diffusely infiltrating astrocytoma and its marginal tissue.
  • Cytological differences between infiltrating lesions of the diffusely infiltrating astrocytoma (DIA) and reactive gliosis at its periphery have not yet been established.
  • The cytological findings of this area are important because the surgeon may have to make a rapid diagnosis regarding the existence of the tumor.
  • [MeSH-major] Astrocytoma / pathology. Brain / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Gliosis / pathology
  • [MeSH-minor] Adult. Astrocytes / ultrastructure. Axons / ultrastructure. Biopsy. Carcinoma / secondary. Cell Nucleus / ultrastructure. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Myelin Sheath / ultrastructure. Neoplasm Invasiveness. Neurons / ultrastructure. Oligodendroglia / ultrastructure. Staining and Labeling / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18095107.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


92. Stüer C, Vilz B, Majores M, Becker A, Schramm J, Simon M: Frequent recurrence and progression in pilocytic astrocytoma in adults. Cancer; 2007 Dec 15;110(12):2799-808
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent recurrence and progression in pilocytic astrocytoma in adults.
  • BACKGROUND: Most pilocytic astrocytomas (piloA) are benign growths (World Health Organization [WHO] grade 1) of the deep midline structures, the brainstem, and the cerebellum.
  • METHODS: Between 1995 and 2005, 44 patients (26 women and 18 men) underwent surgery for a primary or recurrent piloA at the authors' institution.
  • RESULTS: There were 20 patients (45%) with supratentorial lobar piloA (including 10 temporal/temporomesial tumors, 5 parietal tumors, 3 insular tumors, 1 frontal tumor, and 1 occipital tumors), 12 patients with cerebellar piloA, 7 patients with brainstem piloA, 2 patients with opticochiasmatic PiloA, 1 patient with intramedullary piloA, and 2 patients with piloA of the basal ganglia.
  • All but 1 patient with a lobar tumor presented with epilepsy.
  • Tumor recurrence or disease progression was observed in 13 of 44 patients (30%).
  • Eight of 44 patients (18%) died from their disease.
  • CONCLUSIONS: PiloA in adult patients, surprisingly, often was not a benign disease.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / radiography. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Disease Progression. Female. Humans. Male. Middle Aged. Prognosis. Recurrence. Treatment Outcome

  • Genetic Alliance. consumer health - Pilocytic astrocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Nat Clin Pract Neurol. 2008 Jun;4(6):296-7 [18414467.001]
  • (PMID = 17973253.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


93. Parsa CF, Givrad S: Juvenile pilocytic astrocytomas do not undergo spontaneous malignant transformation: grounds for designation as hamartomas. Br J Ophthalmol; 2008 Jan;92(1):40-6
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Juvenile pilocytic astrocytomas do not undergo spontaneous malignant transformation: grounds for designation as hamartomas.
  • AIM: To determine whether juvenile pilocytic astrocytomas WHO grade I have the potential for spontaneous malignant transformation.
  • METHODS: A literature search was performed, cross-referencing juvenile pilocytic astrocytoma, pilocytic astrocytoma, astrocytoma grade I, optic glioma, glioma, low-grade gliomas, polar spongioblastoma, gliocytoma embryonale, and malignant transformation, anaplasia or anaplastic change.
  • Twenty-two of these tumours, however, did not initially match criteria for juvenile pilocytic astrocytoma WHO grade I and were excluded.
  • CONCLUSION: Juvenile pilocytic astrocytomas WHO grade I do not undergo spontaneous anaplastic transformation.
  • Earlier clinical and histopathological opinions regarding juvenile pilocytic astrocytomas as hamartomatous lesions are reaffirmed.
  • [MeSH-major] Astrocytoma / pathology. Brain Diseases / pathology. Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Hamartoma / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Progression. Humans. Middle Aged. Neoplasms, Radiation-Induced / etiology. Neoplasms, Second Primary / etiology

  • MedlinePlus Health Information. consumer health - Brain Diseases.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17962395.001).
  • [ISSN] 1468-2079
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
  •  go-up   go-down


94. Zhang H, Wu G, Tu H, Huang F: Discovery of serum biomarkers in astrocytoma by SELDI-TOF MS and proteinchip technology. J Neurooncol; 2007 Sep;84(3):315-23
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discovery of serum biomarkers in astrocytoma by SELDI-TOF MS and proteinchip technology.
  • OBJECTIVE: To discover serum biomarkers in astrocytoma patients for early detection of glioma and evaluation of prognosis.
  • Among those, 73 were sera from astrocytoma patients, 56 from normal controls, and 11 from other brain tumors.
  • RESULTS: Seven serum biomarkers were significantly deregulated in astrocytoma group comparing to the normal control group.
  • A decision tree classification method were developed using these seven markers.
  • A sensitivity of 84.6% and a selectivity of 84.6% were achieved to discriminate astrocytoma from normal controls.
  • In addition, a correlation of these markers with the astrocytoma malignancy was observed.
  • CONCLUSIONS: Proteomics approaches such as SELDI-TOF mass spectrometry could greatly facilitate the discovery of serum biomarkers in astrocytoma.
  • The discovered biomarkers might show great potential for early detection of astrocytoma and evaluation of prognosis for those clinical suspect astrocytoma patients.
  • [MeSH-major] Astrocytoma / blood. Biomarkers, Tumor / blood. Brain Neoplasms / blood. Protein Array Analysis. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17453148.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


95. Malik A, Deb P, Sharma MC, Sarkar C: Neuropathological spectrum of pilocytic astrocytoma: an Indian series of 120 cases. Pathol Oncol Res; 2006;12(3):164-71
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuropathological spectrum of pilocytic astrocytoma: an Indian series of 120 cases.
  • Pilocytic astrocytomas (PAs) are generally well circumscribed, slowly growing, cystic tumors, occurring in the pediatric age group.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology

  • Genetic Alliance. consumer health - Pilocytic astrocytoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16998597.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


96. Nagai S, Kurimoto M, Washiyama K, Hirashima Y, Kumanishi T, Endo S: Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines. J Neurooncol; 2005 Sep;74(2):105-11
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] Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines.
  • In malignant astrocytoma cells, it was reported that NF-kappaB was activated aberrantly and promoted their proliferation.
  • Thus, inhibition of NF-kappaB activity is considered to be a promising therapeutic strategy for malignant astrocytoma.
  • In this study, we investigated inhibitory effects of curcumin on NF-kappaB activity and cellular proliferation, and induction of apoptosis by curcumin in human malignant astrocytoma cell lines.
  • Alteration of NF-kappaB activity in NP-2 human malignant astrocytoma cell line after treatment with curcumin was examined using electrophoretic mobility shift assay.
  • Alterations of DNA synthesis and cellular growth in five human malignant astrocytoma cell lines after treatment with curcumin were examined using [(3)H]thymidine incorporation assay and the trypan blue dye exclusion method, respectively.
  • Induction of apoptosis by curcumin in NP-2 and NP-3 human malignant astrocytoma cell lines was examined by DNA-fragmentation analysis and morphological observation.
  • The DNA synthesis and the cellular growth were inhibited by curcumin in dose-dependent manner in all the five malignant astrocytoma cell lines.
  • These results indicate that curcumin inhibits the cellular proliferation and induces apoptosis in human malignant astrocytoma cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Astrocytoma / drug therapy. Cell Proliferation / drug effects. Curcumin / therapeutic use. NF-kappa B / drug effects
  • [MeSH-minor] Electrophoretic Mobility Shift Assay. Humans. Thymidine / metabolism. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. CURCUMIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16193380.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; IT942ZTH98 / Curcumin; VC2W18DGKR / Thymidine
  •  go-up   go-down


97. Uno M, Oba-Shinjo SM, de Aguiar PH, Leite CC, Rosemberg S, Miura FK, Junior RM, Scaff M, Nagahashi Marie SK: Detection of somatic TP53 splice site mutations in diffuse astrocytomas. Cancer Lett; 2005 Jun 28;224(2):321-7
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] Detection of somatic TP53 splice site mutations in diffuse astrocytomas.
  • Alteration in TP53 is the most common genetic event reported for many tumors, including astrocytomas.
  • TP53 were examined for mutations by polymerase chain reaction, single strand conformation polymorphism and direct sequencing in cases of diffuse astrocytomas.
  • These findings emphasize the importance of thorough screening of TP53 mutations in gliomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, p53. RNA Splice Sites

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15914282.001).
  • [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
  • [Chemical-registry-number] 0 / RNA Splice Sites
  •  go-up   go-down


98. Niranjan R, Nath C, Shukla R: The mechanism of action of MPTP-induced neuroinflammation and its modulation by melatonin in rat astrocytoma cells, C6. Free Radic Res; 2010 Nov;44(11):1304-16
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] The mechanism of action of MPTP-induced neuroinflammation and its modulation by melatonin in rat astrocytoma cells, C6.
  • The 1-methyl-4-phenyl 1,2,3,6 tetrahydropyridine (MPTP) induces reactive astrogliosis, the cellular manifestation of neuroinflammation, in various models of Parkinson's disease (PD), but its mechanism of action on astrocytes is not understood.
  • The present study demonstrated that MPTP treatment of rat astrocytoma cells, C6 for 24 h significantly increased nitrative and oxidative stress and intracellular calcium (Ca2++) level.
  • Study with deprenyl demonstrates that MPTP is inducing neuroinflammation in astrocytoma cells.
  • The present findings elucidated the molecular mechanism of MPTP-induced neuroinflammation and its modulation by melatonin in astrocytoma cells (C6).
  • [MeSH-minor] Animals. Astrocytoma / metabolism. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Gene Expression / drug effects. Immunohistochemistry. NF-kappa B / drug effects. NF-kappa B / metabolism. Oxidative Stress / drug effects. Rats. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction. p38 Mitogen-Activated Protein Kinases / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism

  • Hazardous Substances Data Bank. 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE .
  • Hazardous Substances Data Bank. MELATONIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20815783.001).
  • [ISSN] 1029-2470
  • [Journal-full-title] Free radical research
  • [ISO-abbreviation] Free Radic. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Neurotoxins; 0 / Reactive Oxygen Species; 9P21XSP91P / 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; JL5DK93RCL / Melatonin
  •  go-up   go-down


99. El-Habr EA, Tsiorva P, Theodorou M, Levidou G, Korkolopoulou P, Vretakos G, Petraki L, Michalopoulos NV, Patsouris E, Saetta AA: Analysis of PIK3CA and B-RAF gene mutations in human astrocytomas: association with activation of ERK and AKT. Clin Neuropathol; 2010 Jul-Aug;29(4):239-45
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] Analysis of PIK3CA and B-RAF gene mutations in human astrocytomas: association with activation of ERK and AKT.
  • OBJECTIVE: The analysis of the presence of PIK3CA and B-RAF gene mutations in relation to ERK and AKT activation in diffusely infiltrating astrocytomas, in order to determine their potential role in tumor aggressiveness.
  • Neither low grade astrocytomas nor anaplastic astrocytomas revealed any mutations in these genes.
  • Moreover, pERK nuclear expression increased in parallel with tumor grade (II, III v/s IV, p = 0.0262).
  • pAKT cytoplasmic expression increased with increasing tumor grade (II,III v/s IV, p = 0.0930), although the latter relationship was of marginal significance. pAKT cytoplasmic expression was also positively correlated with pERK nuclear expression (p = 0.0156).
  • CONCLUSIONS: Our study reports the low frequency of PIK3CA and B-RAF mutations in astrocytomas, despite the presence of activated ERK and AKT proteins.
  • Moreover, the correlation of pERK nuclear and pAKT cytoplasmic expression with tumor grade suggests the possible crucial role of the activation of these proteins in human gliomagenesis.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. MAP Kinase Signaling System / physiology. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics. Proto-Oncogene Proteins B-raf / genetics

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20569675.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  •  go-up   go-down


100. Tchaicha JH, Mobley AK, Hossain MG, Aldape KD, McCarty JH: A mosaic mouse model of astrocytoma identifies alphavbeta8 integrin as a negative regulator of tumor angiogenesis. Oncogene; 2010 Aug 5;29(31):4460-72
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] A mosaic mouse model of astrocytoma identifies alphavbeta8 integrin as a negative regulator of tumor angiogenesis.
  • Furthermore, little is known about how cancer cells selectively circumvent the actions of these inhibitors to promote pathological angiogenesis, a requisite event for tumor progression.
  • Using mosaic mouse models of the malignant brain cancer, astrocytoma, we report that tumor cells induce pathological angiogenesis by suppressing expression of the ECM protein receptor alphavbeta8 integrin.
  • Diminished integrin expression in astrocytoma cells leads to reduced activation of latent TGFbetas, resulting in impaired TGFbeta receptor signaling in tumor-associated endothelial cells.
  • These data reveal that astrocytoma cells manipulate their angiogenic balance by selectively suppressing alphavbeta8 integrin expression and function.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • GeneTex Inc. NCBI Redirect Page | Genetex Inc. (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Methods Enzymol. 2006;419:3-23 [17141049.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] J Cell Sci. 2007 May 15;120(Pt 10):1810-7 [17502485.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Jun;8(6):464-78 [17522591.001]
  • [Cites] Glia. 2007 Aug 1;55(10):1023-33 [17549683.001]
  • [Cites] Nat Rev Neurosci. 2007 Aug;8(8):610-22 [17643088.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2683-710 [17974913.001]
  • [Cites] Mech Dev. 2008 May-Jun;125(5-6):508-16 [18343643.001]
  • [Cites] Am J Pathol. 2008 Jun;172(6):1740-7 [18467691.001]
  • [Cites] Cell. 2008 Jul 25;134(2):215-30 [18662538.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1129-33 [18948956.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):45-56 [19111880.001]
  • [Cites] Cancer Res. 2009 Apr 15;69(8):3308-16 [19351861.001]
  • [Cites] Curr Opin Hematol. 2009 May;16(3):209-14 [19318941.001]
  • [Cites] J Cell Sci. 2009 Jun 1;122(Pt 11):1842-51 [19461074.001]
  • [Cites] Cell Adh Migr. 2009 Apr-Jun;3(2):199-204 [19363295.001]
  • [Cites] Cell Adh Migr. 2009 Apr-Jun;3(2):211-5 [19372738.001]
  • [Cites] Nat Rev Cancer. 2010 Jan;10(1):9-22 [20029421.001]
  • [Cites] Oncogene. 2010 Mar 4;29(9):1351-61 [20010874.001]
  • [Cites] Nat Genet. 2000 May;25(1):55-7 [10802656.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14720-5 [11121071.001]
  • [Cites] Cancer Res. 2001 Jul 1;61(13):4956-60 [11431323.001]
  • [Cites] Mol Cell Neurosci. 2001 Jul;18(1):108-18 [11461157.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6674-8 [11559533.001]
  • [Cites] Development. 2002 Jun;129(12):2891-903 [12050137.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):269-77 [12086863.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5551-8 [12359767.001]
  • [Cites] Mol Cell Biol. 2002 Nov;22(21):7667-77 [12370313.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1962-8 [12702589.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2751-8 [15087390.001]
  • [Cites] Anal Biochem. 1994 Feb 1;216(2):276-84 [8179182.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2746-51 [7796398.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8502-7 [8710899.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8761-6 [9238051.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 28;94(22):12081-7 [9342366.001]
  • [Cites] Brain Pathol. 1999 Jul;9(3):469-79 [10416987.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Development. 2005 Jan;132(1):165-76 [15576410.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):229-43 [15674480.001]
  • [Cites] Am J Pathol. 2005 Jun;166(6):1883-94 [15920172.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13479-83 [16157875.001]
  • [Cites] Curr Top Dev Biol. 2005;69:67-99 [16243597.001]
  • [Cites] Am J Pathol. 2005 Nov;167(5):1379-87 [16251422.001]
  • [Cites] J Neurosci. 2005 Oct 26;25(43):9940-8 [16251442.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7843-8 [16912155.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):106-10 [17122772.001]
  • (PMID = 20531304.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NINDS NIH HHS / NS / R01 NS059876-03; United States / NINDS NIH HHS / NS / R01NS059876; United States / NCI NIH HHS / CA / P50CA127001; United States / NINDS NIH HHS / NS / R01 NS059876-02S2; United States / NINDS NIH HHS / NS / R01 NS059876; United States / NCI NIH HHS / CA / P50 CA127001; United States / NINDS NIH HHS / NS / NS059876-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrins; 0 / integrin alphavbeta8
  • [Other-IDs] NLM/ NIHMS198457; NLM/ PMC3037767
  •  go-up   go-down






Advertisement