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1. Furnari FB, Fenton T, Bachoo RM, Mukasa A, Stommel JM, Stegh A, Hahn WC, Ligon KL, Louis DN, Brennan C, Chin L, DePinho RA, Cavenee WK: Malignant astrocytic glioma: genetics, biology, and paths to treatment. Genes Dev; 2007 Nov 1;21(21):2683-710
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant astrocytic glioma: genetics, biology, and paths to treatment.
  • Malignant astrocytic gliomas such as glioblastoma are the most common and lethal intracranial tumors.
  • This progress is fueling new opportunities for understanding the fundamental basis for development of this devastating disease and also novel therapies that, for the first time, portend meaningful clinical responses.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Brain Neoplasms / therapy
  • [MeSH-minor] Animals. Animals, Genetically Modified. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Models, Animal. Gene Regulatory Networks. Humans. Models, Biological. Necrosis / chemically induced. Neoplasm Invasiveness. Neoplasm Staging. Neovascularization, Pathologic / drug therapy

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  • (PMID = 17974913.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099041; United States / NCI NIH HHS / CA / CA95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 306
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2. Blough MD, Zlatescu MC, Cairncross JG: O6-methylguanine-DNA methyltransferase regulation by p53 in astrocytic cells. Cancer Res; 2007 Jan 15;67(2):580-4
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  • [Title] O6-methylguanine-DNA methyltransferase regulation by p53 in astrocytic cells.
  • In this study, we tested the hypothesis that MGMT is regulated by p53 in astrocytic cells, the precursors of which may give rise to glioblastoma. p53 is of interest because, in addition to often being mutated in glioblastoma, inactivation sensitizes some astrocytoma cell lines to temozolomide.
  • MGMT expression was examined in neonatal murine astrocytes and SF767 human astrocytic glioma cells following p53 inactivation by knockout (murine only) or RNAi methods.
  • In SF767 human astrocytic glioma cells, transient knockdown of p53 led to the down-regulation of MGMT gene expression.
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA Methylation. Gene Silencing. Glioma / enzymology. Glioma / genetics. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. Promoter Regions, Genetic

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  • (PMID = 17234766.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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3. Ritch PS, Carroll SL, Sontheimer H: Neuregulin-1 enhances survival of human astrocytic glioma cells. Glia; 2005 Aug 15;51(3):217-28
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  • [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.

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  • (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
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4. 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.

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  • (PMID = 28184642.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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5. Ernst A, Hofmann S, Ahmadi R, Becker N, Korshunov A, Engel F, Hartmann C, Felsberg J, Sabel M, Peterziel H, Durchdewald M, Hess J, Barbus S, Campos B, Starzinski-Powitz A, Unterberg A, Reifenberger G, Lichter P, Herold-Mende C, Radlwimmer B: Genomic and expression profiling of glioblastoma stem cell-like spheroid cultures identifies novel tumor-relevant genes associated with survival. Clin Cancer Res; 2009 Nov 1;15(21):6541-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic and expression profiling of glioblastoma stem cell-like spheroid cultures identifies novel tumor-relevant genes associated with survival.
  • PURPOSE: Glioblastoma spheroid cultures are enriched in tumor stem-like cells and therefore may be more representative of the respective primary tumors than conventional monolayer cultures.
  • We exploited the glioma spheroid culture model to find novel tumor-relevant genes.
  • Microarray-based gene expression analysis was applied to determine genes with differential expression compared with normal brain tissue and to nonneoplastic brain spheroids in glioma spheroid cultures.
  • Immunohistochemistry on tissue microarrays revealed that expression of AJAP1, EMP3, and PDPN was significantly associated with overall survival of astrocytic glioma patients.
  • CONCLUSION: We identified a set of novel candidate genes that likely play a role in glioblastoma pathogenesis and implicate AJAP1, EMP3, and PDPN as molecular markers associated with the clinical outcome of glioma patients.
  • [MeSH-minor] Biomarkers, Tumor. Brain / metabolism. Cell Culture Techniques. Humans. Oligonucleotide Array Sequence Analysis. Tumor Cells, Cultured

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  • (PMID = 19861460.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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6. Lefranc F, Rynkowski M, DeWitte O, Kiss R: Present and potential future adjuvant issues in high-grade astrocytic glioma treatment. Adv Tech Stand Neurosurg; 2009;34:3-35
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  • [Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.
  • Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.
  • Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.
  • Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.
  • Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.
  • Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.
  • Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells.
  • The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy


7. Xu GW, Mymryk JS, Cairncross JG: Pharmaceutical-mediated inactivation of p53 sensitizes U87MG glioma cells to BCNU and temozolomide. Int J Cancer; 2005 Aug 20;116(2):187-92
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  • [Title] Pharmaceutical-mediated inactivation of p53 sensitizes U87MG glioma cells to BCNU and temozolomide.
  • We examined the effect of PFTalpha on the chemosensitivity of a human cancer in which cell cycle arrest, not apoptosis, is the principle cellular consequence of p53 activation.
  • This was of interest because E6 silencing of p53 sensitizes U87MG astrocytic glioma cells to BCNU and temozolomide (TMZ), cytotoxic drugs that are modestly helpful in the treatment of aggressive astrocytic gliomas.
  • Our findings suggest that in addition to protecting normal cells from the toxic effects of radiation and chemotherapy, small molecule inhibitors of p53, like PFTalpha, might play a role in clinical oncology by sensitizing certain resistant cancers to cytotoxic chemotherapies.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Brain Neoplasms / pathology. Carmustine / pharmacology. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Glioma / pathology. Thiazoles / pharmacology. Toluene / analogs & derivatives. Toluene / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Benzothiazoles. DNA Damage. Drug Interactions. Humans. Tumor Cells, Cultured

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15800902.001).
  • [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 / Antineoplastic Agents, Alkylating; 0 / Benzothiazoles; 0 / Thiazoles; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 3FPU23BG52 / Toluene; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; U68WG3173Y / Carmustine
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8. Xu GW, Mymryk JS, Cairncross JG: Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin. J Neurooncol; 2005 Sep;74(2):141-9
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  • [Title] Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin.
  • p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.
  • In this report, we examined the effect of p53 inactivation on the chemosensitivity of two additional human astrocytic glioma cell lines, D54 and A172, in order to assess whether sensitization is a general property of astrocytic tumor cells.
  • Sensitization to both BCNU and TMZ was associated with failure of p21(WAF1) induction, lack of a sustained G2 cell cycle arrest and significant tumor cell death.
  • These findings suggest that enhanced sensitivity to BCNU and TMZ is a general property of human astrocytic glioma cells in which p53 was disrupted.
  • In contrast, p53 inactivation rendered D54 and U87MG cells significantly more resistant to cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which high-grade astrocytomas sometimes respond.
  • These results indicate that p53 status influences the chemosensitivity of astrocytic glioma cells in a drug-type specific manner, a finding that may have implications for the selection of drug treatments for patients with astrocytic gliomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Carmustine / therapeutic use. Cisplatin / therapeutic use. Dacarbazine / analogs & derivatives. Gene Silencing. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. Tumor Cells, Cultured. Tumor Stem Cell Assay

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  • (PMID = 16193384.001).
  • [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 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Tumor Suppressor Protein p53; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine
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9. 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.

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  • (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
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10. Pu P, Zhang Z, Kang C, Jiang R, Jia Z, Wang G, Jiang H: Downregulation of Wnt2 and beta-catenin by siRNA suppresses malignant glioma cell growth. Cancer Gene Ther; 2009 Apr;16(4):351-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of Wnt2 and beta-catenin by siRNA suppresses malignant glioma cell growth.
  • Increasing evidence suggests that aberrant activation of Wnt signaling is involved in tumor development and progression.
  • Our earlier study on gene expression profile in human gliomas by microarray found that some members of Wnt family were overexpressed.
  • To further investigate the involvement of Wnt signaling in gliomas, the expression of core components of Wnt signaling cascade in 45 astrocytic glioma specimens with different tumor grades was examined by reverse transcription-PCR and immunohistochemistry.
  • Wnt2, Wnt5a, frizzled2 and beta-catenin were overexpressed in gliomas.
  • Knockdown of Wnt2 and its key mediator beta-catenin in the canonical Wnt pathway by siRNA in human U251 glioma cells inhibited cell proliferation and invasive ability, and induced apoptotic cell death.
  • Furthermore, treating the nude mice carrying established subcutaneous U251 gliomas with siRNA targeting Wnt2 and beta-catenin intratumorally also delayed the tumor growth.
  • In conclusion, the canonical Wnt pathway is of critical importance in the gliomagenesis and intervention of this pathway may provide a new therapeutic approach for malignant gliomas.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Female. Humans. Mice. Neoplasm Invasiveness. Neoplasm Transplantation. RNA Interference. Signal Transduction / physiology

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  • (PMID = 18949017.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Wnt2 Protein; 0 / beta Catenin
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11. Kim YJ, Cho YE, Kim YW, Kim JY, Lee S, Park JH: Suppression of putative tumour suppressor gene GLTSCR2 expression in human glioblastomas. J Pathol; 2008 Oct;216(2):218-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Glioma tumour-suppressor candidate region gene 2 (GLTSCR2/PICT-1) is localized within the well-known 1.4 Mb tumour-suppressive region of chromosome 19q, which is frequently altered in various human tumours, including diffuse gliomas.
  • Finally, our immunohistochemical study demonstrates that GLTSCR2 is sequentially down-regulated according to the histological malignant progression of the astrocytic glial tumour.
  • Taken together, our results suggest that GLTSCR2 is involved in astrocytic glioma progression.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / pathology. Cell Line, Tumor. Chi-Square Distribution. Female. Gene Deletion. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18729076.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLTSCR2 protein, human; 0 / Tumor Suppressor Proteins
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12. Kachkov IA, Biktimirov RG, Zakharov AV, Chumakov VA, Suchkov SV: [Glial tumors of the brain: classification, present-day aspects of immunopathogenesis and immunogenetic diagnostics]. Vestn Ross Akad Med Nauk; 2005;(6):36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Glial tumors of the brain: classification, present-day aspects of immunopathogenesis and immunogenetic diagnostics].
  • The complexity of treatment, which includes surgical removal of a tumor, radiotherapy, chemotherapy, and immune correction, makes the problem even more topical.
  • Modem classification of glial neoplasms is of no less importance, because treatment depends on the histologic structure of a tumor.
  • Thereupon, the authors of the article pay special attention to the modem WHO classification of gliomas.
  • However, there are no objective tests to verify the diagnosis of astrocytic glioma with reliable accuracy.

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  • (PMID = 16022111.001).
  • [ISSN] 0869-6047
  • [Journal-full-title] Vestnik Rossiiskoi akademii meditsinskikh nauk
  • [ISO-abbreviation] Vestn. Akad. Med. Nauk SSSR
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Lymphocyte Function-Associated Antigen-1; 0 / alpha-Fetoproteins; 126547-89-5 / Intercellular Adhesion Molecule-1
  • [Number-of-references] 45
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13. 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.

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  • (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
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14. 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).

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  • (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
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15. 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.

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  • (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
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16. 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.

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  • (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
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17. 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.

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  • (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
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18. 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.

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  • (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
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19. 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).

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  • (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
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20. 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.

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  • (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
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21. Ochsenbein AF, Schubert AD, Vassella E, Mariani L: Quantitative analysis of 0&lt;sup&gt;6&lt;/sup&gt;-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.

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  • (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
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22. 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.

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  • (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
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23. 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.

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  • (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
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24. 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.

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  • (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
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25. Houben MP, Aben KK, Teepen JL, Schouten-Van Meeteren AY, Tijssen CC, Van Duijn CM, Coebergh JW: Stable incidence of childhood and adult glioma in The Netherlands, 1989-2003. Acta Oncol; 2006;45(3):272-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stable incidence of childhood and adult glioma in The Netherlands, 1989-2003.
  • Time trends in the incidence of glioma may reflect changes in the prevalence of environmental risk factors for glioma.
  • We therefore investigated trends in the incidence of childhood and adult glioma in The Netherlands from 1989 to 2003.
  • We calculated European standardised incidence rates for glioma, and stratified for age, gender and glioma subgroups.
  • Similar to other countries, the overall incidence of glioma was fairly stable in The Netherlands during the period 1989 to 2003, for both children and adults.
  • In adult astrocytic glioma, a significantly increasing incidence of high-grade astrocytoma was balanced by simultaneous decreases of low-grade astrocytoma, astrocytoma with unknown malignancy grade and glioma of uncertain histology.
  • Stable incidence rates of adult and childhood glioma suggest that no major changes in environmental risk factors have occurred, which influenced the incidence of glioma in the studied period.
  • [MeSH-major] Glioma / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / epidemiology. Child. Child, Preschool. Cohort Studies. Ependymoma / epidemiology. Europe / epidemiology. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Netherlands / epidemiology. Oligodendroglioma / epidemiology. Sex Characteristics. United States / epidemiology

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  • (PMID = 16644569.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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26. Wang XL, Chen XM, Gao HJ, Huang ZG: [Preparation and distribution of polyclonal antibodies against human PIWIL3 protein in tumor tissues]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2008 Jul;24(7):714-6

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  • [Title] [Preparation and distribution of polyclonal antibodies against human PIWIL3 protein in tumor tissues].
  • The expression and distribution of PIWIL3 protein were detected by human tumor tissue biochips.
  • PIWIL3 proteins were expressed in the cytoplasma of human astrocytic glioma and meningioma.
  • These antibodies will have potential value for human PIWIL3 protein in human specific tumor pathogenesis.
  • [MeSH-minor] Astrocytoma / metabolism. Humans. Meningioma / metabolism. Peptides / chemical synthesis. Peptides / chemistry. Peptides / immunology

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  • (PMID = 18616918.001).
  • [ISSN] 1007-8738
  • [Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
  • [ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies; 0 / Peptides; 0 / Proteins
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27. Zhou YH, Wu X, Tan F, Shi YX, Glass T, Liu TJ, Wathen K, Hess KR, Gumin J, Lang F, Yung WK: PAX6 suppresses growth of human glioblastoma cells. J Neurooncol; 2005 Feb;71(3):223-9
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  • We have reported that the expression of PAX6 was significantly reduced in GBMs and that a low level of PAX6 expression is a harbinger of an unfavorable prognosis for patients with malignant astrocytic glioma.
  • Thus it is interesting to determine if repression of PAX6 expression is involved in anti-tumor suppression function in GBM.
  • Repeated subcutaneous and intracranial implantation experiments in nude mice using PAX6-stable transfectants provided solid evidence that PAX6 suppressed tumor growth in vivo and significantly extended mouse survival.
  • CONCLUSION: Our data demonstrate that PAX6exerts a tumor suppressor function that limits the growth of GBM cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Genes, Tumor Suppressor. Humans. Loss of Heterozygosity / genetics. Mice. Mice, Nude. Paired Box Transcription Factors. Transfection

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  • (PMID = 15735909.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Repressor Proteins
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28. Bergonzini V, Calistri A, Salata C, Del Vecchio C, Sartori E, Parolin C, Palù G: Nef and cell signaling transduction: a possible involvement in the pathogenesis of human immunodeficiency virus-associated dementia. J Neurovirol; 2009 May;15(3):238-48
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  • Here we show that HIV-1 Nef has an effect on the transcriptional levels of a cellular protein, anaplastic lymphoma kinase (ALK), that is preferentially expressed in the central and peripheral nervous system at late embryonic stages.
  • By its overexpression along with Nef, the authors demonstrate ALK ability to influence, at least in the U87MG astrocytic glioma cells, the mytogen-activated protein kinase (MAP-K)-dependent pathway.
  • Moreover, although in the absence of a physical direct interaction, Nef and ALK activate matrix metalloproteinases (MMPs), which are likely to contribute to blood-brain barrier (BBB) damage in HAD.
  • [MeSH-minor] Cell Line, Transformed. Cell Line, Tumor. Chemokine CCL5 / metabolism. Chemokine CXCL12 / metabolism. Humans. Receptor Protein-Tyrosine Kinases. Transcriptional Activation

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  • (PMID = 19455469.001).
  • [ISSN] 1538-2443
  • [Journal-full-title] Journal of neurovirology
  • [ISO-abbreviation] J. Neurovirol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CCL5; 0 / Chemokine CXCL12; 0 / nef Gene Products, Human Immunodeficiency Virus; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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29. Ren ZP, Olofsson T, Qu M, Hesselager G, Soussi T, Kalimo H, Smits A, Nistér M: Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors. J Neuropathol Exp Neurol; 2007 Oct;66(10):944-54
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  • [Title] Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors.
  • We investigated genetic heterogeneity of astrocytic gliomas using p53 gene mutations as a marker.
  • Different parts of morphologically heterogeneous astrocytic gliomas were microdissected, and direct DNA sequencing of p53 gene exons 5 through 8 was performed.
  • Thirty-five glioma samples and tumor-adjacent normal-appearing brain tissue from 11 patients were analyzed.
  • The mutations were present in grade II, III, and IV astrocytic glioma areas.
  • Both severe functionally dead mutants and mutants with remaining transcriptional activity could be observed in the same tumor.
  • We observed that morphologically different parts of a glioma could carry different or similar mutations in the p53 gene and could be either associated or not associated with the locus of heterozygosity at the mutant site.
  • Coexistence of p53 gene mutations and the locus of heterozygosity was common, at least in astrocytomas grade III and in glioblastomas, and also occurred in astrocytoma grade II areas.
  • Our results are of importance for a further understanding of the molecular mechanisms behind failure to treat glioma patients.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, p53 / genetics
  • [MeSH-minor] Adult. Aged. DNA Primers. DNA, Neoplasm / genetics. Female. Gene Frequency. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Microdissection. Middle Aged. Mutation / genetics. Mutation / physiology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17917588.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm
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30. Bodey B, Siegel SE, Kaiser HE: Up-regulation of VEGF expression and related neo-angiogenesis in childhood high-grade gliomas: implications for anti-angiogenic anti-neoplastic therapy. In Vivo; 2006 Jul-Aug;20(4):511-8
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  • [Title] Up-regulation of VEGF expression and related neo-angiogenesis in childhood high-grade gliomas: implications for anti-angiogenic anti-neoplastic therapy.
  • There is considerable experimental evidence that VEGF isoforms are strongly involved in provoking neoangiogenesis of neoplastic cells and, consequently, the growth and progression of primary neoplasms (i.e., astrocytic gliomas), including the formation of an invasive and metastatic immunophenotype (IP).
  • During this immunohistochemical study, the presence and tissue localization of VEGF121 was observed in anaplastic, high-grade astrocytomas (AAs) and in glioblastoma multiforme (GBMs) employing the specific monoclonal antibody against it.
  • The immunoreactivity demonstrated a cytoplasmic, cell surface and extracellular matrix localization pattern in more than 90% of the tumor cells, with high intensity immunoreactivity (++++, A,B) in every high-grade astrocytic glioma tissue.
  • VEGF121 expression was identified mostly within the cytoplasm of tumor cells, suggesting an embryonic, undifferentiated and more malignant cellular IP of high-grade gliomas.
  • Tumor-related neo-angiogenesis and endothelial cell proliferation were also present.
  • The great majority of high-grade astrocytic gliomas are incurable with the three classic therapeutic modalities.
  • In the future, the development of targeted anti-neoplastic treatment strategies, adapted to individual patients, will require molecular identification of the different classes of neoplasm (including subtypes of astrocytomas) according to their stages, biology, prognosis and therapeutic options.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Glioma / blood supply. Glioma / pathology. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16900782.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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31. Seiz M, Tuettenberg J, Meyer J, Essig M, Schmieder K, Mawrin C, von Deimling A, Hartmann C: Detection of IDH1 mutations in gliomatosis cerebri, but only in tumors with additional solid component: evidence for molecular subtypes. Acta Neuropathol; 2010 Aug;120(2):261-7
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  • The current WHO classification of brain tumors defines gliomatosis cerebri (GC) as an extensively infiltrating astrocytic glioma involving at least three cerebral lobes.
  • The relation of GC to diffuse astrocytomas and glioblastoma is uncertain.
  • Recent reports showed IDH1 mutations in astrocytic and oligodendroglial tumors WHO grades II and III and in secondary glioblastomas with a frequency of up to 90%, whereas IDH1 mutations occurred in only 5% of primary glioblastomas.
  • We identified IDH1 mutations in 10/24 (42%) cases, which also included a solid tumor portion (type 2 GC), but not in 11 "classical" cases without solid tumor mass (type 1 GC).
  • Our data suggest that GC consists of two histological/molecular subtypes, type 1 being clearly distinct from diffuse astrocytoma, and type 2 sharing features with diffuse astrocytoma.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Arginine / genetics. Astrocytoma / secondary. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Mutational Analysis. Female. Histidine / genetics. Humans. In Situ Hybridization, Fluorescence / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged. Oligodendroglioma / secondary. Polymorphism, Single Nucleotide / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism


32. 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.

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  • (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
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33. Robe PA, Martin D, Albert A, Deprez M, Chariot A, Bours V: A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668]. BMC Cancer; 2006;6:29
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  • [Title] A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668].
  • BACKGROUND: The prognosis of patients suffering from WHO grade 3 and 4 astrocytic glioma remains poor despite surgery, radiation therapy and the use of current chemotherapy regimen.
  • Indeed, the median survival of glioblastoma multiforme (WHO grade 4) patients is at best 14.6 month with only 26.5 percent of the patients still alive after 2 years and the median survival of anaplastic astrocytomas (WHO grade 3) is 19.2 month.
  • Recent evidence suggests that the transcription factor NF-kappaB is constitutively expressed in malignant gliomas and that its inhibition by drugs like Sulfasalazine may block the growth of astrocytic tumors in vitro and in experimental models of malignant gliomas.
  • A total of twenty patients with progressive malignant glioma despite surgery, radiation therapy and a first line of chemotherapy will be recruited and assigned to four dosage regimen of Sulfasalazine.
  • Primary endpoints are drug safety in the setting of malignant gliomas and tumor response as measured according to MacDonald's criteria.
  • DISCUSSION: The aim of this study is to evaluate the safety and efficacy of Sulfasalazine as a treatment for recurring malignant gliomas.
  • [MeSH-minor] Administration, Oral. Adult. Aged. Brain Neoplasms. Disease Progression. Double-Blind Method. Female. Glioma. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 16448552.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN45828668
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 3XC8GUZ6CB / Sulfasalazine
  • [Other-IDs] NLM/ PMC1368982
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34. Wang Y, Yang J, Zheng H, Tomasek GJ, Zhang P, McKeever PE, Lee EY, Zhu Y: Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model. Cancer Cell; 2009 Jun 2;15(6):514-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model.
  • Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2(+) transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.

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  • (PMID = 19477430.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS053900-03; United States / NINDS NIH HHS / NS / R01 NS053900; United States / NINDS NIH HHS / NS / 1R01 NS053900; United States / NINDS NIH HHS / NS / R01 NS053900-01; United States / NINDS NIH HHS / NS / NS053900-01; United States / NINDS NIH HHS / NS / R01 NS053900-02; United States / NINDS NIH HHS / NS / NS053900-02; United States / NINDS NIH HHS / NS / R01 NS073762; United States / NINDS NIH HHS / NS / NS053900-03
  • [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 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS112275; NLM/ PMC2721466
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35. Shapiro WR, Carpenter SP, Roberts K, Shan JS: (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma. Expert Opin Biol Ther; 2006 May;6(5):539-45
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  • [Title] (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma.
  • Treatment of malignant glioma is therapeutically challenging.
  • Despite improvements in neurosurgery, radiotherapy and chemotherapy, few patients diagnosed with anaplastic astrocytoma (AA) or glioblastoma multiforme (GBM) (WHO grades 3 and 4, respectively) will live beyond 2 years.
  • Most malignant gliomas cannot be completely resected or irradiated due to their ability to infiltrate diffusely into normal brain tissue.
  • Brain tissue is protected from the systemic circulation via the blood-brain barrier (BBB), which impedes entry of water-soluble chemotherapeutic agents into the tumour at therapeutic concentrations. (131)I-chTNT-1/B mAb (Cotara) employs an innovative strategy to treat the invasive portion of the tumour and the core lesion. (131)I-chTNT-1/B mAb is a genetically engineered, radiolabelled, chimeric monoclonal antibody specific for a universal intracellular antigen (i.e., DNA/histone H1 complex) exposed in the necrotic core of malignant gliomas.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Astrocytoma / radiotherapy. Iodine Radioisotopes / therapeutic use

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  • (PMID = 16610983.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Histones; 0 / Iodine Radioisotopes; 9007-49-2 / DNA
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36. 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.

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  • (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
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37. Götze S, Wolter M, Reifenberger G, Müller O, Sievers S: Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas. Int J Cancer; 2010 Jun 1;126(11):2584-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas.
  • Recent studies suggested a role of Wnt signaling in gliomas, the most common primary brain tumors.
  • We investigated 70 gliomas of different malignancy grades for promoter hypermethylation in 8 genes encoding members of the secreted frizzled-related protein (SFRP1, SFRP2, SFRP4, SFRP5), dickkopf (DKK1, DKK3) and naked (NKD1, NKD2) families of Wnt pathway inhibitors.
  • While none of the tumors carried CTNNB1 mutations, we found frequent promoter hypermethylation of Wnt pathway inhibitor genes, with at least one of these genes being hypermethylated in 6 of 16 diffuse astrocytomas (38%), 4 of 14 anaplastic astrocytomas (29%), 7 of 10 secondary glioblastomas (70%) and 23 of 30 primary glioblastomas (77%).
  • Furthermore, SFRP1-hypermethylated gliomas showed significantly lower expression of the respective transcripts when compared with unmethylated tumors.
  • Taken together, our results suggest an important role of epigenetic silencing of Wnt pathway inhibitor genes in astrocytic gliomas, in particular, in glioblastomas, with distinct patterns of hypermethylated genes distinguishing primary from secondary glioblastomas.
  • [MeSH-major] Astrocytoma / genetics. DNA Methylation / genetics. Promoter Regions, Genetic. Wnt Proteins / genetics
  • [MeSH-minor] Carrier Proteins / genetics. Cell Line, Tumor. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Exons. Eye Proteins / genetics. Glioblastoma / genetics. Glioblastoma / secondary. Glioma / genetics. Glioma / pathology. Humans. Intercellular Signaling Peptides and Proteins / genetics. Membrane Proteins / genetics. Mutation. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. beta Catenin / genetics

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  • (PMID = 19847810.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NKD1 protein, human; 0 / NKD2 protein, human; 0 / Proto-Oncogene Proteins; 0 / SFRP1 protein, human; 0 / SFRP2 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
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38. Liu L, Bäcklund LM, Nilsson BR, Grandér D, Ichimura K, Goike HM, Collins VP: Clinical significance of EGFR amplification and the aberrant EGFRvIII transcript in conventionally treated astrocytic gliomas. J Mol Med (Berl); 2005 Nov;83(11):917-26
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  • [Title] Clinical significance of EGFR amplification and the aberrant EGFRvIII transcript in conventionally treated astrocytic gliomas.
  • The aim of this study was to evaluate the clinical value of assessing epidermal growth factor receptor (EGFR) amplification and the common 5' rearrangement of EGFR resulting in the EGFRvIII transcript in astrocytic gliomas.
  • Amplification of EGFR was found in 41% (65/160) of glioblastomas (GBs) and 10% (4/41) of anaplastic astrocytomas (AAs).
  • There were no abnormalities of the EFGR or its transcript in grade II astrocytoma (AII).
  • We noted a tendency towards decreased survival with any EGFR abnormality in the 41 patients with AAs.
  • [MeSH-major] Astrocytoma / genetics. Central Nervous System Neoplasms / genetics. Gene Amplification. Glioblastoma / genetics. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 16133418.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / CRUK/ A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2815848; NLM/ UKMS2690
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39. Zhou YH, Hess KR, Liu L, Linskey ME, Yung WK: Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables. Neuro Oncol; 2005 Oct;7(4):485-94
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  • [Title] Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables.
  • The disparate lengths of survival among patients with malignant astrocytic gliomas (anaplastic astrocytomas [AAs] and glioblastoma multiforme [GBM]) cannot be adequately accounted for by clinical variables (patient age, histology, and recurrent status).
  • We previously explicated the expression and prognostic value of PAX6, PTEN, VEGF, and EGFR in these glioma tissues and established a comprehensive prognostic model (Zhou et al., 2003).
  • This study attempts to improve that model by including four additional genetic markers, which exhibited a differential expression (P < 0.001) among tumor grades and between tumor and normal tissues.
  • This finding suggests that the expression of IGFBP2 is associated with pathways activated specifically in GBMs that result in enhancing invasiveness and angiogenesis.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical

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  • (PMID = 16212813.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ribosomal Proteins; 0 / ribosomal protein S9; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC1871729
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40. Li H, Wang Q, Gao F, Zhu F, Wang X, Zhou C, Liu C, Chen Y, Ma C, Sun W, Zhang L: Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas. Oncol Rep; 2008 Sep;20(3):573-9
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  • [Title] Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas.
  • However, the expression level of PDCD5 in human gliomas has not been investigated.
  • In the present study, we examined the expression of PDCD5 in 88 human glioma samples at both mRNA and protein levels by RT-PCR, Western blotting and immunohistochemistry.
  • We found that 53.3% (16/30) of the glioma samples had a reduced expression of PDCD5 mRNA and 70.5% (62/88) had a reduced expression of the PDCD5 protein as compared to normal brain tissue.
  • Furthermore, we studied the correlation of the expression level of PDCD5 with the clinicopathological grade and survival of patients with astrocytomas.
  • Although longitudinal studies of a cohort of patients with astrocytoma revealed that PDCD5 expression was not able to predict clinical outcome (p>0.05), a decreased expression of PDCD5 correlated significantly with high-grade astrocytomas (p<0.001).
  • In conclusion, our data suggest that reduced PDCD5 expression may contribute to the pathogenesis of human gliomas.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Female. Humans. Immunoenzyme Techniques. Male. Neoplasm Staging. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tumor Cells, Cultured

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  • (PMID = 18695908.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / RNA, Messenger
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41. Dong L, Pu PY, Wang H, Wang GX, Kang CS, Jiao DR: [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):232-6
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  • [Title] [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].
  • OBJECTIVE: To study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas. METHODS:.
  • (1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.
  • RESULTS: The frequency of p53 mutation in diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas and secondary glioblastomas was 1/10, 4/19 (21.1%), 4/6 and 2/2, respectively and the frequency of EGFR overexpression was 5/10, 10/19 (52.6%), 5/6 and 2/2, respectively.
  • Both p53 accumulation and EGFR overexpression increased accompanied by a successive increase of degree of the glioma malignancy.
  • CONCLUSIONS: EGFR overexpression is not infrequently seen, however, p53 mutation is rarely seen in the low grade gliomas.
  • Consequently, EGFR overexpression and p53 gene mutation are not mutually exclusive in astrocytic gliomagenesis but synergistically to promote the glioma progression.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16776982.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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42. Hagemann C, Gloger J, Anacker J, Said HM, Gerngras S, Kühnel S, Meyer C, Rapp UR, Kämmerer U, Vordermark D, Flentje M, Roosen K, Vince GH: RAF expression in human astrocytic tumors. Int J Mol Med; 2009 Jan;23(1):17-31
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  • [Title] RAF expression in human astrocytic tumors.
  • Only for A-RAF no link to tumorigenesis has been published so far.
  • Malignant gliomas are the most prevalent primary brain tumors of adults.
  • Although a role of the mitogenic Ras-RAF-MEK-ERK signalling cascade in brain tumor development is well established, there are only few reports available addressing alterations in RAF sequence or protein expression and function in human gliomas.
  • We analysed the mutational status of A-RAF and B-RAF in human glioblastomas (GBM) by sequencing.
  • Then we checked for RAF gene amplification by dot blot hybridization and examined RAF mRNA and protein expression patterns in human astrocytic gliomas of WHO grade II (LGA) and IV (GBM) by semiquantitative RT-PCR and Western blotting, respectively.
  • Finally, we performed functional assays to address a putative function of A-RAF in glioma cell proliferation and migration.
  • A-raf gene amplification was more often detected and overexpression of all three RAF proteins on mRNA and protein level was regularly found in human malignant gliomas.
  • Since neither A-RAF, nor C-RAF expression had any influence on proliferation and migration of GBM cells, putative functions of C-RAF in angiogenesis and of A-RAF in regulation of metabolism are discussed.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Proto-Oncogene Proteins A-raf / genetics. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins c-raf / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Cell Proliferation. Gene Expression Regulation. Humans. Mutant Proteins / genetics. Prognosis. RNA, Messenger / genetics. Sequence Analysis, DNA

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  • (PMID = 19082503.001).
  • [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 / Mutant Proteins; 0 / RNA, Messenger; EC 2.7.11.1 / Proto-Oncogene Proteins A-raf; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
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43. Eckerich C, Zapf S, Ulbricht U, Müller S, Fillbrandt R, Westphal M, Lamszus K: Contactin is expressed in human astrocytic gliomas and mediates repulsive effects. Glia; 2006 Jan 1;53(1):1-12
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  • [Title] Contactin is expressed in human astrocytic gliomas and mediates repulsive effects.
  • Analyzing different types of astrocytic tumors, we detected an association between increasing malignancy grade and contactin expression.
  • Functionally, contactin had repellent effects on glioma cells in vitro, as demonstrated by adhesion and migration assays.
  • Our findings suggest that contactin has repellent effects on glioma cells to which it is presented as a ligand, but it does not alter the proliferative or adhesive capacities of cells that overexpress the molecule.
  • The repulsive properties of contactin may be a key factor in glioma disaggregation, and may contribute to the diffuse infiltration pattern characteristic of glioma cells in human brain.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Cell Adhesion Molecules, Neuronal / metabolism
  • [MeSH-minor] Cell Adhesion / physiology. Cell Aggregation / physiology. Cell Communication / physiology. Cell Line, Tumor. Cell Movement / physiology. Cell Proliferation. Contactins. Extracellular Matrix Proteins / metabolism. Gene Expression Regulation, Neoplastic / physiology. Glial Fibrillary Acidic Protein / metabolism. Humans. Ligands. Neoplasm Invasiveness. Protein Tyrosine Phosphatases / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16078236.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules, Neuronal; 0 / Contactins; 0 / Extracellular Matrix Proteins; 0 / Glial Fibrillary Acidic Protein; 0 / Ligands; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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44. Xu P, Qiu M, Zhang Z, Kang C, Jiang R, Jia Z, Wang G, Jiang H, Pu P: The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo. J Neurooncol; 2010 Mar;97(1):41-51
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  • [Title] The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo.
  • Deregulation of Notch signaling has been implicated in some genetic diseases and tumorigenesis.
  • The function of Notch signaling in a variety of tumors can be either oncogenic or tumor-suppressive, depending on the cellular context.
  • In this study, Notch1 overexpression was observed in the majority of 45 astrocytic gliomas with different grades and in U251MG glioma cells.
  • Meanwhile, tumor growth was delayed in established subcutaneous gliomas in nude mice treated with Notch1 siRNA in vivo.
  • These results suggest that Notch1 plays an important oncogenic role in the development and progression of astrocytic gliomas.
  • [MeSH-major] Astrocytoma / genetics. Gene Expression Regulation, Neoplastic / physiology. Receptor, Notch1 / genetics
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Disease Models, Animal. Flow Cytometry / methods. Humans. In Situ Nick-End Labeling / methods. Matrix Metalloproteinase 9 / metabolism. Mice. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Transfection / methods

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  • (PMID = 19771395.001).
  • [ISSN] 1573-7373
  • [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] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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45. Kitai R, Horita R, Sato K, Yoshida K, Arishima H, Higashino Y, Hashimoto N, Takeuchi H, Kubota T, Kikuta K: Nestin expression in astrocytic tumors delineates tumor infiltration. Brain Tumor Pathol; 2010 Apr;27(1):17-21
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  • [Title] Nestin expression in astrocytic tumors delineates tumor infiltration.
  • Nestin is an intermediate filament protein expressed in undifferentiated cells during central nervous system development, and glioma is known to be a highly infiltrative tumor.
  • We determined whether nestin was expressed in astrocytic tumors and could identify infiltrating tumor cells.
  • We screened 65 archival, paraffin-embedded adult astrocytic tumors using immunohistochemical staining and computerized overlaid photographs.
  • The intensity of nestin expression corresponded to the tumor grade.
  • All 33 glioblastoma cases showed positive and extensive staining, which was less positive in diffuse astrocytoma.
  • Overlaid images showed that nestin immunostaining delineated tumor invasion into adjacent gray and white matter.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Intermediate Filament Proteins / metabolism. Intermediate Filament Proteins / physiology. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Child. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Nestin. Young Adult

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  • (PMID = 20425043.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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46. 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
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  • [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.

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  • [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
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47. Waha A, Felsberg J, Hartmann W, von dem Knesebeck A, Mikeska T, Joos S, Wolter M, Koch A, Yan PS, Endl E, Wiestler OD, Reifenberger G, Pietsch T, Waha A: Epigenetic downregulation of mitogen-activated protein kinase phosphatase MKP-2 relieves its growth suppressive activity in glioma cells. Cancer Res; 2010 Feb 15;70(4):1689-99
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  • [Title] Epigenetic downregulation of mitogen-activated protein kinase phosphatase MKP-2 relieves its growth suppressive activity in glioma cells.
  • Critical tumor suppression pathways in brain tumors have yet to be fully defined.
  • Using differential methylation hybridization, we identified a CpG-rich region of the promoter of the dual-specificity mitogen-activated protein kinase phosphatase-2 gene (DUSP4/MKP-2) that is hypermethylated in gliomas.
  • In 83 astrocytic gliomas and 5 glioma cell lines examined, hypermethylation of the MKP-2 promoter was found to occur relatively more frequently in diffuse or anaplastic astrocytomas and secondary glioblastomas relative to primary glioblastomas.
  • Our findings reveal MKP-2 as a common epigenetically silenced gene in glioma, the inactivation of which may play a significant role in glioma development.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Proliferation. Dual-Specificity Phosphatases / genetics. Epigenesis, Genetic / physiology. Glioma / pathology. Mitogen-Activated Protein Kinase Phosphatases / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. DNA Methylation. Down-Regulation / physiology. Female. Gene Expression Regulation, Neoplastic / physiology. Gene Silencing / physiology. Genes, Tumor Suppressor / physiology. Humans. Male. Middle Aged

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  • (PMID = 20124482.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / DUSP4 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases
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48. Hu X, Pandolfi PP, Li Y, Koutcher JA, Rosenblum M, Holland EC: mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma. Neoplasia; 2005 Apr;7(4):356-68
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  • [Title] mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma.
  • Combined activation of Ras and AKT leads to the formation of astrocytic glioblastoma multiforme (GBM) in mice.
  • We demonstrate here that loss of Pten is similar to AKT activation in the context of glioma formation in mice.
  • Blockade of mTOR results in regional apoptosis in these tumors and conversion in the character of surviving tumor cells from astrocytoma to oligodendroglioma.
  • These data suggest that mTOR activity is required for the survival of some cells within these GBMs, and mTOR appears required for the maintenance of astrocytic character in the surviving cells.
  • Furthermore, our study provides the first example of conversion between two distinct tumor types usually thought of as belonging to specific lineages, and provides evidence for signal transduction-mediated transdifferentiation between glioma subtypes.

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  • (PMID = 15967113.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01CA894134-1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 147336-22-9 / Green Fluorescent Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.67 / PTEN Phosphohydrolase; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1501155
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49. McCarthy BJ, Propp JM, Davis FG, Burger PC: Time trends in oligodendroglial and astrocytic tumor incidence. Neuroepidemiology; 2008;30(1):34-44
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  • [Title] Time trends in oligodendroglial and astrocytic tumor incidence.
  • BACKGROUND: We hypothesized that the incidences of oligodendrogliomas, anaplastic oligodendrogliomas, and mixed gliomas have significantly increased from the early 1990 s forward, while the incidences of anaplastic and grade II astrocytic tumors have significantly decreased.
  • METHODS: Data for the years 1973-2004 from the Surveillance, Epidemiology and End Results (SEER) public-use data and for 1985-2004 from six collaborating registries of the Central Brain Tumor Registry of the US (CBTRUS) were obtained.
  • RESULTS: Using CBTRUS data, the incidences (per 100,000 person-years) of oligodendrogliomas (APC = 4.7), mixed gliomas (APC = 3.9) and anaplastic oligodendrogliomas (APC = 12.5) have all increased over time, while the incidences of astrocytoma not otherwise specified (APC = -8.1) and fibrillary astrocytoma (APC = -2.1) have decreased.
  • CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18259099.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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50. 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
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  • [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

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  • (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
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51. Lapointe M, Lanthier J, Moumdjian R, Régina A, Desrosiers RR: Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors. Brain Res Mol Brain Res; 2005 Apr 27;135(1-2):93-103
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  • [Title] Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors.
  • Here we investigated PIMT regulation in astrocytic tumors, which are the most common human brain tumors.
  • PIMT expression and enzyme activity were significantly decreased in all grades of human astrocytic tumors.
  • More precisely, PIMT levels were significantly lower by 76% in pilocytic astrocytomas (grade I), 46% in astrocytomas (grade II), 69% in anaplastic astrocytomas (grade III), and a marked 80% in glioblastomas (grade IV) as compared to normal brains.
  • Furthermore, the reduced PIMT levels correlated closely with a decrease in the number of neuron cells in astrocytic tumors as assessed by measuring the neuron-specific enolase level.
  • Many proteins with abnormal aspartyl residues accumulated in brain tumors and some were specific to individual grades of astrocytic tumors.
  • Similar results were obtained, either by measuring the reduction in PIMT activity and expression or by measuring the formation of abnormal proteins, in an orthotopic rat brain tumor model implanted with invasive CNS-1 glioma cells.
  • The novelty of these findings was to provide the first evidence for a marked reduction of PIMT expression and activity during stage progression of astrocytic tumors in humans.
  • [MeSH-major] Brain / enzymology. Brain Neoplasms / enzymology. Gene Expression Regulation, Neoplastic / physiology. Glioma / enzymology. Protein D-Aspartate-L-Isoaspartate Methyltransferase / metabolism
  • [MeSH-minor] Animals. Blotting, Northern. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry / methods. Male. Methylation. Neoplasm Transplantation / methods. Phosphopyruvate Hydratase / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred Lew. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 15857672.001).
  • [ISSN] 0169-328X
  • [Journal-full-title] Brain research. Molecular brain research
  • [ISO-abbreviation] Brain Res. Mol. Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / RNA, Messenger; EC 2.1.1.77 / Protein D-Aspartate-L-Isoaspartate Methyltransferase; EC 4.2.1.11 / Phosphopyruvate Hydratase
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52. Conti A, Aguennouz M, La Torre D, Tomasello C, Cardali S, Angileri FF, Maio F, Cama A, Germanò A, Vita G, Tomasello F: miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors. J Neurooncol; 2009 Jul;93(3):325-32
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  • [Title] miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors.
  • Recent evidence indicates that miRNAs can function both as tumor suppressors and as oncogenes.
  • Expression of miR-21, 221, 128a, 128b, 128c, 181a, 181b, 181c was studied using real-time quantitative reverse transcriptase polymerase chain reaction and northern blotting for human astrocytic tumors with different grade of malignancy. miR-21 and 221 were overexpressed in glioma samples, whereas miRNA 181b was downregulated compared with normal brain tissue. miRNA-21 was hyperexpressed in all tumor samples whereas higher levels of miRNA-221 were found in high-grade gliomas.
  • This study is the first analysis of miRNAs in astrocytic tumor at different stages of malignancy.

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  • (PMID = 19159078.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MIRN21 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
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53. Kim D, Cho SH, Kim JS, Jo SH, Lee SJ, Kim KT, Choi SY: Human astrocytic bradykinin B(2) receptor modulates zymosan-induced cytokine expression in 1321N1 cells. Peptides; 2010 Jan;31(1):101-7
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  • [Title] Human astrocytic bradykinin B(2) receptor modulates zymosan-induced cytokine expression in 1321N1 cells.
  • Bradykinin secreted from neurons affects astrocytic functions such as neurovascular coupling and astrocytic cytokine production.
  • In human astrocytes, however, the detailed mechanism of bradykinin-mediated modulation of astrocytic functions has not yet been fully elucidated.
  • Here, we report the functional expression of the bradykinin B(2) receptor and its modulation of zymosan-induced cytokine expression in human astrocytoma 1321N1 cells.
  • In contrast to the result in human glioma cells, bradykinin inhibits the zymosan-induced expression of TNF-alpha and IL-1beta in rat astrocytes, which shows a species-dependent manner.
  • These data suggest that bradykinin B(2) receptors are expressed in human astrocytoma cells and that they modulate the expression pattern of inflammatory cytokines.
  • [MeSH-minor] Animals. Bradykinin / analogs & derivatives. Bradykinin / metabolism. Calcium Signaling / physiology. Cell Line, Tumor. Humans. Inflammation / chemically induced. Inflammation / physiopathology. Interleukin-1beta / immunology. Rats. Species Specificity. Toll-Like Receptor 2 / metabolism. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 19854233.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Receptor, Bradykinin B2; 0 / Toll-Like Receptor 2; 0 / Tumor Necrosis Factor-alpha; 9010-72-4 / Zymosan; S8TIM42R2W / Bradykinin
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54. Rousseau A, Nutt CL, Betensky RA, Iafrate AJ, Han M, Ligon KL, Rowitch DH, Louis DN: Expression of oligodendroglial and astrocytic lineage markers in diffuse gliomas: use of YKL-40, ApoE, ASCL1, and NKX2-2. J Neuropathol Exp Neurol; 2006 Dec;65(12):1149-56
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  • [Title] Expression of oligodendroglial and astrocytic lineage markers in diffuse gliomas: use of YKL-40, ApoE, ASCL1, and NKX2-2.
  • The phenotypic heterogeneity of astrocytic and oligodendroglial tumor cells complicates establishing accurate diagnostic criteria, and lineage-specific markers would facilitate diagnosis of glioma subtypes.
  • Based on data from the literature and from expression microarrays, we selected molecules relevant to gliogenesis and glial lineage specificity and then used immunohistochemistry to assess expression of these molecules in 55 diffuse gliomas, including 8 biphasic oligoastrocytomas, 21 oligodendrogliomas (all with 1p/19qloss), 21 astrocytomas, and 5 glioblastomas.
  • For the astrocytic lineage markers (GFAP, YKL-40, and ApoE), GFAP expression was significantly higher in the astrocytic component of oligoastrocytomas compared with the oligodendroglial part; similar patterns were detected for YKL-40 and ApoE, although the differences were not significant.
  • GFAP, YKL-40, and ApoE reliably distinguished grade II-III oligodendrogliomas from grade II-IV astrocytomas (p < 0.0001, p = 0.002, and p < 0.0001, respectively).
  • Among the oligodendroglial lineage markers (Olig2, Sox10, ASCL1, and NKX2-2), ASCL1 and NKX2-2 displayed significantly different immunostaining between oligodendrogliomas and astrocytomas (p = 0.017 and 0.004, respectively), but none clearly differentiated between the 2 glial populations of oligoastrocytomas.
  • In addition to GFAP, therefore, YKL-40, ApoE, ASCL1, and NKX2-2 represent promising tumor cell markers to distinguish oligodendrogliomas from astrocytomas.
  • [MeSH-major] Astrocytes / pathology. Biomarkers, Tumor / metabolism. Brain Neoplasms / diagnosis. Cell Lineage / genetics. Glioma / diagnosis. Oligodendroglia / pathology
  • [MeSH-minor] Adipokines. Apolipoproteins E / analysis. Apolipoproteins E / metabolism. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / analysis. Basic Helix-Loop-Helix Transcription Factors / metabolism. Diagnosis, Differential. Glial Fibrillary Acidic Protein / analysis. Glial Fibrillary Acidic Protein / metabolism. Glycoproteins / analysis. Glycoproteins / metabolism. Homeodomain Proteins / analysis. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Lectins. Oligodendroglioma / diagnosis. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Predictive Value of Tests. Transcription Factors / analysis. Transcription Factors / metabolism

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  • (PMID = 17146289.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASCL1 protein, human; 0 / Adipokines; 0 / Apolipoproteins E; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / CHI3L1 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Glycoproteins; 0 / Homeodomain Proteins; 0 / Lectins; 0 / Nkx-2.2 homedomain protein; 0 / Transcription Factors; 0 / apolipoprotein E1
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55. Mulholland PJ, Thirlwell C, Brock CS, Newlands ES: Emerging targeted treatments for malignant glioma. Expert Opin Emerg Drugs; 2005 Nov;10(4):845-54
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  • [Title] Emerging targeted treatments for malignant glioma.
  • This paper focuses on the medical management of malignant gliomas, which is currently undergoing change.
  • The current therapies for glioma and the targeted agents in clinical trials are reviewed.
  • There is a general acceptance that temozolomide in combination with radiotherapy is replacing radiotherapy alone as first-line therapy in high-grade astrocytic gliomas.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Drug Delivery Systems / methods. Drugs, Investigational / administration & dosage. Glioma / drug therapy

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  • (PMID = 16262566.001).
  • [ISSN] 1744-7623
  • [Journal-full-title] Expert opinion on emerging drugs
  • [ISO-abbreviation] Expert Opin Emerg Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational
  • [Number-of-references] 56
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56. Liebrich M, Guo LH, Schluesener HJ, Schwab JM, Dietz K, Will BE, Meyermann R: Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors. Arch Immunol Ther Exp (Warsz); 2007 Jan-Feb;55(1):41-7
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  • [Title] Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors.
  • MATERIALS AND METHODS: Expression of IL-16 was analyzed by immunohistochemistry in human astrocytic brain tumors and the rat C6 glioblastoma tumor model.
  • IL-16 was detected in both human astrocytic brain tumors and rat C6 glioma.
  • RESULTS: Compared with human control brains, a significant increase in the percentages of parenchymal IL-16+ macrophages/microglia was observed already in grade II astrocytomas, indicating that IL-16+ immunostaining could be a descriptor of a macrophage/microglia subset in astrocytic brain tumors.
  • A further increase was observed at the transition from grade II to III astrocytomas.
  • This increase in IL-16 immunoreactivity correlated with WHO grades of human astrocytic brain tumors.
  • CONCLUSIONS: Therefore, IL-16 might be a so far unknown factor in the regulation of the local inflammatory milieu of human and experimental astrocytomas.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Glioblastoma / immunology. Interleukin-16 / biosynthesis. Macrophages / immunology. Microglia / immunology
  • [MeSH-minor] Adult. Aged. Animals. Cell Line, Tumor. Female. Humans. Inflammation Mediators / metabolism. Male. Middle Aged. Rats. Rats, Sprague-Dawley

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  • (PMID = 17221335.001).
  • [ISSN] 0004-069X
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / Interleukin-16
  • [Other-IDs] NLM/ PMC3234149
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57. Katoh N, Shirato H, Aoyama H, Onimaru R, Suzuki K, Hida K, Miyasaka K, Iwasaki Y: Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor. J Neurooncol; 2006 May;78(1):63-9

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  • [Title] Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.
  • PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord glioma with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumors.
  • MATERIALS AND METHODS: Forty-one patients with spinal cord glioma received post-operative radiotherapy between 1979 and 2003.
  • There were 12 low-grade astrocytic tumors, 11 high-grade astrocytic tumors, 16 low-grade ependymal tumors and 2 high-grade ependymal tumors.
  • Among 11 patients with high-grade astrocytic tumors, 5 with anaplastic astrocytoma and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation.
  • RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the astrocytic tumors and 84% for the ependymal tumors, respectively (P=0.009).
  • Among 11 patients with high-grade astrocytic tumors, the actuarial survival rate at 10 years was 35%.
  • DISCUSSION: The results for ependymal tumors and low-grade astrocytic tumors were comparable to those reported in the literature.
  • Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-grade astrocytic tumors.
  • [MeSH-major] Dose Fractionation. Glioma / radiotherapy. Spinal Cord Neoplasms / radiotherapy

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  • (PMID = 16314938.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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58. Kostianovsky AM, Maier LM, Anderson RC, Bruce JN, Anderson DE: Astrocytic regulation of human monocytic/microglial activation. J Immunol; 2008 Oct 15;181(8):5425-32
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  • [Title] Astrocytic regulation of human monocytic/microglial activation.
  • Recent reports have described reduced immunological responsiveness and stimulatory capacity among monocytes/microglia that infiltrate malignant human gliomas.
  • Herein, we demonstrate that culture of ex vivo human monocytes or primary human microglia with tumor cells isolated from glioblastoma multiforme (GBM) specimens renders them tolerogenic, capable of suppressing the function of ex vivo monocytes in the absence of tumor cells or their soluble factors.
  • We demonstrate that the tolerance induced in monocytes/microglia by GBM tumor cells is not associated with interference with the signaling cascade associated with TLR- or CD40-induced monocyte activation.
  • Rather, these tumor cells appear to up-regulate pathways that antagonize positive signaling pathways, including but not limited to STAT3 and STAT5.
  • Finally, we demonstrate that the tolerogenic properties of GBM tumor cells amplify properties inherent to nontransformed astrocytes.
  • Future studies that identify all of the molecular mechanisms by which astrocytes and malignant gliomas suppress monocyte/microglial function will have dual therapeutic benefits: suppressing these pathways may benefit patients with astrocytic tumors, while enhancing them may benefit patients with autoimmune processes within the CNS, such as multiple sclerosis.
  • [MeSH-major] Astrocytes / immunology. Glioma / immunology. Microglia / immunology. Monocytes / immunology
  • [MeSH-minor] Antigens, CD40 / immunology. Humans. Multiple Sclerosis / immunology. Multiple Sclerosis / pathology. Multiple Sclerosis / therapy. STAT3 Transcription Factor / immunology. STAT5 Transcription Factor / immunology. Signal Transduction / immunology. Toll-Like Receptors / immunology. Tumor Cells, Cultured

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  • (PMID = 18832699.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 0 / Toll-Like Receptors
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59. Burgoyne AM, Palomo JM, Phillips-Mason PJ, Burden-Gulley SM, Major DL, Zaremba A, Robinson S, Sloan AE, Vogelbaum MA, Miller RH, Brady-Kalnay SM: PTPmu suppresses glioma cell migration and dispersal. Neuro Oncol; 2009 Dec;11(6):767-78
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  • [Title] PTPmu suppresses glioma cell migration and dispersal.
  • Glioblastomas (GBMs) are the highest grade of primary brain tumors with astrocytic similarity and are characterized by marked dispersal of tumor cells.
  • PTPmu expression was examined in human GBM, low-grade astrocytoma, and normal brain tissue.
  • These studies revealed a striking loss of PTPmu protein expression in highly dispersive GBMs compared to less dispersive low-grade astrocytomas and normal brain.
  • The migration of brain tumor cells was assessed in vitro using a scratch wound assay.
  • To assess migration, labeled U-87 MG glioma cells were injected into adult rat brain slices, and their movement was followed over time.
  • Together, these data suggest that loss of PTPmu in human GBMs contributes to tumor cell migration and dispersal, implicating loss of PTPmu in glioma progression.

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  • (PMID = 19304959.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS051520-04; United States / NEI NIH HHS / EY / P30 EY011373; United States / NINDS NIH HHS / NS / R01 NS051520; United States / NINDS NIH HHS / NS / R01-NS051520; United States / NCI NIH HHS / CA / K08 CA101954; United States / NINDS NIH HHS / NS / NS051520-04; United States / NEI NIH HHS / EY / P30 EY011373-119002; United States / NCI NIH HHS / CA / P20 CA103736; United States / NEI NIH HHS / EY / P30 EY011373-129002; United States / NCI NIH HHS / CA / P30 CA043703; United States / NEI NIH HHS / EY / P30 EY011373-139002; United States / NCI NIH HHS / CA / T32 CA059366; United States / NINDS NIH HHS / NS / NS051520-02; United States / NINDS NIH HHS / NS / NS051520-01A1; United States / NEI NIH HHS / EY / EY011373-139002; United States / NIGMS NIH HHS / GM / T32-GM007250; United States / NEI NIH HHS / EY / P30-EY11373; United States / NEI NIH HHS / EY / EY011373-119002; United States / NINDS NIH HHS / NS / NS051520-03; United States / NINDS NIH HHS / NS / R01 NS051520-02; United States / NINDS NIH HHS / NS / R01 NS051520-01A1; United States / NEI NIH HHS / EY / EY011373-129002; United States / NCI NIH HHS / CA / K08-CA101954; United States / NCI NIH HHS / CA / R01-CA116257; United States / NCI NIH HHS / CA / P30-CA043703; United States / NCI NIH HHS / CA / T32-CA059366; United States / NCI NIH HHS / CA / R01 CA116257; United States / NIGMS NIH HHS / GM / T32 GM007250; United States / NINDS NIH HHS / NS / R01 NS051520-03; United States / NCI NIH HHS / CA / P20-CA103736
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 2
  • [Other-IDs] NLM/ PMC2802397
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60. Zhou YH, Hess KR, Raj VR, Yu L, Liu L, Yung AW, Linskey ME: Establishment of prognostic models for astrocytic and oligodendroglial brain tumors with standardized quantification of marker gene expression and clinical variables. Biomark Insights; 2010 Dec 22;5:153-68
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  • [Title] Establishment of prognostic models for astrocytic and oligodendroglial brain tumors with standardized quantification of marker gene expression and clinical variables.
  • BACKGROUND: Prognosis models established using multiple molecular markers in cancer along with clinical variables should enable prediction of natural disease progression and residual risk faced by patients.
  • In this study, multivariate Cox proportional hazards analyses were done based on overall survival (OS) of 100 glioblastoma multiformes (GBMs, 92 events), 49 anaplastic astrocytomas (AAs, 33 events), 45 gliomas with oligodendroglial features, including anaplastic oligodendroglioma (AO, 13 events) and oligodendraglioma (O, 9 events).
  • The modeling included two clinical variables (patient age and recurrence at the time of sample collection) and the expression variables of 13 genes selected based on their proven biological and/or prognosis functions in gliomas (ABCG2, BMI1, MELK, MSI1, PROM1, CDK4, EGFR, MMP2, VEGFA, PAX6, PTEN, RPS9, and IGFBP2).
  • Univariate models revealed opposing prognostic effects of ABCG2, MELK, BMI1, PROM1, IGFBP2, PAX6, RPS9, and MSI1 expressions for astrocytic (GBM and AA) and oligodendroglial tumors (AO_O).
  • Our success in establishing prognosis models for AA and AO_O was largely based on identification of a set of genes with independent prognostic values and application of standardized gene expression quantification to allow formation of a large cohort in analysis.

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  • (PMID = 21234290.001).
  • [ISSN] 1177-2719
  • [Journal-full-title] Biomarker insights
  • [ISO-abbreviation] Biomark Insights
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3018892
  • [Keywords] NOTNLM ; gene expression markers / glioma / model / prognosis
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61. Mertsch S, Schmitz N, Jeibmann A, Geng JG, Paulus W, Senner V: Slit2 involvement in glioma cell migration is mediated by Robo1 receptor. J Neurooncol; 2008 Mar;87(1):1-7
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  • [Title] Slit2 involvement in glioma cell migration is mediated by Robo1 receptor.
  • Because similar molecular mechanisms may be utilized in glioma cell invasion and neuroblast migration, we studied the expression of Slit2 and its transmembrane receptor Robo1 as well as their functional role in migration in glioma cells. qRT-PCR and immunohistochemistry of human specimens revealed that Slit2 was distinctly expressed by non-neoplastic neurons, but at only very low levels in fibrillary astrocytoma and glioblastoma.
  • Robo1 also was mainly restricted to neurons in the normal brain, whereas astrocytic tumor cells in situ as well as glioblastoma cell lines overexpressed Robo1 at mRNA and protein levels.
  • Recombinant human Slit2 in a concentration of 0.45 nM was repulsive for glioma cell lines in a modified Boyden chamber assay.
  • RNAi-mediated knockdown of Robo1 in glioma cell lines neutralized the repulsive effect of Slit2, demonstrating that Robo1 served as the major Slit2 receptor.
  • Our findings suggest that a chemorepulsive effect mediated by interaction of Slit2 and Robo1 participates in glioma cell guidance in the brain.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Glioma / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Nerve Tissue Proteins / metabolism. Receptors, Immunologic / metabolism
  • [MeSH-minor] Astrocytes / metabolism. Blotting, Western. Cell Line, Tumor. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Neurons / metabolism. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17968499.001).
  • [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 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Immunologic; 0 / Slit homolog 2 protein; 0 / roundabout protein
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62. Witte HT, Jeibmann A, Klämbt C, Paulus W: Modeling glioma growth and invasion in Drosophila melanogaster. Neoplasia; 2009 Sep;11(9):882-8
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  • [Title] Modeling glioma growth and invasion in Drosophila melanogaster.
  • Glioblastoma is the most common and most malignant intrinsic human brain tumor, characterized by extensive invasion and proliferation of glial (astrocytic) tumor cells, frequent activation of tyrosine kinase receptor signaling pathways, relative resistance to chemotherapy and radiotherapy, and poor prognosis.
  • Using the Gal4-UAS system, we have produced glioma models in Drosophila by overexpressing homologs of human tyrosine kinase receptors under control of the glia-specific promoter reversed polarity (repo).
  • Glial overexpression of activated epidermal growth factor receptor (EGFR) resulted in enhanced proliferation and migration of larval glial cells with increased numbers in the eye imaginal disc, diffuse tumor-like enlargement of the optic stalk, and marked ectopic invasion of glial cells along the optic nerve.
  • We suggest that Drosophila models will be useful for deciphering signaling cascades underlying abnormal behavior of glioma cells for genetic screens to reveal interacting genes involved in gliomagenesis and for experimental therapy approaches.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Drosophila melanogaster / metabolism. Glioma / pathology
  • [MeSH-minor] Animals. Eye / cytology. Eye / metabolism. Humans. Immunoenzyme Techniques. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Platelet-Derived Growth Factor / metabolism. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Receptors, Platelet-Derived Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 19724682.001).
  • [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 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2735809
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63. Tsunoda K, Kitange G, Anda T, Shabani HK, Kaminogo M, Shibata S, Nagata I: Expression of the constitutively activated RelA/NF-kappaB in human astrocytic tumors and the in vitro implication in the regulation of urokinase-type plasminogen activator, migration, and invasion. Brain Tumor Pathol; 2005;22(2):79-87
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  • [Title] Expression of the constitutively activated RelA/NF-kappaB in human astrocytic tumors and the in vitro implication in the regulation of urokinase-type plasminogen activator, migration, and invasion.
  • Although malignant gliomas are highly invasive tumors, a characteristic that contributes to the commonly observed therapeutic failures and local disease recurrences, the molecular events that regulate invasion in these tumors remain poorly understood.
  • Because the transcription factor RelA/NF-kappaB has been shown to regulate invasion during several cellular processes, we have examined immunohistochemically expression of the constitutively activated RelA/NF-kappaB in tissues obtained from 49 astrocytic tumors [8 diffuse astrocytomas, 9 anaplastic astrocytomas (AAs) and 32 glioblastomas (GBMs)].
  • In addition, we examined the in vitro effects of antisense oligonucleotides and curcumin on the expression and activation of RelA/NF-kappaB, urokinase-type plasminogen activator (u-PA) expression, migration, and invasion in the T98G glioma cell line.
  • Expression of the constitutively activated RelA/NF-kappaB was observed in 2 (25%) of 8 cases of diffuse astrocytomas, 5 (55.6%) of 9 cases of AAs, and 30 (93.8%) of 32 cases of GBMs.
  • This expression was significantly correlated with the malignant potential in astrocytic tumors (P < 0.001).
  • Moreover, antisense oligonucleotides and curcumin inhibited phorbol-12-myristate-13-acetate (PMA)-induced RelA/NF-kappaB expression or activation (or both), down-regulated u-PA expression, and reduced the migration and invasive potentials of T98G glioma cells.
  • Thus, the expression of constitutively activated RelA/NF-kappaB is associated with malignancy potential in astrocytic tumors and may play a critical role in the regulation of u-PA expression and invasiveness in gliomas.
  • RelA/NF-kappaB may therefore be an intriguing candidate for studies aimed at understanding and prevention of the invasiveness of gliomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. NF-kappa B / biosynthesis. Neoplasm Proteins / biosynthesis. Transcription Factor RelA / biosynthesis. Urokinase-Type Plasminogen Activator / biosynthesis
  • [MeSH-minor] Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Movement / drug effects. Cell Nucleus / metabolism. Culture Media, Conditioned. Curcumin / pharmacology. Enzyme Induction / genetics. Humans. Neoplasm Invasiveness. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Retrospective Studies. Single-Blind Method. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 18095109.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / RELA protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factor RelA; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; IT942ZTH98 / Curcumin; NI40JAQ945 / Tetradecanoylphorbol Acetate
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64. Fuller GN, Mircean C, Tabus I, Taylor E, Sawaya R, Bruner JM, Shmulevich I, Zhang W: Molecular voting for glioma classification reflecting heterogeneity in the continuum of cancer progression. Oncol Rep; 2005 Sep;14(3):651-6
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  • [Title] Molecular voting for glioma classification reflecting heterogeneity in the continuum of cancer progression.
  • Gliomas, the most common brain tumors, are generally categorized into two lineages (astrocytic and oligodendrocytic) and further classified as low-grade (astrocytoma and oligodendroglioma), mid-grade (anaplastic astrocytoma and anaplastic oligodendroglioma), and high-grade (glioblastoma multiforme) based on morphological features.
  • A strict classification scheme has limitations because a specific glioma can be at any stage of the continuum of cancer progression and may contain mixed features.
  • Thus, a more comprehensive classification based on molecular signatures may reflect the biological nature of specific tumors more accurately.
  • In this study, we used microarray technology to profile the gene expression of 49 human brain tumors and applied the k-nearest neighbor algorithm for classification.
  • We first trained the classification gene set with 19 of the most typical glioma cases and selected a set of genes that provide the lowest cross-validation classification error with k=5.
  • We then applied this gene set to the 30 remaining cases, including several that do not belong to gliomas such as atypical meningioma.
  • The results showed that not only does the algorithm correctly classify most of the gliomas, but the detailed voting results also provide more subtle information regarding the molecular similarities to neighboring classes.
  • For atypical meningioma, the voting was equally split among the four classes, indicating a difficulty in placement of meningioma into the four classes of gliomas.
  • Thus, the actual voting results, which are typically used only to decide the winning class label in k-nearest neighbor algorithms, provide a useful method for gaining deeper insight into the stage of a tumor in the continuum of cancer development.
  • [MeSH-major] Brain Neoplasms / classification. Gene Expression Profiling. Glioma / classification. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Algorithms. Disease Progression. Gene Expression Regulation, Neoplastic / genetics. Genetic Heterogeneity

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  • (PMID = 16077969.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
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65. Ichimura K, Vogazianou AP, Liu L, Pearson DM, Bäcklund LM, Plant K, Baird K, Langford CF, Gregory SG, Collins VP: 1p36 is a preferential target of chromosome 1 deletions in astrocytic tumours and homozygously deleted in a subset of glioblastomas. Oncogene; 2008 Mar 27;27(14):2097-108
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  • [Title] 1p36 is a preferential target of chromosome 1 deletions in astrocytic tumours and homozygously deleted in a subset of glioblastomas.
  • Astrocytic, oligodendroglial and mixed gliomas are the commonest gliomas in adults.
  • The 1p status of astrocytomas has not yet been thoroughly examined.
  • Using a chromosome 1 tile path array, we investigated 108 adult astrocytic tumours for copy number alterations.
  • Total 1p deletions were rare (2%), however partial deletions involving 1p36 were frequently identified in anaplastic astrocytomas (22%) and glioblastomas (34%).
  • However, the CpG island of TNFRSF9 was hypermethylated in 19% of astrocytic tumours and 87% of glioma cell lines.
  • TNFRSF9 expression was upregulated after demethylation of glioma cell lines.
  • Our results indicate that 1p deletions are common anaplastic astrocytomas and glioblastomas but are distinct from the 1p abnormalities in oligodendrogliomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Glioblastoma / genetics

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  • (PMID = 17934521.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / CRUK/ A6618; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2650419; NLM/ UKMS4022
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66. Figarella-Branger D, Bouvier C: [Histological classification of human gliomas: state of art and controversies]. Bull Cancer; 2005 Apr;92(4):301-9
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  • [Title] [Histological classification of human gliomas: state of art and controversies].
  • [Transliterated title] Classification anatomopathologique des gliomes: faits et controverses.
  • The histological classification of human gliomas remains in 2005 a challenge.
  • The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.
  • Although the standard remains the WHO classification, this classification suffered from lack of reproducibility among pathologists.
  • In particular this classification does not take into account the intrinsic morphological heterogeneity of infiltrative gliomas and does not discriminate the tumour cells from the residual brain parenchyma.
  • According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).
  • Circumscribed gliomas mainly corresponds to pilocytic astrocytomas (grade I).
  • In contrast, the Sainte Anne classification takes into account the macroscopic informations provided by imaging techniques and the tumour growth patterns.
  • Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.
  • According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).
  • In the future the glioma classification has to be unique and should take into account clinical data, neuroradiological and histological features and results of molecular biology.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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  • (PMID = 15888386.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
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67. You F, Osawa Y, Hayashi S, Nakashima S: Immediate early gene IEX-1 induces astrocytic differentiation of U87-MG human glioma cells. J Cell Biochem; 2007 Jan 1;100(1):256-65
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  • [Title] Immediate early gene IEX-1 induces astrocytic differentiation of U87-MG human glioma cells.
  • In order to increase the apoptotic sensitivity to chemotherapeutic drugs and gamma-ray, we attempted to establish U87-MG human glioma cell line expressing IEX-1.
  • Unexpectedly, however, transfection of IEX-1 into U87-MG glioma cells resulted in morphological changes to astrocytic phenotype and increase in glial differentiation marker proteins, S-100 and glial fibrillary acidic protein (GFAP).
  • Glial cell differentiation was used to examine in rat C6 glioma cell line, since this cell line express astrocytic phenotypes by increase in intracellular cAMP concentration.
  • Stimulation of human U87-MG glioma cells by membrane-permeable dibutyryl cAMP (dbcAMP) not only elicited their morphological changes but also induced expression of IEX-1 as well as S-100 and GFAP.
  • These results indicate that IEX-1 plays an important role in astrocytic differentiation of human glioma cells and that IEX-1 functions at downstream of PKA.
  • [MeSH-major] Apoptosis Regulatory Proteins / physiology. Astrocytes / metabolism. Cell Differentiation. Glioma / metabolism. Membrane Proteins / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cyclic AMP-Dependent Protein Kinases / metabolism. Cyclic CMP / analogs & derivatives. Cyclic CMP / metabolism. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / metabolism. Humans. Isoquinolines / pharmacology. Rats. S100 Proteins / metabolism. Sulfonamides / pharmacology

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  • [Copyright] 2006 Wiley-Liss, Inc.
  • (PMID = 16960879.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Glial Fibrillary Acidic Protein; 0 / IER3 protein, human; 0 / Isoquinolines; 0 / Membrane Proteins; 0 / S100 Proteins; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 3616-08-8 / Cyclic CMP; 64649-87-2 / dibutyryl cyclic-3',5'-cytidine monophosphate; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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68. Cui XL, Zhao ZG, Ren XH, Sui DL, Chu JS, Tang K, Zeng C, Lin S: [Characteristics of combining loss of heterozygosity of 1p/19q in glioma]. Zhonghua Wai Ke Za Zhi; 2010 Jun 1;48(11):852-5
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  • [Title] [Characteristics of combining loss of heterozygosity of 1p/19q in glioma].
  • METHODS: The status of 1p and 19q of 138 glioma specimen from January 2009 to December 2009 was evaluated by Fluorescence in situ hybridization (FISH) method, and the frequencies of combining LOH of 1p/19q were compared between different pathologies, brain sub-regions, genders and ages.
  • RESULTS: The frequencies of combined LOH of 1p and 19q of oligodendroglial (81.3%) and oligo astrocytic tumors (55.8%) were significantly higher than that of astrocytic tumor (22.2%) (P < 0.01), and the frequency of oligodendroglial tumor was significantly higher than that of oligo astrocytic tumor (P < 0.05).
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Loss of Heterozygosity

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  • (PMID = 21163056.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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69. Khattab AZ, Ahmed MI, Fouad MA, Essa WA: Significance of p53 and CD31 in astrogliomas. Med Oncol; 2009;26(1):86-92
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  • [Title] Significance of p53 and CD31 in astrogliomas.
  • BACKGROUND: Astrogliomas are the most common primary brain tumor.
  • Its progression is the result of activation of oncogenes, inactivation of tumor suppressor genes (TSGs), and expression of various growth factors.
  • The angiogenesis and p53 in astrogliomas play an important role in its grading, treatment strategies, and hence its clinical outcome.
  • OBJECTIVES: To analyze the frequency of presentation and the possible co-expression of p53 and angiogenesis marker (CD31) and their clinical implications in astrogliomas.
  • MATERIAL AND METHODS: This retrograde study included 45 cases with astrocytomas in the form of paraffin blocks.
  • Sections were stained with hematoxylin and eosin to determine the type and histological grade according to WHO (2007) classification of CNS tumors.
  • RESULTS: Both p53 and CD31 expressions were correlated well with the histopathological grades of different subtypes of astrogliomas with good discrimination between low and high grades.
  • Overall, a highly significant statistical correlation was observed between the grades of astrocytomas and the p53 and CD31 labeling indices.
  • Obviously, these observations demonstrate that the co-expression and increased levels of p53 and CD31 in astrogliomas are increasing as the tumor grade is increasing.
  • Thus, the two markers can be used as adjunct to the diagnosis and stratification of the high grade from the low-grade intrinsic brain astrogliomas.
  • [MeSH-major] Antigens, CD31 / biosynthesis. Astrocytoma / metabolism. Biomarkers, Tumor. Brain Neoplasms / metabolism. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 18821037.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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70. Taomoto K, Ohnishi H, Kamada Y, Kuga Y, Kohaya N, Nakashima K, Ichioka T, Tominaga T, Nakamura M, Nakazato Y: A rare case of malignant glioma suspected to have arisen from a cavernous sinus. Brain Tumor Pathol; 2007;24(2):75-80
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  • [Title] A rare case of malignant glioma suspected to have arisen from a cavernous sinus.
  • The extraparenchymal tumor located around the right trigeminal ganglion was totally removed, except for an intracavernous lesion, by the orbitozygomatic approach.
  • The solid tumor was completely separated from the brainstem and seemed to be a trigeminal schwannoma arising from the trigeminal ganglion or cavernous sinus at surgery.
  • A histological examination, however, found a typical malignant glioma that consisted primarily of astrocytic tumor cells.
  • Immunohistochemical staining showed the tumor cells stained intensely for GFAP, S-100 protein, and vimentin, but not for NFP, Schwann/2E, CD34, and CD68.
  • The tumor recurred after a short time, and then it rapidly disseminated into the subarachnoid space and left the cerebral hemisphere.
  • There are no previous reports of a malignant glioma arising from either the cavernous sinus or the trigeminal ganglion.
  • From the pathogenetic point of view, this malignant glioma is an extremely rare case that developed clinically and neuroradiologically from the cavernous sinus and was suspected be being derived from ectopic glial tissue.
  • [MeSH-major] Brain Neoplasms / pathology. Cavernous Sinus / pathology. Glioma / pathology. Neoplasm Recurrence, Local / pathology

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  • (PMID = 18095135.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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71. Pu P, Kang C, Zhang Z, Liu X, Jiang H: Downregulation of PIK3CB by siRNA suppresses malignant glioma cell growth in vitro and in vivo. Technol Cancer Res Treat; 2006 Jun;5(3):271-80
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  • [Title] Downregulation of PIK3CB by siRNA suppresses malignant glioma cell growth in vitro and in vivo.
  • EGFR overexpression is the most frequent and important molecular event in the development of astrocytic gliomas, and the P13K signaling pathway is one of the most important downstream pathways of EGFR.
  • EGFR and other members of the receptor tyrosine kinases (RTKs) family, such as VEGFR, PDGFR, and IGFR, et cetera, are often overexpressed in most of malignant gliomas and share common downstream signaling pathways.
  • The PIK3CB gene encoding the class 1A PI3K catalytic subunit p110beta was selected as the target of therapeutic approach for malignant gliomas in the present study.
  • In addition, the growth of the subcutaneous U251 glioma in the nude mice treated with siRNA targeting PIK3CB was significantly inhibited.
  • These results demonstrate that PIK3CB overexpression may play an oncogenic role in the PI3K pathway, and the plasmid-based siRNA targeting of PIK3CB is a potential and promising approach for the treatment of malignant gliomas.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy. Phosphatidylinositol 3-Kinases / metabolism. RNA, Small Interfering
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Down-Regulation. Female. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transfection. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 16700623.001).
  • [ISSN] 1533-0346
  • [Journal-full-title] Technology in cancer research & treatment
  • [ISO-abbreviation] Technol. Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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72. Nawashiro H, Otani N, Shinomiya N, Fukui S, Ooigawa H, Shima K, Matsuo H, Kanai Y, Endou H: L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors. Int J Cancer; 2006 Aug 1;119(3):484-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors.
  • LAT1 has been identified as a light chain of the CD98 heterodimer from C6 glioma cells.
  • We have investigated for the first time, the expression of the transporter in the human primary astrocytic tumor tissue from 60 patients.
  • On the basis of these findings, we also investigated the effect of the specific inhibitor to LAT1, 2-aminobicyclo-2 (2,2,1)-heptane-2-carboxylic acid (BCH), on the survival of C6 glioma cells in vitro and in vivo using a rat C6 glioma model.
  • BCH inhibited the growth of C6 glioma cells in vitro and in vivo in a dose-dependent manner.
  • These findings suggest that LAT1 could be one of the molecular targets in glioma therapy.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Large Neutral Amino Acid-Transporter 1 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acids, Cyclic / pharmacology. Animals. Antigens, CD98 Heavy Chain / analysis. Cell Line, Tumor. Cell Survival / drug effects. Child. Female. Glioma / drug therapy. Glioma / mortality. Glioma / pathology. Humans. Immunohistochemistry. Infant, Newborn. Male. Middle Aged. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / mortality. Neoplasms, Experimental / pathology. Rats. Rats, Wistar. Survival Analysis. Survival Rate

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16496379.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Cyclic; 0 / Antigens, CD98 Heavy Chain; 0 / Large Neutral Amino Acid-Transporter 1; 20448-79-7 / 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid
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73. Boor I, Nagtegaal M, Kamphorst W, van der Valk P, Pronk JC, van Horssen J, Dinopoulos A, Bove KE, Pascual-Castroviejo I, Muntoni F, Estévez R, Scheper GC, van der Knaap MS: MLC1 is associated with the dystrophin-glycoprotein complex at astrocytic endfeet. Acta Neuropathol; 2007 Oct;114(4):403-10
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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  • [Title] MLC1 is associated with the dystrophin-glycoprotein complex at astrocytic endfeet.
  • Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a progressive cerebral white matter disease with onset in childhood, caused by mutations in the MLC1 gene.
  • MLC1 is a protein with unknown function that is mainly expressed in the brain in astrocytic endfeet at the blood-brain and cerebrospinal fluid-brain barriers.
  • It shares its localization at astrocytic endfeet with the dystrophin-associated glycoprotein complex (DGC).
  • From these results we conclude that MLC1 is associated with the DGC at astrocytic endfeet.
  • [MeSH-minor] Aquaporin 4 / metabolism. Blotting, Western. Brain Neoplasms / metabolism. Glioma / metabolism. Glycoproteins / metabolism. Humans. Immunohistochemistry. Immunoprecipitation. Multiple Sclerosis / metabolism. Potassium Channels, Inwardly Rectifying / metabolism

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  • (PMID = 17628813.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0502130
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / AQP4 protein, human; 0 / Aquaporin 4; 0 / Dystrophin-Associated Protein Complex; 0 / Glycoproteins; 0 / Kcnj10 (channel); 0 / MLC1 protein, human; 0 / Membrane Proteins; 0 / Potassium Channels, Inwardly Rectifying
  • [Other-IDs] NLM/ PMC2039857
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74. Mizoguchi M, Betensky RA, Batchelor TT, Bernay DC, Louis DN, Nutt CL: Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival. J Neuropathol Exp Neurol; 2006 Dec;65(12):1181-8
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  • [Title] Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival.
  • Diffuse astrocytic gliomas are the most common human glial tumors with glioblastoma being the most malignant form.
  • In this study, we investigated the activation status of these 3 signaling molecules as well as wild-type (EGFRwt) and mutant (EGFRvIII) EGFR in 82 malignant astrocytic gliomas (55 glioblastomas and 27 anaplastic astrocytomas) using immunohistochemistry.
  • The distribution of these 3 activated molecules varied significantly with tumor grade; although activation of STAT3 was essentially identical between anaplastic astrocytomas and glioblastomas, an increase in the activation of MAPK and AKT appeared to correlate with the progression of anaplastic astrocytoma to glioblastoma.
  • Taken together, these findings begin to elucidate the interrelationship between these signaling pathways in astrocytic gliomas in vivo.
  • [MeSH-major] Astrocytoma / enzymology. Brain Neoplasms / enzymology. Glioblastoma / enzymology. Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / biosynthesis. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Disease Progression. Enzyme Activation / genetics. Genetic Predisposition to Disease / genetics. Humans. Immunohistochemistry. Mutation / genetics. Predictive Value of Tests. Prognosis. Signal Transduction / physiology. Survival Rate / trends. Transcriptional Activation / genetics

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  • (PMID = 17146292.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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75. Sen S, Dong M, Kumar S: Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology. PLoS One; 2009 Dec 23;4(12):e8427
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  • [Title] Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology.
  • Glioblastoma Multiforme (GBM) is a malignant astrocytic tumor associated with low survival rates because of aggressive infiltration of tumor cells into the brain parenchyma.
  • To probe the cellular basis of this correlation, we have suppressed expression of the nonmuscle isoforms alpha-actinin-1 and alpha-actinin-4 and examined the contribution of each isoform to the structure, mechanics, and motility of human glioma tumor cells in culture.
  • Our results demonstrate that both alpha-actinin-1 and alpha-actinin-4 make critical and distinct contributions to cytoskeletal organization, rigidity-sensing, and motility of glioma cells, thereby yielding mechanistic insight into the observed correlation between alpha-actinin expression and GBM invasiveness in vivo.

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  • (PMID = 20037648.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / DP2 OD004213; United States / NIH HHS / OD / 1DP2OD004213
  • [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 / Protein Isoforms; 11003-00-2 / Actinin; 125361-02-6 / Vinculin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2793025
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76. Liang Y, Bollen AW, Nicholas MK, Gupta N: Id4 and FABP7 are preferentially expressed in cells with astrocytic features in oligodendrogliomas and oligoastrocytomas. BMC Clin Pathol; 2005 Jul 15;5:6
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  • [Title] Id4 and FABP7 are preferentially expressed in cells with astrocytic features in oligodendrogliomas and oligoastrocytomas.
  • We examined the expression patterns and localization of these survival-associated genes in ODG and OAC in order to analyze their possible roles in the oncogenesis of these two tumor types.
  • RESULTS: Transcripts of most survival-associated genes as well as Id4 were present in both GBM and ODG tumors, whereas protein expression of Id4 and one of the survival-associated genes, brain-type fatty acid-binding protein (FABP7), was present in cells with astrocytic features, including reactive and neoplastic astrocytes, but not in neoplastic oligodendrocytes.
  • However, protein expression of Id4 and FABP7 in GBM, ODG, and OAC suggests that this group of functionally important genes might demonstrate two patterns of expression in these glioma subtypes: one group is universally expressed in glioma cells, and the other group of genes is expressed primarily in neoplastic astrocytes but not in neoplastic oligodendrocytes.

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  • (PMID = 16018821.001).
  • [ISSN] 1472-6890
  • [Journal-full-title] BMC clinical pathology
  • [ISO-abbreviation] BMC Clin Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1182359
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77. de Groot JF, Liu TJ, Fuller G, Yung WK: The excitatory amino acid transporter-2 induces apoptosis and decreases glioma growth in vitro and in vivo. Cancer Res; 2005 Mar 1;65(5):1934-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The excitatory amino acid transporter-2 induces apoptosis and decreases glioma growth in vitro and in vivo.
  • Astrocytic tumors have been shown to release glutamate at high levels, which may stimulate tumor cell proliferation and motility via activation of glutamate receptors.
  • Excess glutamate has also been found to facilitate tumor invasion by causing excitotoxic damage to normal brain thereby paving a pathway for tumor migration.
  • Results from tissue microarray analyses showed decreased excitatory amino acid transporter-2 (EAAT-2) expression in high-grade glial tumors compared with low-grade astrocytomas and normal brain.
  • EAAT-2 expression was inversely correlated with tumor grade, implicating its potential role in glial tumor progression, which was reflected by an undetectable level of EAAT-2 protein in glioma cell lines.
  • In this study, we sought to investigate the effect of reconstituted EAAT-2 on glioma cell growth in vitro and in vivo by adenoviral-mediated gene transfer.
  • Infection of glioma cells with Ad-EAAT-2 resulted in a physiologic level of functional EAAT-2, and a subsequent dose-dependent reduction in cell proliferation in all glioma cell lines tested compared with controls.
  • Interestingly, results from analyses of Annexin V staining, detection of poly(ADP-ribose)polymerase cleavage and caspase-3 activation all indicated that Ad-EAAT-2 infection elicited apoptosis in glioma cells.
  • Ex vivo experiments in nude mice showed a total suppression of tumor growth at sites that received Ad-EAAT-2-infected cells.
  • Collectively, our results uncovered a new function of EAAT-2 in controlling glioma proliferation.
  • Further studies will improve our knowledge of the role of glutamate in glioma growth and may provide useful prognostic information and alternative therapeutic targets for the treatment of glioma.
  • [MeSH-minor] Adenoviridae / genetics. Animals. Annexin A5 / metabolism. Astrocytoma / metabolism. Astrocytoma / pathology. Astrocytoma / prevention & control. Brain / metabolism. Brain / pathology. Caspase 3. Caspases / metabolism. Cell Proliferation. Disease Progression. Enzyme Activation. Female. Glioblastoma / metabolism. Glioblastoma / pathology. Glioblastoma / prevention & control. Humans. In Vitro Techniques. Mice. Mice, Nude. Microarray Analysis. Poly(ADP-ribose) Polymerases / metabolism. Tumor Cells, Cultured / transplantation

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  • (PMID = 15753393.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Excitatory Amino Acid Transporter 2; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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78. Beckner ME, Gobbel GT, Abounader R, Burovic F, Agostino NR, Laterra J, Pollack IF: Glycolytic glioma cells with active glycogen synthase are sensitive to PTEN and inhibitors of PI3K and gluconeogenesis. Lab Invest; 2005 Dec;85(12):1457-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glycolytic glioma cells with active glycogen synthase are sensitive to PTEN and inhibitors of PI3K and gluconeogenesis.
  • Recently, we found that glycolytic enzymes were abundant and some were increased in pseudopodia formed by U87 glioma (astrocytoma) cells.
  • In this study, we examined cell migration, adhesion (a step in migration), and Matrigel invasion of U87 and LN229 glioma cells when their mitochondria were inhibited with sodium azide or limited by 1% O(2).
  • Upon discovering that glycolysis alone can support glioma cell migration, unique features of glucose metabolism in astrocytic cells were investigated.
  • The ability of astrocytic cells to remove lactate, the inhibitor of glycolysis, via gluconeogenesis and incorporation into glycogen led to consideration of supportive genetic mutations.
  • We hypothesize that glycolysis in gliomas can support invasive migration, especially when aided by loss of PTEN's regulation on the phosphatidylinositol-3 kinase (PI3K)/Akt pathway leading to inhibition of GSK3.
  • These findings confirm that glycolytic glioma cells can migrate invasively and that the loss of PTEN is supportive, with activated glycogenic potential included among the relevant downstream effects.
  • [MeSH-major] Astrocytoma / metabolism. Enzyme Inhibitors / pharmacology. Gluconeogenesis / drug effects. Glycogen Synthase Kinase 3 / metabolism. Glycolysis / physiology. PTEN Phosphohydrolase / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors
  • [MeSH-minor] Cell Adhesion. Cell Line, Tumor. Cell Movement. Collagen. Drug Combinations. Gene Expression Regulation, Neoplastic. Humans. Lactic Acid / metabolism. Laminin. Mitochondria / drug effects. Mitochondria / metabolism. Neoplasm Invasiveness / physiopathology. Phosphorylation. Proteoglycans. RNA, Messenger / metabolism. Sodium Azide / pharmacology. Transfection

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  • (PMID = 16170333.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 119978-18-6 / matrigel; 33X04XA5AT / Lactic Acid; 9007-34-5 / Collagen; 968JJ8C9DV / Sodium Azide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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79. Perdiki M, Korkolopoulou P, Thymara I, Agrogiannis G, Piperi C, Boviatsis E, Kotsiakis X, Angelidakis D, Diamantopoulou K, Thomas-Tsagli E, Patsouris E: Cyclooxygenase-2 expression in astrocytomas. Relationship with microvascular parameters, angiogenic factors expression and survival. Mol Cell Biochem; 2007 Jan;295(1-2):75-83

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 expression in astrocytomas. Relationship with microvascular parameters, angiogenic factors expression and survival.
  • The role of the up-regulation of COX-2 in the formation and progression of gliomas has been dealt with in earlier reports, which describe increased levels of PGs within gliomas.
  • In the present study, we examined the expression of COX-2 in diffuse gliomas of astrocytic origin in relation to microvascular parameters, angiogenic factors and survival.
  • MATERIALS AND METHODS: A total of 83 cases of diffuse astrocytomas (grade II-IV) were analyzed by immunohistochemistry for the presence of COX-2.
  • CONCLUSION: These results implicate COX-2 in the angiogenesis and biological aggressiveness of diffuse astrocytomas, and suggest that it would be worthwhile to examine how the inhibition of COX-2 expression may influence astrocytoma patients' survival.
  • [MeSH-major] Angiogenesis Inducing Agents / metabolism. Astrocytoma / blood supply. Astrocytoma / enzymology. Cyclooxygenase 2 / metabolism. Glioma / blood supply. Glioma / enzymology. Membrane Proteins / metabolism

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  • (PMID = 16868662.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / Membrane Proteins; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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80. Strojnik T, Kavalar R, Zajc I, Diamandis EP, Oikonomopoulou K, Lah TT: Prognostic impact of CD68 and kallikrein 6 in human glioma. Anticancer Res; 2009 Aug;29(8):3269-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of CD68 and kallikrein 6 in human glioma.
  • AIMS: To evaluate the expression of CD68 and kallikrein 6 in human gliomas, and investigate their prognostic significance for survival of brain cancer patients in comparison to some known prognostic markers.
  • PATIENTS AND METHODS: Histological sections of 51 primary astrocytic tumours (11 benign, 40 malignant) were immunohistochemically stained for CD68, cathepsin B, kallikrein 6 and Ki-67.
  • Strong CD68 staining was of greater predictive value in the subgroup of anaplastic astrocytomas (p=0.021).
  • CONCLUSION: Kallikrein 6 was down-regulated in malignant glioma, but this differential expression did not have an impact on patient prognosis.
  • In contrast, immunostaining of glioma tissue for CD68 and for cathepsin B may be used for prognosis of survival in these patients.
  • This finding suggests that besides the known role of cathepsin B in invasion and angiogenesis, CD68 may be also associated with glioma progression.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. Kallikreins / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19661345.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / RNA, Messenger; EC 3.4.21.- / KLK6 protein, human; EC 3.4.21.- / Kallikreins
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81. Guo D, Nilsson J, Haapasalo H, Raheem O, Bergenheim T, Hedman H, Henriksson R: Perinuclear leucine-rich repeats and immunoglobulin-like domain proteins (LRIG1-3) as prognostic indicators in astrocytic tumors. Acta Neuropathol; 2006 Mar;111(3):238-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Perinuclear leucine-rich repeats and immunoglobulin-like domain proteins (LRIG1-3) as prognostic indicators in astrocytic tumors.
  • We have previously characterized three human leucine-rich repeats and immunoglobulin-like domains (LRIG) genes and proteins, named LRIG1-3 and proposed that they may act as suppressors of tumor growth.
  • In this study, we evaluated the mRNA expression level of LRIG1-3 in human glioma cell lines and control-matched glioma tissues, characterized the sub-cellular localization of an LRIG3-GFP fusion protein, and analyzed the relationship between sub-cellular localization of LRIG1-3 and clinical parameters in 404 astrocytic tumors by immunohistochemistry.
  • LRIG1-3 mRNA was detected in all human glioma cell lines and matched glioma samples, with large differences in the expression levels.
  • Ectopically expressed LRIG3-GFP localized to perinuclear and cytoplasmic compartments, and to the cell surface of transfected glioma cells.
  • Perinuclear staining of LRIG3 was associated with a lower proliferation index and was in addition to tumor grade, an independent prognostic factor.
  • These results indicate that expression and sub-cellular localization of LRIG1-3 might be of importance in the pathogenesis and prognosis of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Cell Proliferation. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Survival Rate


82. Wrensch M, Wiencke JK, Wiemels J, Miike R, Patoka J, Moghadassi M, McMillan A, Kelsey KT, Aldape K, Lamborn KR, Parsa AT, Sison JD, Prados MD: Serum IgE, tumor epidermal growth factor receptor expression, and inherited polymorphisms associated with glioma survival. Cancer Res; 2006 Apr 15;66(8):4531-41
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  • [Title] Serum IgE, tumor epidermal growth factor receptor expression, and inherited polymorphisms associated with glioma survival.
  • In population-based glioma patients, we examined survival in relation to potentially pertinent constitutive polymorphisms, serologic factors, and tumor genetic and protein alterations in epidermal growth factor receptor (EGFR), MDM2, and TP53.
  • We obtained 595 of 697 astrocytic tumors for marker studies.
  • Using a stringent P < 0.001, glioma survival was associated with ERCC1 C8092A [hazard ratio (HR), 0.72; 95% confidence limits (95% CL), 0.60-0.86; P = 0.0004] and GSTT1 deletion (HR, 1.64; 95% CL, 1.25-2.16; P = 0.0004); glioblastoma patients with elevated IgE had 9 months longer survival than those with normal or borderline IgE levels (HR, 0.62; 95% CL, 0.47-0.82; P = 0.0007), and EGFR expression in anaplastic astrocytoma was associated with nearly 3-fold poorer survival (HR, 2.97; 95% CL, 1.70-5.19; P = 0.0001).
  • We also suggest that tumor EGFR expression be incorporated into clinical evaluation of anaplastic astrocytoma patients.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Immunoglobulin E / blood. Receptor, Epidermal Growth Factor / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / genetics. Humans. Middle Aged. Polymorphism, Genetic

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  • (PMID = 16618782.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA097257; United States / NCI NIH HHS / CA / CA52689; United States / NCI NIH HHS / CA / CA89032; United States / NIEHS NIH HHS / ES / ES04705; United States / NIEHS NIH HHS / ES / ES06717
  • [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 / Biomarkers, Tumor; 37341-29-0 / Immunoglobulin E; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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83. Hayashi S, Yamamoto M, Tachibana K, Ueno Y, Bu G, Fukushima T: Mechanism of photofrin-enhanced ultrasound-induced human glioma cell death. Anticancer Res; 2009 Mar;29(3):897-905
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  • [Title] Mechanism of photofrin-enhanced ultrasound-induced human glioma cell death.
  • BACKGROUND: Low-intensity ultrasound showed tumor cell killing by a non-thermal effect in human leukemia cells.
  • The aim of our study was to investigate the efficacy of low-intensity ultrasound on malignant astrocytic tumor cells with the photosensitizer, Photofrin, which is taken up by the cell surface receptor, low density lipoprotein receptor-related protein/alpha2-macroglobulin receptor (LRP/alpha2MR).
  • MATERIALS AND METHODS: Cells were sonicated with continuous wave ultrasound with or without the presence of Photofrin (75 mg/ml) at an intensity of 0.3 W/cm(2) for a duration of 5, 15, or 30 s.
  • RESULTS: Ultrasound alone induced instant cell killing immediately after sonication in both U251MG and U105MG malignant gliomas cells.
  • CONCLUSION: This is the first report to demonstrate the usefulness of low-intensity ultrasound for the cell killing of malignant glioma cells.
  • [MeSH-major] Brain Neoplasms / therapy. Cell Survival / drug effects. Dihematoporphyrin Ether / therapeutic use. Glioma / therapy. Photosensitizing Agents / therapeutic use. Ultrasonic Therapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Low Density Lipoprotein Receptor-Related Protein-1 / genetics. Low Density Lipoprotein Receptor-Related Protein-1 / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. alpha-Macroglobulins / genetics. alpha-Macroglobulins / metabolism

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  • (PMID = 19414325.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Low Density Lipoprotein Receptor-Related Protein-1; 0 / Photosensitizing Agents; 0 / RNA, Messenger; 0 / alpha-Macroglobulins; 97067-70-4 / Dihematoporphyrin Ether
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84. Vila-Carriles WH, Zhou ZH, Bubien JK, Fuller CM, Benos DJ: Participation of the chaperone Hsc70 in the trafficking and functional expression of ASIC2 in glioma cells. J Biol Chem; 2007 Nov 23;282(47):34381-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Participation of the chaperone Hsc70 in the trafficking and functional expression of ASIC2 in glioma cells.
  • High-grade glioma cells express subunits of the ENaC/Deg superfamily, including members of ASIC subfamily.
  • Our previous work has shown that glioma cells exhibit a basally active cation current, which is not present in low-grade tumor cells or normal astrocytes, and that can be blocked by amiloride.
  • We have previously shown that high-grade glioma cells functionally express this current because of the lack of ASIC2 in the plasma membrane.
  • We now hypothesize that ASIC2 trafficking in glioma cells is regulated by a specific chaperone protein, namely Hsc70.
  • Our results demonstrated that Hsc70 co-immunoprecipitates with ASIC2 and that it is overexpressed in glioma cells as compared with normal astrocytes.
  • In addition, glycerol and sodium 4-phenylbutyrate reduced the amount of Hsc70 expressed in glioma cells to levels found in normal astrocytes.
  • Transfection of Hsc70 siRNA inhibited the constitutively activated amiloride-sensitive current, decreased migration, and increased ASIC2 surface expression in glioma cells.
  • These results support an association between Hsc70 and ASIC2 that may underlie the increased retention of ASIC2 in the endoplasmic reticulum of glioma cells.
  • The data also suggest that decreasing Hsc70 expression promotes reversion of a high-grade glioma cell to a more normal astrocytic phenotype.

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  • (PMID = 17878160.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK037206; United States / NCI NIH HHS / CA / CA 101952; United States / NIDDK NIH HHS / DK / DK 37206; United States / NCI NIH HHS / CA / P50 CA 97247
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acid Sensing Ion Channels; 0 / HSC70 Heat-Shock Proteins; 0 / HSPA8 protein, human; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Small Interfering; 0 / Sodium Channels; 139873-08-8 / Calnexin
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85. Hwang SY, Yoo BC, Jung JW, Oh ES, Hwang JS, Shin JA, Kim SY, Cha SH, Han IO: Induction of glioma apoptosis by microglia-secreted molecules: The role of nitric oxide and cathepsin B. Biochim Biophys Acta; 2009 Nov;1793(11):1656-68
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  • [Title] Induction of glioma apoptosis by microglia-secreted molecules: The role of nitric oxide and cathepsin B.
  • Microglia contributes significantly to brain tumor mass, particularly in astrocytic gliomas.
  • Here, we examine the cytotoxic effects of soluble components secreted from microglia culture on glioma cells.
  • Microglia conditioned culture medium (MCM) actively stimulated apoptotic death of glioma cells, and the effects of MCM prepared from LPS- or IFN-gamma-activated microglia were more pronounced.
  • The cytotoxic effects were glioma-specific in that primary cultured rat astrocytes were not affected by MCM.
  • A donor of peroxynitrite induced glioma-specific cell death.
  • In addition, NO synthase inhibitor suppressed glioma cell death induced by activated MCM, indicating that NO is one of the key molecules responsible for glioma cytotoxicity mediated by activated MCM.
  • However, since unstimulated resting microglia produces low or very limited level of NO, MCM may contain other critical molecule(s) that induce glioma apoptosis.
  • In particular, suppression of cathepsin B by the chemical inhibitors significantly reversed MCM-induced glioma cell death, implying a critical role of this protease in cytotoxicity.
  • Our findings provide evidence on the functional implications of specific microglial-secreted proteins in glioma cytotoxicity, as well as a basis to develop a proteomic databank of both basal and activation-related proteins in microglia.
  • [MeSH-major] Apoptosis. Cathepsin B / metabolism. Glioma / metabolism. Microglia / secretion. Nitric Oxide / secretion

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  • (PMID = 19748528.001).
  • [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 / Antiviral Agents; 0 / Culture Media, Conditioned; 0 / Enzyme Inhibitors; 0 / Lipopolysaccharides; 31C4KY9ESH / Nitric Oxide; 82115-62-6 / Interferon-gamma; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.1 / Ctsb protein, mouse; EC 3.4.22.1 / Ctsb protein, rat
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86. Bajenaru ML, Garbow JR, Perry A, Hernandez MR, Gutmann DH: Natural history of neurofibromatosis 1-associated optic nerve glioma in mice. Ann Neurol; 2005 Jan;57(1):119-27
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  • [Title] Natural history of neurofibromatosis 1-associated optic nerve glioma in mice.
  • Children affected with the inherited tumor predisposition syndrome, neurofibromatosis 1 (NF1), are prone to the development of low-grade astrocytic optic pathway tumors (optic pathway glioma [OPG]).
  • Previously, we developed a model of NF1-associated astrocytoma (GFAPCre; Nf1(flox/mut) mice) in which mice develop optic nerve and chiasm glioma.
  • Last, we observed neovascularization and microglial cell infiltration by 3 weeks of age before overt neoplastic transformation, suggesting that these cellular changes participate in the early stages of tumor formation.
  • [MeSH-major] Glioma / complications. Neurofibromatosis 1 / complications. Optic Nerve Neoplasms / complications
  • [MeSH-minor] Age Factors. Animals. Animals, Newborn. Antigens / metabolism. Blood Vessels / physiology. Disease Models, Animal. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry / methods. Indoles / metabolism. Intermediate Filament Proteins / metabolism. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging / methods. Mice. Mice, Transgenic. Nerve Tissue Proteins / metabolism. Nestin. Staining and Labeling / methods. von Willebrand Factor / immunology

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  • (PMID = 15622533.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R24 CA 83060; United States / NEI NIH HHS / EY / 5T32 EY 13360-03; United States / NINDS NIH HHS / NS / NS 36996; United States / NCI NIH HHS / CA / P30 CA 91842
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Glial Fibrillary Acidic Protein; 0 / Indoles; 0 / Intermediate Filament Proteins; 0 / Ki-67 Antigen; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Von Willebrand antigen; 0 / von Willebrand Factor; 47165-04-8 / DAPI
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87. Akimoto J, Fukami S, Tsutsumi M, Hashimoto T, Miki T, Haraoka J, Kudo M: Radiopathological characteristics of cerebellar malignant glioma in adults. Brain Tumor Pathol; 2009;26(2):59-68
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  • [Title] Radiopathological characteristics of cerebellar malignant glioma in adults.
  • Our aim was to extract the radiopathological features of cerebellar malignant glioma in adults from the four cases we encountered.
  • All four cases (two men and two women, aged 52-80 years; mean age, 67 years) had a floating sensation or vertigo at the onset of their disease.
  • These patients were followed up for 2-14 months (mean, 6 months), and the tumor was detected when their clinical symptoms deteriorated.
  • The tumor was located in the hemisphere in one patient and in the vermis in three patients.
  • All patients underwent subtotal tumor resection, followed by postoperative radiochemotherapy.
  • The pathological features were typical of malignant glioma, partially presenting the features of low-grade glioma, such as pilocytic, astrocytic, or oligodendroglial components.
  • At the onset of cerebellar malignant glioma, diagnostic imaging shows few signs of brain tumor.
  • Because cerebellar malignant glioma is a rare disease, it is difficult to differentiate it from metastatic brain tumors and primary central nervous system lymphoma by preoperative imaging.
  • Some patho logical features suggesting malignant transformation from low-grade glioma were detected.
  • [MeSH-major] Cerebellar Neoplasms / radiography. Cerebellum / radiography. Glioma / radiography
  • [MeSH-minor] Aged. Aged, 80 and over. Fatal Outcome. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Staining and Labeling. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19856216.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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88. Puustinen P, Junttila MR, Vanhatupa S, Sablina AA, Hector ME, Teittinen K, Raheem O, Ketola K, Lin S, Kast J, Haapasalo H, Hahn WC, Westermarck J: PME-1 protects extracellular signal-regulated kinase pathway activity from protein phosphatase 2A-mediated inactivation in human malignant glioma. Cancer Res; 2009 Apr 1;69(7):2870-7
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  • [Title] PME-1 protects extracellular signal-regulated kinase pathway activity from protein phosphatase 2A-mediated inactivation in human malignant glioma.
  • Sustained ERK pathway activity is commonly observed in human malignancies; however, the mechanisms by which the pathway is protected from phosphatase-mediated inactivation in the tumor tissue remain obscure.
  • In malignant gliomas, PME-1 expression levels correlate with both ERK activity and cell proliferation in vivo.
  • Moreover, PME-1 expression significantly correlates with disease progression in human astrocytic gliomas (n=222).
  • Together, these observations identify PME-1 expression as one mechanism by which ERK pathway activity is maintained in cancer cells and suggest an important functional role for PME-1 in the disease progression of human astrocytic gliomas.


89. Hartmann C, Meyer J, Balss J, Capper D, Mueller W, Christians A, Felsberg J, Wolter M, Mawrin C, Wick W, Weller M, Herold-Mende C, Unterberg A, Jeuken JW, Wesseling P, Reifenberger G, von Deimling A: Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas. Acta Neuropathol; 2009 Oct;118(4):469-74
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  • [Title] Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas.
  • Somatic mutations in the IDH1 gene encoding cytosolic NADP+-dependent isocitrate dehydrogenase have been shown in the majority of astrocytomas, oligodendrogliomas and oligoastrocytomas of WHO grades II and III.
  • Preliminary data suggest an importance of IDH1 mutation for prognosis showing that patients with anaplastic astrocytomas, oligodendrogliomas and oligoastrocytomas harboring IDH1 mutations seem to fare much better than patients without this mutation in their tumors.
  • To determine mutation types and their frequencies, we examined 1,010 diffuse gliomas.
  • We found 165 IDH1 (72.7%) and 2 IDH2 mutations (0.9%) in 227 diffuse astrocytomas WHO grade II, 146 IDH1 (64.0%) and 2 IDH2 mutations (0.9%) in 228 anaplastic astrocytomas WHO grade III, 105 IDH1 (82.0%) and 6 IDH2 mutations (4.7%) in 128 oligodendrogliomas WHO grade II, 121 IDH1 (69.5%) and 9 IDH2 mutations (5.2%) in 174 anaplastic oligodendrogliomas WHO grade III, 62 IDH1 (81.6%) and 1 IDH2 mutations (1.3%) in 76 oligoastrocytomas WHO grade II and 117 IDH1 (66.1%) and 11 IDH2 mutations (6.2%) in 177 anaplastic oligoastrocytomas WHO grade III.
  • We report on an inverse association of IDH1 and IDH2 mutations in these gliomas and a non-random distribution of the mutation types within the tumor entities.
  • IDH1 mutations of the R132C type are strongly associated with astrocytoma, while IDH2 mutations predominantly occur in oligodendroglial tumors.
  • In addition, patients with anaplastic glioma harboring IDH1 mutations were on average 6 years younger than those without these alterations.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Isocitrate Dehydrogenase / genetics
  • [MeSH-minor] Adult. Age Factors. Brain / pathology. Cell Differentiation. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Mutation. Prognosis. Tumor Cells, Cultured

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  • (PMID = 19554337.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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90. Bajetto A, Barbieri F, Dorcaratto A, Barbero S, Daga A, Porcile C, Ravetti JL, Zona G, Spaziante R, Corte G, Schettini G, Florio T: Expression of CXC chemokine receptors 1-5 and their ligands in human glioma tissues: role of CXCR4 and SDF1 in glioma cell proliferation and migration. Neurochem Int; 2006 Oct;49(5):423-32
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  • [Title] Expression of CXC chemokine receptors 1-5 and their ligands in human glioma tissues: role of CXCR4 and SDF1 in glioma cell proliferation and migration.
  • The expression of five CXC chemokine receptors and their main ligands was analysed by RT-PCR in 31 human astrocytic neoplasms.
  • CXCR4 and SDF1 were the most frequently mRNA identified (29/31 and 13/31 of the gliomas studied, respectively).
  • These results provide evidence of the expression of multiple CXC chemokines and their receptors in brain tumours and that in particular CXCR4 and SDF1 sustain proliferation and migration of glioma cells to promote malignant progression.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Cell Proliferation. Chemokines, CXC / physiology. Glioma / metabolism. Receptors, Chemokine / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. DNA Primers. Humans. Immunohistochemistry. Ligands. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16621164.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines, CXC; 0 / DNA Primers; 0 / Ligands; 0 / Receptors, Chemokine
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91. Likavcanová K, Dobrota D, Liptaj T, Prónayová N, Mlynárik V, Belan V, Galanda M, Béres A, De Riggo J: In vitro study of astrocytic tumour metabolism by proton magnetic resonance spectroscopy. Gen Physiol Biophys; 2005 Sep;24(3):327-35
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  • [Title] In vitro study of astrocytic tumour metabolism by proton magnetic resonance spectroscopy.
  • In vivo magnetic resonance spectroscopy (MRS) studies of glial brain tumours reported that higher grade of astrocytoma is associated with increased level of choline-containing compounds (Cho) and decreased levels of N-acetylaspartate (NAA) and creatine and phosphocreatine (Cr).
  • In this work, we studied the metabolism of glioma tumours by in vitro proton magnetic resonance spectroscopy (1H-MRS).
  • 1H-MR spectra were recorded in vitro from perchloric acid extracts of astrocytoma (WHO II) and glioblastoma multiforme (WHO IV) samples.
  • We observed differences between astrocytoma and glioblastoma multiforme in the levels of Cho, alanine, lactate, NAA, and glutamate/glutamine.
  • In astrocytoma samples, we found higher MR signal of NAA and lower signal of Cho and alanine.
  • The NAA/Cr ratio was higher in astrocytomas than in glioblastomas multiforme.
  • [MeSH-major] Astrocytes / pathology. Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Spectroscopy / methods. Neoplasms / metabolism
  • [MeSH-minor] Aspartic Acid / analogs & derivatives. Aspartic Acid / therapeutic use. Brain / metabolism. Brain / pathology. Choline / chemistry. Choline / pharmacology. Chromium / chemistry. Creatine / chemistry. Glioblastoma / chemistry. Glioblastoma / metabolism. Glioma / pathology. Humans. In Vitro Techniques. Phosphocreatine / chemistry. Spectrophotometry

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  • (PMID = 16308427.001).
  • [ISSN] 0231-5882
  • [Journal-full-title] General physiology and biophysics
  • [ISO-abbreviation] Gen. Physiol. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 020IUV4N33 / Phosphocreatine; 0R0008Q3JB / Chromium; 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; MU72812GK0 / Creatine; N91BDP6H0X / Choline
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92. Korkolopoulou P, Perdiki M, Thymara I, Boviatsis E, Agrogiannis G, Kotsiakis X, Angelidakis D, Rologis D, Diamantopoulou K, Thomas-Tsagli E, Kaklamanis L, Gatter K, Patsouris E: Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX. Hum Pathol; 2007 Apr;38(4):629-38

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX.
  • In the present study, we examined the expression of this enzyme in diffuse gliomas of astrocytic origin in relation to vascular endothelial growth factor (VEGF) and HIF-1alpha expression, proliferation rate (as assessed with Ki-67 antigen), microvessel morphology, and survival.
  • We conclude that CAIX may be used as a prognostic indicator in diffuse astrocytomas to refine the information provided by grade.
  • Given the role of CAIX in the acidification of tumor environment and its up-regulation by hypoxia, it is thought that CAIX expression may be linked to resistance of tumor cells to radiotherapy by allowing them to acclimatize to a hypoxic and acidic microenvironment.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Astrocytoma / metabolism. Astrocytoma / pathology. Carbonic Anhydrases / biosynthesis

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  • (PMID = 17367605.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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93. Wiencke JK, Aldape K, McMillan A, Wiemels J, Moghadassi M, Miike R, Kelsey KT, Patoka J, Long J, Wrensch M: Molecular features of adult glioma associated with patient race/ethnicity, age, and a polymorphism in O6-methylguanine-DNA-methyltransferase. Cancer Epidemiol Biomarkers Prev; 2005 Jul;14(7):1774-83
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  • [Title] Molecular features of adult glioma associated with patient race/ethnicity, age, and a polymorphism in O6-methylguanine-DNA-methyltransferase.
  • BACKGROUND: Risk factors for adult glioma in the San Francisco Bay Area include well-known demographic features such as age and race/ethnicity, and our previous studies indicated that these characteristics are associated with the TP53 mutation status of patients' tumors.
  • METHODS: Molecular analyses were carried out on 556 incident astrocytic tumors.
  • RESULTS: The tumor data confirm the inverse relationships between TP53 mutation and MDM2 (P = 0.04) or EGFR (P = 0.004) amplification and that patients whose tumors contain TP53 mutations are younger than those without (P < 0.001).
  • Although there was little difference in age of patient by EGFR amplification or expression among glioblastoma multiforme cases, EGFR gene amplification was associated with much older age of onset of anaplastic astrocytoma; for example, EGFR-amplified anaplastic astrocytoma cases were on average 63 years old compared with 48 years for nonamplified cases (P = 0.005).
  • CONCLUSIONS: Our results are consistent with ethnic variation in glioma pathogenesis.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Molecular Biology. Nuclear Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Polymorphism, Genetic. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Biomarkers, Tumor / genetics. Ethnic Groups. Female. Gene Amplification. Genes, p53. Humans. Male. Middle Aged. Prevalence. Proto-Oncogene Proteins c-mdm2. San Francisco / epidemiology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16030116.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES04705; United States / NIEHS NIH HHS / ES / ES06717; United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01CA52689
  • [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 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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94. Rosenzweig T, Ziv-Av A, Xiang C, Lu W, Cazacu S, Taler D, Miller CG, Reich R, Shoshan Y, Anikster Y, Kazimirsky G, Sarid R, Brodie C: Related to testes-specific, vespid, and pathogenesis protein-1 (RTVP-1) is overexpressed in gliomas and regulates the growth, survival, and invasion of glioma cells. Cancer Res; 2006 Apr 15;66(8):4139-48
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  • [Title] Related to testes-specific, vespid, and pathogenesis protein-1 (RTVP-1) is overexpressed in gliomas and regulates the growth, survival, and invasion of glioma cells.
  • In this study, we examined the expression and functions of related to testes-specific, vespid, and pathogenesis protein 1 (RTVP-1) in glioma cells.
  • RTVP-1 was expressed in high levels in glioblastomas, whereas its expression in low-grade astrocytomas and normal brains was very low.
  • Transfection of glioma cells with small interfering RNAs targeting RTVP-1 decreased cell proliferation in all the cell lines examined and induced cell apoptosis in some of them.
  • Overexpression of RTVP-1 increased astrocyte and glioma cell proliferation and the anchorage-independent growth of the cells.
  • In addition, overexpression of RTVP-1 rendered glioma cells more resistant to the apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand and serum deprivation.
  • Finally, we found that RTVP-1 regulated the invasion of glioma cells as was evident by their enhanced migration through Matrigel and by their increased invasion in a spheroid confrontation assay.
  • Our results suggest that the expression of RTVP-1 is correlated with the degree of malignancy of astrocytic tumors and that RTVP-1 is involved in the regulation of the growth, survival, and invasion of glioma cells.
  • Collectively, these findings suggest that RTVP-1 is a potential therapeutic target in gliomas.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioma / metabolism. Glioma / pathology. Neoplasm Proteins / biosynthesis. Nerve Tissue Proteins / biosynthesis
  • [MeSH-minor] Amino Acid Sequence. Apoptosis / physiology. Astrocytoma / enzymology. Astrocytoma / metabolism. Astrocytoma / pathology. Cell Growth Processes / physiology. Cell Line, Tumor. Cell Survival / physiology. Glioblastoma / enzymology. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Matrix Metalloproteinase 2 / metabolism. Molecular Sequence Data. Neoplasm Invasiveness

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  • (PMID = 16618735.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-R21-96965
  • [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 / GLIPR1 protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; EC 3.4.24.24 / Matrix Metalloproteinase 2
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95. Dasgupta B, Yi Y, Hegedus B, Weber JD, Gutmann DH: Cerebrospinal fluid proteomic analysis reveals dysregulation of methionine aminopeptidase-2 expression in human and mouse neurofibromatosis 1-associated glioma. Cancer Res; 2005 Nov 1;65(21):9843-50
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  • [Title] Cerebrospinal fluid proteomic analysis reveals dysregulation of methionine aminopeptidase-2 expression in human and mouse neurofibromatosis 1-associated glioma.
  • Individuals affected with the neurofibromatosis 1 (NF1) tumor predisposition syndrome are prone to the development of multiple nervous system tumors, including optic pathway gliomas (OPG).
  • The NF1 tumor suppressor gene product, neurofibromin, functions as a Ras GTPase-activating protein, and has been proposed to regulate cell growth by inhibiting Ras activity.
  • As part of a larger effort to identify protein markers for NF1-associated astrocytomas that could be exploited for therapeutic drug design, we did an objective proteomic analysis of the cerebrospinal fluid from genetically engineered Nf1 mice with optic glioma.
  • In this study, we show that Nf1 mouse OPGs and NF1-associated human astrocytic tumors, but not sporadic pilocytic or other low-grade astrocytomas, specifically expressed high levels of MetAP2.
  • These observations suggest that MetAP2 is regulated by neurofibromin, and that MetAP2 inhibitors could be potentially employed to treat NF1-associated tumor proliferation.
  • [MeSH-major] Aminopeptidases / cerebrospinal fluid. Glioma / cerebrospinal fluid. Metalloendopeptidases / cerebrospinal fluid. Neurofibromatosis 1 / cerebrospinal fluid. Optic Nerve Neoplasms / cerebrospinal fluid
  • [MeSH-minor] Amino Acid Sequence. Animals. Astrocytes / cytology. Astrocytes / drug effects. Astrocytes / pathology. Astrocytoma / cerebrospinal fluid. Astrocytoma / complications. Astrocytoma / enzymology. Astrocytoma / genetics. Cell Growth Processes / drug effects. Cyclohexanes. Fatty Acids, Unsaturated / pharmacology. Gene Silencing. Glycoproteins / antagonists & inhibitors. Glycoproteins / biosynthesis. Glycoproteins / cerebrospinal fluid. Glycoproteins / genetics. Humans. Mice. Mice, Transgenic. Molecular Sequence Data. Neurofibromin 1 / deficiency. Neurofibromin 1 / genetics. Proteomics. Sesquiterpenes. Tumor Suppressor Proteins / genetics

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  • (PMID = 16267007.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclohexanes; 0 / Fatty Acids, Unsaturated; 0 / Glycoproteins; 0 / Neurofibromin 1; 0 / Sesquiterpenes; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; 7OW73204U1 / fumagillin; EC 3.4.11.- / Aminopeptidases; EC 3.4.11.18 / Metap2 protein, mouse; EC 3.4.11.18 / methionine aminopeptidase 2; EC 3.4.24.- / Metalloendopeptidases
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96. Elgamal EA, Coakham HB: Hemifacial spasm caused by pontine glioma: case report and review of the literature. Neurosurg Rev; 2005 Oct;28(4):330-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemifacial spasm caused by pontine glioma: case report and review of the literature.
  • The case of an adult man harbouring brain stem glioma (BSG) whose only neurological signs were left HFS and mild facial weakness is reported.
  • No responsible vessel could be identified during surgery, but the causative lesion was found to be an astrocytic tumour encasing the facial nerve at its root exit zone from the brain stem.
  • [MeSH-major] Astrocytoma / complications. Brain Stem Neoplasms / complications. Hemifacial Spasm / etiology
  • [MeSH-minor] Electrophysiology. Facial Nerve Diseases / etiology. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Nerve Compression Syndromes / etiology. Neurologic Examination. Neurosurgical Procedures. Tomography, X-Ray Computed

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  • (PMID = 16001287.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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97. Konan KE, Diabate AS, N'Guessan ND, Anzouan KE, Yapi-Yapo CP, Assouan C, Assa A, Ouattara DN: [Diagnostic and surgical approach to an hourglass-shaped nasopalatine glioma in an infant]. Odontostomatol Trop; 2010 Sep;33(131):5-10
MedlinePlus Health Information. consumer health - Nose Injuries and Disorders.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnostic and surgical approach to an hourglass-shaped nasopalatine glioma in an infant].
  • [Transliterated title] Approche diagnostique et chirurgicale d'un gliome naso-palatin "en sablier" chez un nourrisson.
  • The authors report a case of glioma nasopalatine Multifoil in wallet, location-intra nasal and palatal left.
  • The nasal glioma is a rare congenital malformation presenting as a nasal mass composed of neuroglial tissue heteropias resulting from an abnormality in embryonic development.
  • It is a benign tumor that fits into the nosology of the masses of the midline.
  • This abnormality arises primarily a diagnostic problem because often mistaken for a meningo-encephalocele or a nasal dermoid cyst.
  • Histology examination of the surgical specimen confirmed the nature of astrocytic neuroglial tumor.
  • The location of the tumor pedide palate to that of the left nostril is special and especially histological diagnosis of this congenital malformation.
  • [MeSH-major] Choristoma / congenital. Maxillary Diseases / congenital. Nose Diseases / congenital. Palate / pathology

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  • (PMID = 21328923.001).
  • [ISSN] 0251-172X
  • [Journal-full-title] Odonto-stomatologie tropicale = Tropical dental journal
  • [ISO-abbreviation] Odontostomatol Trop
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Senegal
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98. Andreiuolo F, Junier MP, Hol EM, Miquel C, Chimelli L, Leonard N, Chneiweiss H, Daumas-Duport C, Varlet P: GFAPdelta immunostaining improves visualization of normal and pathologic astrocytic heterogeneity. Neuropathology; 2009 Feb;29(1):31-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GFAPdelta immunostaining improves visualization of normal and pathologic astrocytic heterogeneity.
  • We therefore evaluated GFAPdelta immunostaining in a wide panel of astrogliosis and gliomas, and compared these with GFAP and vimentin.
  • In normal tissue, gliosis and gliomas, GFAPdelta immunostaining was observed in astrocytes with relatively high GFAP levels.
  • Interestingly GFAPdelta and vimentin immunostainings coincided in normal tissues and gliosis, but not in gliomas.
  • [MeSH-major] Astrocytes / cytology. Astrocytes / pathology. Brain Diseases / pathology. Brain Neoplasms / pathology. Glial Fibrillary Acidic Protein / analysis. Glioma / pathology

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  • (PMID = 18564099.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
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99. Hai J, Lin Q, Zhang H, Lu Y, Yi J: Cyclic AMP-dependent regulation of differentiation of rat C6 glioma cells by panaxydol. Neurol Res; 2009 Apr;31(3):274-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclic AMP-dependent regulation of differentiation of rat C6 glioma cells by panaxydol.
  • OBJECTIVES: Preliminary works have indicated that panaxydol possesses growth inhibition and induces differentiation in rat C6 glioma cells.
  • Astrocytic processes were quantified under a phase-contrasted microscope.
  • CONCLUSION: These results suggest that the cAMP-dependent pathway may regulate cellular proliferation, migration and differentiation in C6 glioma cells by panaxydol.
  • [MeSH-major] Cell Differentiation / drug effects. Cyclic AMP / metabolism. Diynes / pharmacology. Fatty Alcohols / pharmacology. Glial Fibrillary Acidic Protein / metabolism. Glioma / pathology
  • [MeSH-minor] Animals. Astrocytes / pathology. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Growth Inhibitors / administration & dosage. Male. Mice. Mice, Nude. Rats. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 19040798.001).
  • [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 / Diynes; 0 / Fatty Alcohols; 0 / Glial Fibrillary Acidic Protein; 0 / Growth Inhibitors; 72800-72-7 / panaxydol; E0399OZS9N / Cyclic AMP
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100. Elsir T, Eriksson A, Orrego A, Lindström MS, Nistér M: Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas. J Neuropathol Exp Neurol; 2010 Feb;69(2):129-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas.
  • PROX1 is a prospero-related transcription factor that plays a critical role in the development of various organs including the mammalian lymphatic and central nervous systems; it controls cell proliferation and differentiation through different transcription pathwaysand has both oncogenic and tumor-suppressive functions.
  • We investigated PROX1 expression patterns in 56 human astrocytic gliomas of different grades using immunohistochemistry.
  • An average of 79% of cells in World Health Organization Grade IV (glioblastoma, n = 15) and 57% of cells in World Health Organization Grade III (anaplastic astrocytoma, n = 13) were strongly PROX1 positive; low-grade diffuse astrocytomas (Grade II, n = 13) had 21% of cells that were strongly positive; Grade I tumors (n = 15) had 1.5%; and non-neoplastic brain tissue (n = 15) had 3.7% of cells that were PROX1 positive.
  • Analyses of coexpression with proliferation markers suggest that PROX1+ cells have a marginally lower rate of proliferation than other tumor cells but are still mitotically active.
  • We conclude that PROX1 may constitute a useful tool for the diagnosis and grading ofastrocytic gliomas and for distinguishing Grade III and Grade IV tumors from Grade I and Grade II tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Homeodomain Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Antigens, Nuclear / metabolism. Biomarkers / metabolism. Brain Diseases / metabolism. Cell Proliferation. Humans. Immunohistochemistry. Microtubule-Associated Proteins / metabolism. Microvessels / metabolism. Mitosis. Nerve Tissue Proteins / metabolism. Tubulin / metabolism

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  • (PMID = 20084020.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / neuronal nuclear antigen NeuN, human; 0 / prospero-related homeobox 1 protein
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