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1. Haapasalo J, Hilvo M, Nordfors K, Haapasalo H, Parkkila S, Hyrskyluoto A, Rantala I, Waheed A, Sly WS, Pastorekova S, Pastorek J, Parkkila AK: Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas. Neuro Oncol; 2008 Apr;10(2):131-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas.
  • CA XII has been proposed to be involved in acidification of the extracellular milieu, creating an appropriate microenvironment for rapid tumor growth.
  • Because RNA sequence databases have indicated that two isoforms of CA XII might exist in human tissues, and because alternatively spliced protein forms have been linked to aggressive behavior of cancer cells, we designed a study to evaluate the presence of the two forms of CA XII in diffuse astrocytomas, a tumor type known for its aggressive and often noncurable behavior.
  • Reverse transcription PCR of tumor samples surprisingly revealed that CA XII present in diffuse astrocytomas is mainly encoded by a shorter mRNA variant.
  • We further showed by Western blotting that anti-CA XII antibody recognized both isoforms in the glioblastoma cell lines, and we then evaluated the expression of CA XII in astrocytomas using immunohistochemistry and correlated the results with various clinicopathological and molecular factors.
  • Of 370 diffusely infiltrating astrocytomas, 363 cases (98%) showed immunoreactions for CA XII.
  • From these results, we conclude that CA XII is commonly expressed in diffuse astrocytomas and that it might be used as a biomarker of poor prognosis.
  • The absence of 11 amino acids in the shorter isoform, which seems to be common in astrocytomas, may affect the normal quaternary structure and biological function of CA XII.
  • [MeSH-major] Astrocytoma / enzymology. Biomarkers, Tumor / analysis. Brain Neoplasms / enzymology. Carbonic Anhydrases / genetics. Carbonic Anhydrases / metabolism

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  • (PMID = 18322268.001).
  • [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 / Isoenzymes; EC 4.2.1.1 / CA13 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2613815
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2. 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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  • [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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3. 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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4. 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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5. 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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  • [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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6. 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.


7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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8. 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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9. Koos B, Peetz-Dienhart S, Riesmeier B, Frühwald MC, Hasselblatt M: O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation is significantly less frequent in ependymal tumours as compared to malignant astrocytic gliomas. Neuropathol Appl Neurobiol; 2010 Jun;36(4):356-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] O(6)-methylguanine-DNA methyltransferase (MGMT) promoter methylation is significantly less frequent in ependymal tumours as compared to malignant astrocytic gliomas.
  • [MeSH-major] Astrocytoma / genetics. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Ependymoma / genetics. Promoter Regions, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 20202118.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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10. Arjona D, Bello MJ, Rey JA: EGFR intragenic loss and gene amplification in astrocytic gliomas. Cancer Genet Cytogenet; 2006 Jan 1;164(1):39-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR intragenic loss and gene amplification in astrocytic gliomas.
  • We have studied EGFR gene amplification and allelic status of chromosome 7 in 68 tumors consisting of 34 WHO grade IV glioblastomas (26 primary and 8 secondary), 14 WHO grade III anaplastic astrocytomas, and 20 WHO grade II astrocytomas, by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP), quantitative PCR, and microsatellite analysis.
  • [MeSH-major] Astrocytoma / genetics. Gene Amplification. Genes, erbB-1. Loss of Heterozygosity

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  • (PMID = 16364761.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Shostak KO, Dmitrenko VV, Vudmaska MI, Naidenov VG, Beletskii AV, Malisheva TA, Semenova VM, Zozulya YP, Demotes-Mainard J, Kavsan VM: Patterns of expression of TSC-22 protein in astrocytic gliomas. Exp Oncol; 2005 Dec;27(4):314-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of expression of TSC-22 protein in astrocytic gliomas.
  • AIM: To evaluate expression patterns of protein product of putative tumor suppressor gene TSC-22 in human astrocytic tumors by immunohistochemical approach.
  • Immunohistochemical analysis of TSC-22 and GFAP expression with the use of anti-human-TSC-22- and anti-human-GFAP-antibodies was performed on histological slides of astrocytic tumors.
  • RESULTS: Immunohistochemical analysis has shown that the number of cells expressing TSC-22 was significantly lower in glioblastoma tissues than that in diffuse astrocytoma.
  • Double immunohistochemical staining of astrocytic tumors using anti-human-TSC-2- and anti-human-GFAP-antibodies showed that both TSC-22 and GFAP expression is co-localized in astrocytes.
  • In more aggressive forms of astrocytic tumors decreased expression of TSC-22 mRNA correlates with its lowered expression on protein level.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Repressor Proteins / biosynthesis
  • [MeSH-minor] Amino Acid Sequence. Astrocytes / metabolism. Base Sequence. Biomarkers, Tumor / analysis. Gene Expression Profiling. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Microglia / metabolism. Molecular Sequence Data. Recombinant Proteins / biosynthesis. Recombinant Proteins / genetics

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  • (PMID = 16404353.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / TSC22D1 protein, human
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12. 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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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. Völker HU, Hagemann C, Coy J, Wittig R, Sommer S, Stojic J, Haubitz I, Vince GH, Kämmerer U, Monoranu CM: Expression of transketolase-like 1 and activation of Akt in grade IV glioblastomas compared with grades II and III astrocytic gliomas. Am J Clin Pathol; 2008 Jul;130(1):50-7
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  • [Title] Expression of transketolase-like 1 and activation of Akt in grade IV glioblastomas compared with grades II and III astrocytic gliomas.
  • This study was performed to compare the expression of transketolase-like 1 (TKTL1) and p-Akt in glioblastoma multiforme (GBM) and other astrocytic gliomas (AGs, grades II and III).
  • Immunohistochemically, the tumor grade significantly correlated with expression of TKTL1.
  • Compared with grades II and III AGs, GBMs showed higher expression of TKTL1, more positive tumors, and a higher percentage of positive tumor cells.
  • [MeSH-major] Astrocytoma / enzymology. Glioblastoma / enzymology. Proto-Oncogene Proteins c-akt / metabolism. Transketolase / biosynthesis

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  • (PMID = 18550470.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.2.1.1 / TKTL1 protein, human; EC 2.2.1.1 / Transketolase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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15. Arjona D, Bello MJ, Alonso ME, Isla A, De Campos JM, Vaquero J, Sarasa JL, Gutierrez M, Rey JA: Real-time quantitative PCR analysis of regions involved in gene amplification reveals gene overdose in low-grade astrocytic gliomas. Diagn Mol Pathol; 2005 Dec;14(4):224-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Real-time quantitative PCR analysis of regions involved in gene amplification reveals gene overdose in low-grade astrocytic gliomas.
  • We have studied gene amplification of genes located in 1q32 (GAC1, ELF3, MDM4, and ren1), 4q11 (PDGFR-alpha), and in 12q13-14 (MDM2 and CDK4) using quantitative real-time PCR in a group of 86 tumors consisting of 44 WHO grade IV glioblastomas (GBM) (34 primary and 10 secondary tumors), 21 WHO grade III anaplastic astrocytomas (AA), and 21 WHO grade II astrocytomas (AII).
  • GAC1 (51%) and MDM4 (27%) were the most frequently amplified genes within the 1q32 amplicon, and their higher amplification frequency was statistically significant (P<0.05, chi) in the low-grade astrocytomas.
  • The present study shows that gene amplification in the studied regions is already present in low-grade astrocytic tumors and that amplification of some genes may represent another molecular marker to differentiate primary from secondary GBM.
  • [MeSH-major] Astrocytoma / genetics. Gene Amplification. Gene Dosage. Proto-Oncogenes / genetics
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Polymerase Chain Reaction

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  • (PMID = 16319692.001).
  • [ISSN] 1052-9551
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [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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16. 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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17. 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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18. 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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19. 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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20. 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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21. 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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22. 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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23. 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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24. 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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25. 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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26. 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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27. Landriscina M, Schinzari G, Di Leonardo G, Quirino M, Cassano A, D'Argento E, Lauriola L, Scerrati M, Prudovsky I, Barone C: S100A13, a new marker of angiogenesis in human astrocytic gliomas. J Neurooncol; 2006 Dec;80(3):251-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] S100A13, a new marker of angiogenesis in human astrocytic gliomas.
  • Indeed, S100A13 is a copper binding protein able to enhance the export of FGF1 in response to stress in vitro and to induce the formation of a multiprotein aggregate responsible for FGF1 release.
  • We investigated the expression of S100A13 in human astrocytic gliomas in relation to tumour grading and vascularization.
  • A series of 26 astrocytic gliomas was studied to evaluate microvessel density and to assess FGF1, S100A13 and VEGF-A expression.
  • FGF1 was equally expressed in the vast majority of tumours, whereas S100A13 and VEGF-A were significantly up-regulated in high-grade vascularized gliomas.
  • These data suggest that the up-regulation of S100A13 and VEGF-A expression correlates with the activation of angiogenesis in high-grade human astrocytic gliomas.
  • [MeSH-major] Astrocytoma / blood supply. Biomarkers, Tumor / metabolism. Brain Neoplasms / blood supply. Neovascularization, Pathologic / metabolism. S100 Proteins / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16773219.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL32348; United States / NHLBI NIH HHS / HL / HL35627; United States / NCRR NIH HHS / RR / RR1555
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / S100 Proteins; 0 / S100A13 protein, human; 0 / Vascular Endothelial Growth Factor A; 62031-54-3 / Fibroblast Growth Factors
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28. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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29. 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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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Katsetos CD, Reddy G, Dráberová E, Smejkalová B, Del Valle L, Ashraf Q, Tadevosyan A, Yelin K, Maraziotis T, Mishra OP, Mörk S, Legido A, Nissanov J, Baas PW, de Chadarévian JP, Dráber P: Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines. J Neuropathol Exp Neurol; 2006 May;65(5):465-77
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  • [Title] Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines.
  • Centrosome amplification is a pivotal mechanism underlying tumorigenesis but its role in gliomas is underinvestigated.
  • The present study specifically examines the expression and distribution of the centrosome-associated cytoskeletal protein gamma-tubulin in 56 primary diffuse astrocytic gliomas (grades II-IV) and in 4 human glioblastoma cell lines (U87MG, U118MG, U138MG, and T98G).
  • In tumors in adults (n = 46), varying degrees of localization were detected in all tumor grades, but immunoreactivity was significantly increased in high-grade anaplastic astrocytomas and glioblastomas multiforme as compared to low-grade diffuse astrocytomas (p = 0.0001).
  • A similar trend was noted in diffuse gliomas in children but the sample of cases was too small as to be statistically meaningful.
  • Our results indicate that overexpression and ectopic cellular distribution of gamma-tubulin in astrocytic gliomas may be significant in the context of centrosome protein amplification and may be linked to tumor progression and anaplastic potential.
  • [MeSH-minor] Antigens / metabolism. Blotting, Northern / methods. Cell Line, Tumor. Humans. Immunohistochemistry / methods

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  • (PMID = 16772870.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
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32. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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33. Zscharnack K, Kessler R, Bleichert F, Warnke JP, Eschrich K: The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells. Neuropathol Appl Neurobiol; 2009 Dec;35(6):566-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells.
  • Here, we studied the role of the PFKFB3 splice variants in human astrocytic gliomas.
  • METHODS: We analysed the PFKFB3 splice variants in 48 astrocytic gliomas by RT-PCR and real-time PCR.
  • RESULTS: UBI2K5 and UBI2K6 are the predominant splice variants in rapidly proliferating high-grade astrocytomas while the expression of UBI2K3 and UBI2K4 is mainly restricted to low-grade astrocytomas and nonneoplastic brain tissue.
  • The UBI2K4 mRNA level is downregulated in astrocytic gliomas with increasing malignancy grade.
  • CONCLUSIONS: Our results demonstrate that the splice variant UBI2K4 impedes the tumour cell growth and might serve as a tumour suppressor in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Phosphofructokinase-2 / metabolism
  • [MeSH-minor] Brain / metabolism. Cell Count. Cell Line, Tumor. Cell Proliferation. Cell Survival. Down-Regulation. Humans. Neoplasm Staging. Polymerase Chain Reaction. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transfection

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  • (PMID = 19490427.001).
  • [ISSN] 1365-2990
  • [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 / Protein Isoforms; 0 / RNA, Messenger; EC 2.7.1.105 / PFKFB3 protein, human; EC 2.7.1.105 / Phosphofructokinase-2
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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. Katsetos CD, Dráberová E, Smejkalová B, Reddy G, Bertrand L, de Chadarévian JP, Legido A, Nissanov J, Baas PW, Dráber P: Class III beta-tubulin and gamma-tubulin are co-expressed and form complexes in human glioblastoma cells. Neurochem Res; 2007 Aug;32(8):1387-98
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  • We have previously shown that the neuronal-associated class III beta-tubulin isotype and the centrosome-associated gamma-tubulin are aberrantly expressed in astrocytic gliomas (Cell Motil Cytoskeleton 2003, 55:77-96; J Neuropathol Exp Neurol 2006, 65:455-467).
  • Here we determined the expression, distribution and interaction of betaIII-tubulin and gamma-tubulin in diffuse-type astrocytic gliomas (grades II-IV) (n = 17) and the human glioblastoma cell line T98G.
  • By immunohistochemistry and immunofluorescence microscopy, betaIII-tubulin and gamma-tubulin were co-distributed in anaplastic astrocytomas and glioblastomas and to a lesser extent, in low-grade diffuse astrocytomas (P < 0.05).
  • [MeSH-minor] Adult. Antineoplastic Agents, Phytogenic / pharmacology. Cell Line, Tumor / cytology. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Child. Humans. Multiprotein Complexes. Nocodazole / pharmacology. Paclitaxel / pharmacology. Tubulin Modulators / pharmacology. Vinblastine / pharmacology

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  • (PMID = 17406983.001).
  • [ISSN] 0364-3190
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Multiprotein Complexes; 0 / TUBB3 protein, human; 0 / Tubulin; 0 / Tubulin Modulators; 5V9KLZ54CY / Vinblastine; P88XT4IS4D / Paclitaxel; SH1WY3R615 / Nocodazole
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36. Nutt CL: Molecular genetics of oligodendrogliomas: a model for improved clinical management in the field of neurooncology. Neurosurg Focus; 2005 Nov;19(5):E2
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  • Oligodendrogliomas, in contrast to astrocytic gliomas, frequently respond to chemotherapy and have a better overall prognosis.
  • Furthermore, 1p/19q loss has been shown to correlate with unequivocal oligodendroglial tumor histology, location and growth pattern of tumors within the brain, and magnetic resonance imaging characteristics.
  • Although much is also known about the molecular pathological characteristics of astrocytic gliomas, the significance of this information to clinical management in patients with these tumors has not been as striking as has been the case for oligodendrogliomas; possible reasons for this are discussed.
  • [MeSH-minor] Disease Management. Humans. Medical Oncology / methods


37. Yoo H, Sohn S, Nam BH, Min HS, Jung E, Shin SH, Gwak HS, Lee SH: The expressions of carbonic anhydrase 9 and vascular endothelial growth factor in astrocytic tumors predict a poor prognosis. Int J Mol Med; 2010 Jul;26(1):3-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expressions of carbonic anhydrase 9 and vascular endothelial growth factor in astrocytic tumors predict a poor prognosis.
  • Hypoxia in the tumor microenvironment triggers a variety of genetic and adoptive responses that regulate tumor growth.
  • Tumor hypoxia is often associated with a malignant phenotype, resistance to therapy, and poor survival.
  • The objectives of this study were to evaluate the expressions of carbonic anhydrase 9 (CA9) and vascular endothelial growth factor (VEGF) in astrocytic gliomas and to relate patterns of expression with prognosis, that is with histological grade and survival.
  • We investigated 78 World Health Organization (WHO) grade II, III, and IV astrocytic gliomas.
  • Furthermore, VEGF expression was found to be significantly related to tumor grade (p=0.02) and tended to be related to overall survival (p=0.1).
  • Nevertheless, the expressions of CA9 and VEGF were found to be associated with tumor grade and possibly with survival.
  • Further studies on a larger patient population are needed to determine the correlation between the expressions of CA9, and VEGF in astrocytic gliomas and clinical outcome.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Astrocytoma / metabolism. Carbonic Anhydrases / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 20514415.001).
  • [ISSN] 1791-244X
  • [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 / Antigens, Neoplasm; 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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38. 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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39. Kessler R, Bleichert F, Warnke JP, Eschrich K: 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is up-regulated in high-grade astrocytomas. J Neurooncol; 2008 Feb;86(3):257-64
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  • [Title] 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is up-regulated in high-grade astrocytomas.
  • We investigated the PFKFB3 expression in 40 human astrocytic gliomas and 20 non-neoplastic brain tissue specimens.
  • The PFKFB3 protein levels were markedly elevated in high-grade astrocytomas relative to low-grade astrocytomas and corresponding non-neoplastic brain tissue, whereas no significant increase of PFKFB3 mRNA was observed in high-grade astrocytomas when compared with control tissue.
  • The findings demonstrate that PFKFB3 up-regulation is a hallmark of high-grade astrocytomas offering an explanation for high glycolytic flux and lactate production in these tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Phosphofructokinase-2 / metabolism. Up-Regulation / physiology


40. 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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41. 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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42. 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

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  • [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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43. Hogervorst JG, Schouten LJ, Konings EJ, Goldbohm RA, van den Brandt PA: Dietary acrylamide intake and brain cancer risk. Cancer Epidemiol Biomarkers Prev; 2009 May;18(5):1663-6
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  • At baseline, a random subcohort of 5,000 participants was randomly selected from the total cohort for a case-cohort approach.
  • Subgroup analyses were done for microscopically verified brain cancer, astrocytic gliomas, high-grade astrocytic gliomas, and never-smokers.

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  • (PMID = 19383886.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 20R035KLCI / Acrylamide
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44. 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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45. Miura FK, Alves MJ, Rocha MC, da Silva R, Oba-Shinjo SM, Marie SK: Xenograft transplantation of human malignant astrocytoma cells into immunodeficient rats: an experimental model of glioblastoma. Clinics (Sao Paulo); 2010 Mar;65(3):305-9
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  • [Title] Xenograft transplantation of human malignant astrocytoma cells into immunodeficient rats: an experimental model of glioblastoma.
  • INTRODUCTION: Astrocytic gliomas are the most common intracranial central nervous system neoplasias, accounting for about 60% of all primary central nervous system tumors.
  • Despite advances in the treatment of gliomas, no effective therapeutic approach is yet available; hence, the search for a more realistic model to generate more effective therapies is essential.
  • OBJECTIVE: To develop an experimental malignant astrocytoma model with the characteristics of the human tumor.
  • METHOD: Primary cells from subcutaneous xenograft tumors produced with malignant astrocytoma U87MG cells were inoculated intracerebrally by stereotaxis into immunosuppressed (athymic) Rowett rats.
  • CONCLUSION: A malignant astrocytoma intracerebral xenograft model with poorly invasive behavior was achieved in athymic Rowett rats.
  • Tumor invasiveness in an experimental animal model may depend on a combination of several factors, including the cell line used to induce tumor formation, the rat strains and the status of the animal's immune system.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Immunocompromised Host
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Female. Humans. Neoplasm Transplantation. Rats. Rats, Nude. Transplantation, Heterologous

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  • [Cites] Anticancer Res. 2006 Jul-Aug;26(4B):2887-900 [16886610.001]
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  • (PMID = 20360922.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC2845772
  • [Keywords] NOTNLM ; Athymic Rowett rats / Brain tumor / Experimental model / U87MG cells
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46. Lièvre A, Landi B, Côté JF, Veyrie N, Zucman-Rossi J, Berger A, Laurent-Puig P: Absence of mutation in the putative tumor-suppressor gene KLF6 in colorectal cancers. Oncogene; 2005 Nov 3;24(48):7253-6
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  • [Title] Absence of mutation in the putative tumor-suppressor gene KLF6 in colorectal cancers.
  • The KLF6 gene encodes the Krüppel-like factor 6, a transcription factor that has been individualized as a tumor-suppressor gene involved in the regulation of cell proliferation and differentiation.
  • Recently, high frequency (42%) of KLF6 mutations have been reported in colorectal cancers (CRC) as in prostate cancers, astrocytic gliomas and hepatocellular carcinomas.
  • [MeSH-major] Colorectal Neoplasms / genetics. Genes, Tumor Suppressor. Kruppel-Like Transcription Factors / genetics. Mutation. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Aged. Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 10. Exons. Female. Genetic Variation. Germ-Line Mutation. Humans. Introns. Loss of Heterozygosity. Male. Microsatellite Repeats. Neoplasm Staging. Nucleic Acid Amplification Techniques. Polymorphism, Single Nucleotide. Sequence Analysis, DNA. Zinc Fingers

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  • [Copyright] Oncogene (2005) 24, 7253-7256. doi:10.1038/sj.onc.1208867; published online 25 July 2005.
  • (PMID = 16044160.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / KLF6 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Proto-Oncogene Proteins
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47. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • In addition, we summarize the key genetic alterations that have been attributed to astrocytoma patho-genesis and progression.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • Novel animal models will provide us with the opportunity to comprehensively study this multilayered disease and explore novel therapeutic approaches in vivo.
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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48. Kunitz A, Wolter M, van den Boom J, Felsberg J, Tews B, Hahn M, Benner A, Sabel M, Lichter P, Reifenberger G, von Deimling A, Hartmann C: DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas. Brain Pathol; 2007 Oct;17(4):363-70
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  • [Title] DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas.
  • Allelic losses on 19q are found in the majority of oligodendroglial tumors and approximately one-third of diffuse astrocytomas.
  • However, the tumor suppressor genes (TSG) on 19q are still elusive.
  • In line with this, other authors reported EMP3 as being epigenetically silenced in neuroblastomas and astrocytomas.
  • To further investigate EMP3 as a TSG candidate on 19q13.3, we performed molecular analysis of this gene in 162 human gliomas.
  • Mutation analysis did not reveal EMP3 alteration in 132 gliomas.
  • In astrocytomas, EMP3 hypermethylation was also paralleled by reduced expression but was independent of the 19q status.
  • EMP3 hypermethylation was detected in more than 80% of diffuse, anaplastic astrocytomas and secondary glioblastomas.
  • Our data corroborate that oligodendroglial and astrocytic gliomas often show EMP3 hypermethylation and aberrant expression.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic / genetics. Glioma / genetics. Membrane Glycoproteins / genetics
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / physiopathology. Gene Expression Profiling. Gene Silencing / physiology. Genetic Predisposition to Disease / genetics. Humans. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / physiopathology. Oligonucleotide Array Sequence Analysis

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  • (PMID = 17610521.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / EMP3 protein, human; 0 / Membrane Glycoproteins
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49. 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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50. 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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51. Walton NM, Snyder GE, Park D, Kobeissy F, Scheffler B, Steindler DA: Gliotypic neural stem cells transiently adopt tumorigenic properties during normal differentiation. Stem Cells; 2009 Feb;27(2):280-9
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  • An increasing body of evidence suggests that astrocytic gliomas of the central nervous system may be derived from gliotypic neural stem cells.
  • However, when induced to differentiate, neural stem cells give rise to intermediate progenitors that transiently exhibit multiple glioma characteristics, including aneuploidy, loss of growth-contact inhibition, alterations in cell cycle, and growth factor insensitivity.
  • Further examination of progenitor populations revealed a subset of cells defined by the aberrant expression of (the pathological glioma marker) class III beta-tubulin that exhibit intrinsic parental properties of gliomas, including multilineage differentiation and continued proliferation in the absence of a complex cellular regulatory environment.

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  • (PMID = 18988710.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070143; United States / NICHD NIH HHS / HD / T32 HD043730; United States / NINDS NIH HHS / NS / NS055165; United States / NINDS NIH HHS / NS / NS37556; United States / NICHD NIH HHS / HD / T32HD043730; United States / NHLBI NIH HHS / HL / HL70143; United States / NINDS NIH HHS / NS / NS46384; United States / NINDS NIH HHS / NS / R01 NS037556; United States / NINDS NIH HHS / NS / R01 NS055165; United States / NINDS NIH HHS / NS / R21 NS046384
  • [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; 0 / Tubulin
  • [Other-IDs] NLM/ NIHMS686089; NLM/ PMC4425277
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52. Moodbidri MS, Shirsat NV: Induction of BAALC and down regulation of RAMP3 in astrocytes treated with differentiation inducers. Cell Biol Int; 2006 Mar;30(3):210-3
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  • Genes controlling proliferation and differentiation of astrocytes are likely to play an important role in the pathogenesis of astrocytic gliomas and could serve as therapeutic targets. mRNA differential display analysis identified two genes, viz.
  • AM has been suggested to act as autocrine/paracrine growth factor for gliomas.
  • Our studies show RAMP3 down regulation on staurosporine treatment of astrocytes, suggesting protein kinase C inhibition as a possible strategy for inhibiting AM activity and thereby growth of glioma cells.
  • [MeSH-major] Astrocytes / drug effects. Astrocytes / metabolism. Cell Differentiation / drug effects. Down-Regulation / drug effects. Intracellular Signaling Peptides and Proteins / genetics. Membrane Proteins / genetics. Neoplasm Proteins / genetics. Up-Regulation / drug effects

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  • (PMID = 16376586.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Baalc protein, rat; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Ramp3 protein, rat; 0 / Receptor Activity-Modifying Protein 3; 0 / Receptor Activity-Modifying Proteins; E0399OZS9N / Cyclic AMP; H88EPA0A3N / Staurosporine; YOW8V9698H / Dimethyl Sulfoxide
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53. Anan'eva II, Malkarov MS, Korsakova NA, Balkanov AS, Dorofeev AE, Kachkov IA, Suchkov SV: [Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition]. Arkh Patol; 2007 Jan-Feb;69(1):54-60
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  • [Title] [Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition].
  • Gliomas are the most common tumors of the central nervous system (CNS).
  • Malignant astrocytic gliomas account for 50% of all primary brain tumors.
  • Cells of origin are unknown for the majority of brain tumors: CNS tumors have frequently in their content many histological forms and their classification will depend on what the parts of neoplasm that will be clearly identified at the material taking and further investigation.
  • Current immunohistochemical studies may determine the antigenic structure of a tumor cell, compare it with the antigens expressed by a certain cell type and, thus, classify the tumor by its origin, but there are no antibodies which would correctly identify different types of tumors.
  • The lecture reflects the current classifications of glial tumors: the typical three-leveled classification, the Kernokhan classification, the Duma-Duport classification.
  • A part of the lecture deals with the specific features of genetics and molecular biology of gliomas: recent studies cast any doubt on the existing data on the sources of growth of these tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / classification. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Genetic Predisposition to Disease
  • [MeSH-minor] Antigens, Neoplasm / biosynthesis. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Gene Expression Regulation, Neoplastic / genetics. Humans

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  • (PMID = 19385137.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
  • [Number-of-references] 45
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54. 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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55. Libý P, Kostrouchová M, Pohludka M, Yilma P, Hrabal P, Sikora J, Brozová E, Kostrouchová M, Rall JE, Kostrouch Z: Elevated and deregulated expression of HDAC3 in human astrocytic glial tumours. Folia Biol (Praha); 2006;52(1-2):21-33
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  • [Title] Elevated and deregulated expression of HDAC3 in human astrocytic glial tumours.
  • Abnormal expression of histone deacetylases may contribute to the establishment of a cancer specific transcription profile.
  • We examined expression of HDAC3 in human non-malignant gliosis and glial astrocytic tumours.
  • Samples from four non-malignant gliosis and 17 astrocytic gliomas (six of grade II, one of grade III and ten of grade IV) removed for therapeutic purposes were assayed for HDAC3 expression at mRNA and protein levels.
  • Immunohistochemistry and immunofluorescence made on a collection of 35 astrocytic tumours detected nuclear as well as cytoplasmic HDAC3 expression in all of those tumours.
  • While the distribution of HDAC3 was both nuclear as well as cytoplasmic and moderate in intensity in non-malignant tissues and low-grade gliomas, high-grade tumours expressed HDAC3 in a focally deregulated pattern that included strongly pronounced cytoplasmic localization.
  • We conclude that HDAC3 expression is elevated in human astrocytic tumours and its expression pattern is deregulated at the cellular level in high-grade gliomas.
  • [MeSH-major] Astrocytoma / enzymology. Brain Neoplasms / enzymology. Histone Deacetylases / metabolism

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  • (PMID = 17007107.001).
  • [ISSN] 0015-5500
  • [Journal-full-title] Folia biologica
  • [ISO-abbreviation] Folia Biol. (Praha)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3
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56. Waha A, Güntner S, Huang TH, Yan PS, Arslan B, Pietsch T, Wiestler OD, Waha A: Epigenetic silencing of the protocadherin family member PCDH-gamma-A11 in astrocytomas. Neoplasia; 2005 Mar;7(3):193-9
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  • [Title] Epigenetic silencing of the protocadherin family member PCDH-gamma-A11 in astrocytomas.
  • In a microarray-based methylation analysis of astrocytomas [World Health Organization (WHO) grade II], we identified a CpG island within the first exon of the protocadherin-gamma subfamily A11 (PCDH-gamma-A11) gene that showed hypermethylation compared to normal brain tissue.
  • Bisulfite sequencing and combined bisulfite restriction analysis (COBRA) was performed to screen low- and high-grade astrocytomas for the methylation status of this CpG island.
  • Hypermethylation was detected in 30 of 34 (88%) astrocytomas (WHO grades II and III), 20 of 23 (87%) glioblastomas (WHO grade IV), and 8 of 8 (100%) glioma cell lines.
  • There was a highly significant correlation (P = .00028) between PCDH-gamma-A11 hypermethylation and decreased transcription as determined by competitive reverse transcription polymerase chain reaction in WHO grades II and III astrocytomas.
  • After treatment of glioma cell lines with a demethylating agent, transcription of PCDH-gamma-A11 was restored.
  • In summary, we have identified PCDH-gamma-A11 as a new target silenced epigenetically in astrocytic gliomas.
  • The inactivation of this cell-cell contact molecule might be involved in the invasive growth of astrocytoma cells into normal brain parenchyma.

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  • (PMID = 15799819.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA069065; United States / NCI NIH HHS / CA / R29 CA069065; United States / NCI NIH HHS / CA / CA-69065; United States / NCI NIH HHS / CA / CA-86701
  • [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 / Cadherins; 0 / PCDH11X protein, human; 0 / Sulfites; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC1501138
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57. Fathi AR, Vassella E, Arnold M, Curschmann J, Reinert M, Vajtai I, Weis J, Deiana G, Mariani L: Objective response to radiation therapy and long-term survival of patients with WHO grade II astrocytic gliomas with known LOH 1p/19q status. Strahlenther Onkol; 2007 Sep;183(9):517-22

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  • [Title] Objective response to radiation therapy and long-term survival of patients with WHO grade II astrocytic gliomas with known LOH 1p/19q status.
  • BACKGROUND: WHO grade II gliomas are often approached by radiation therapy (RT).
  • However, little is known about tumor response and its potential impact on long-term survival.
  • PATIENTS AND METHODS: Patients subjected to RT were selected from the own database of WHO grade II gliomas diagnosed between 1991 and 2000.
  • The volumetric tumor response after RT was assessed based on magnetic resonance imaging and graded according to standard criteria as complete, partial (PR, >or= 50%), or minor (MR, 25% to <50%).
  • RESULTS: There were 24 astrocytomas and three oligoastrocytomas.
  • CONCLUSION: Approximately 50% of patients with astrocytic WHO grade II gliomas respond to RT despite the absence of LOH for 1p/19q.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / radiotherapy. Chromosomes, Human, Pair 1 / radiation effects. Chromosomes, Human, Pair 19 / radiation effects. Cranial Irradiation. Loss of Heterozygosity / radiation effects. Supratentorial Neoplasms / genetics. Supratentorial Neoplasms / radiotherapy. Survivors
  • [MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Magnetic Resonance Imaging. Male. Microsatellite Repeats. Middle Aged. Neoplasm Staging. Radiotherapy Dosage. Retrospective Studies. Survival Analysis

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  • (PMID = 17762927.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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58. 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

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  • [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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59. 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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60. Hänninen MM, Haapasalo J, Haapasalo H, Fleming RE, Britton RS, Bacon BR, Parkkila S: Expression of iron-related genes in human brain and brain tumors. BMC Neurosci; 2009;10:36
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  • BACKGROUND: Defective iron homeostasis may be involved in the development of some diseases within the central nervous system.
  • We investigated the mRNA levels of hepcidin (HAMP), HFE, neogenin (NEO1), transferrin receptor 1 (TFRC), transferrin receptor 2 (TFR2), and hemojuvelin (HFE2) in normal human brain, brain tumors, and astrocytoma cell lines.
  • The specimens included 5 normal brain tissue samples, 4 meningiomas, one medulloblastoma, 3 oligodendrocytic gliomas, 2 oligoastrocytic gliomas, 8 astrocytic gliomas, and 3 astrocytoma cell lines.
  • In most tumor types, the pattern of gene expression was diverse.
  • Notable findings include high expression of transferrin receptor 1 in the hippocampus and medulla oblongata compared to other brain regions, low expression of HFE in normal brain with elevated HFE expression in meningiomas, and absence of hepcidin mRNA in astrocytoma cell lines despite expression in normal brain and tumor specimens.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antimicrobial Cationic Peptides / genetics. Antimicrobial Cationic Peptides / metabolism. Astrocytoma / genetics. Astrocytoma / metabolism. Cell Line, Tumor. Female. GPI-Linked Proteins. Hepcidins. Humans. Male. Meningioma / genetics. Meningioma / metabolism. Middle Aged. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. RNA, Messenger / analysis. Receptors, Transferrin / genetics. Receptors, Transferrin / metabolism. Statistics, Nonparametric. Young Adult

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  • (PMID = 19386095.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antimicrobial Cationic Peptides; 0 / CD71 antigen; 0 / GPI-Linked Proteins; 0 / HAMP protein, human; 0 / HFE protein, human; 0 / HFE2 protein, human; 0 / Hepcidins; 0 / Histocompatibility Antigens Class I; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Transferrin; 0 / TFR2 protein, human; 0 / neogenin
  • [Other-IDs] NLM/ PMC2679039
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61. Newton HB: Molecular neuro-oncology and the development of targeted therapeutic strategies for brain tumors. Part 4: p53 signaling pathway. Expert Rev Anticancer Ther; 2005 Feb;5(1):177-91
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  • [Title] Molecular neuro-oncology and the development of targeted therapeutic strategies for brain tumors. Part 4: p53 signaling pathway.
  • Molecular neuro-oncology has now begun to clarify the transformed phenotype of brain tumors and identify oncogenic pathways that might be amenable to targeted therapy.
  • Loss of the tumor suppressor gene p53 and its encoded protein are the most common genetic events in human cancer and are a frequent occurrence in brain tumors. p53 functions as a transcription factor and is responsible for the transactivation and repression of key genes involved in cell growth, apoptosis and the cell cycle.
  • Mutation of the p53 gene or dysfunction of its signaling pathway are early events in the transformation process of astrocytic gliomas.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Genes, p53. Signal Transduction. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 15757449.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16058
  • [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.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 111
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62. Mennel HD, Lell B: Ganglioside (GD2) expression and intermediary filaments in astrocytic tumors. Clin Neuropathol; 2005 Jan-Feb;24(1):13-8
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  • [Title] Ganglioside (GD2) expression and intermediary filaments in astrocytic tumors.
  • The search of proliferation markers in astrocytic tumors that may serve as targets for therapeutic interventions, is in full progress.
  • Gangliosides are lipid-sugar compounds localized on the cell membrane that are thought to modify pertinent signals and, therefore, may influence a variety of functions in normal and pathologic conditions including those that act upon tumor growth.
  • Intracranial supratentorial astrocytic gliomas of the adult represent a tumor group, that may be divided into three grades of malignancy, the most anaplastic member being the glioblastoma.
  • Yet, the results were only partly congruent and the correlation to tumor grades rather loose.
  • Thus, the conclusion must be drawn that the correlation of ganglioside patterns to the proliferation of astrocytic tumors is as poor as that of GFAP or vimentin expression, respectively.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gangliosides / metabolism. Intermediate Filaments / metabolism

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  • (PMID = 15696779.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Gangliosides; 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin; 65988-71-8 / ganglioside, GD2
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63. Alaraj A, Chan M, Oh S, Michals E, Valyi-Nagy T, Hersonsky T: Astroblastoma presenting with intracerebral hemorrhage misdiagnosed as dural arteriovenous fistula: review of a rare entity. Surg Neurol; 2007 Mar;67(3):308-13
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  • [Title] Astroblastoma presenting with intracerebral hemorrhage misdiagnosed as dural arteriovenous fistula: review of a rare entity.
  • Immunohistochemically, the tumor cells show diffuse strong positivity for GFAP, S-100 protein, vimentin, as well as neuron-specific enolase and focal positivity for EMA.
  • Because of its high degree of proliferation, the presence of astroblastic pseudorosettes, prominent perivascular hyalinization, regional hyaline changes, and pushing borders with regard to the adjacent brain, the tumor was considered anaplastic.
  • CONCLUSIONS: Astroblastoma is a rare pure pathologic entity--a distinct form of astrocytic gliomas.
  • The diagnosis of astroblastoma is often difficult because of the astroblastic aspects that can be found in astrocytic tumors, in ependymomas, and in nonneuroepithelial tumors.
  • The natural history seems to be between astrocytomas and glioblastomas.
  • [MeSH-minor] Adult. Cerebral Angiography. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging

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  • (PMID = 17320647.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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64. Felsberg J, Yan PS, Huang TH, Milde U, Schramm J, Wiestler OD, Reifenberger G, Pietsch T, Waha A: DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours. Neuropathol Appl Neurobiol; 2006 Oct;32(5):517-24
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  • Cytogenetic and molecular genetic studies have shown frequent losses on the long arm of chromosome 14 in different types of human gliomas.
  • Using differential methylation hybridization as a genome-wide screening approach to determine DNA methylation patterns in gliomas, we recently identified two DNA fragments in 14q23.1 (CGI-clone musical sharp396) and 14q32.12 (CGI-clone musical sharp519) that were differentially methylated between astrocytic gliomas and mixed oligoastrocytomas.
  • To validate this observation, we examined these 14q32.12 locus for methylation in an extended series of 43 astrocytic and oligodendroglial gliomas.
  • Microsatellite analysis showed LOH in seven of 28 (25%) oligodendroglial tumours and three of 15 (20%) astrocytic tumours.
  • Methylation-specific PCR analysis of the 14q32.12 locus revealed hypermethylation in 12 of 43 gliomas (28%).
  • Taken together, our data lend further support for the location of one or more yet to be identified glioma-associated tumour suppressor gene(s) on 14q.
  • In addition, the restriction of 14q32.12 methylation to oligodendroglial tumours suggests a role for epigenetic DNA modifications in these particular gliomas.
  • [MeSH-minor] Adolescent. Adult. Aged. Alleles. Child. Child, Preschool. DNA, Neoplasm / drug effects. Female. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Sulfites / pharmacology

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  • (PMID = 16972885.001).
  • [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 / DNA, Neoplasm; 0 / Sulfites; TZX5469Z6I / sodium bisulfite
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65. Huang H, Held-Feindt J, Buhl R, Mehdorn HM, Mentlein R: Expression of VEGF and its receptors in different brain tumors. Neurol Res; 2005 Jun;27(4):371-7
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  • INTRODUCTION: Vascular endothelial growth factor (VEGF) and its receptors VEGFR-1 and -2 are considered to play a major in tumor angiogenesis, which is a prerequisite for growth of solid tumors.
  • Glioblastoma multiforme is a prominent example of VEGF-induced tumor vascularization; however, little is known about VEGF and in particular VEGFR expression in other types of brain tumors.
  • Interestingly, for the astrocytic gliomas, the expression of VEGFR correlated well to the tumor malignancy, even better than VEGF content.

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  • (PMID = 15949234.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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66. Xiong J, Liu Y, Wang Y, Ke RH, Mao Y, Ye ZR: Chromosome 1p/19q status combined with expression of p53 protein improves the diagnostic and prognostic evaluation of oligodendrogliomas. Chin Med J (Engl); 2010 Dec;123(24):3566-73
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  • In order to improve the diagnostic criteria and to predict the prognosis of oligodendroglioma patients, the status of chromosome 1p/19q deletion, the methylation of O(6)-methylguanine-DNA methyltransferase (MGMT), and the expression of p53 protein were evaluated and investigated in relation to patients' outcomes.
  • RESULTS: Both oligodendrogliomas and astrocytic gliomas exhibited frequent methylation of MGMT.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 19. Oligodendroglioma / genetics. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / genetics. Child. Chromosomes, Human, Pair 1. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Humans. Loss of Heterozygosity. Male. Middle Aged. Prognosis. Tumor Suppressor Proteins / genetics

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  • (PMID = 22166632.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; Chromosome 1, monosomy 1p
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67. Balciūniene N, Tamasauskas A, Valanciūte A, Deltuva V, Vaitiekaitis G, Gudinaviciene I, Weis J, von Keyserlingk DG: Histology of human glioblastoma transplanted on chicken chorioallantoic membrane. Medicina (Kaunas); 2009;45(2):123-31
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  • Glioblastoma is the most malignant tumor in the range of cerebral astrocytic gliomas.
  • Invasion of vessels from the chicken into transplanted tumor is not observed.
  • Chicken erythrocytes did not appear within the transplants, and tumor cells invade chicken tissue at the minimum.
  • The features of original tumor-host reaction of the patient remained too.
  • [MeSH-minor] Animals. Chick Embryo. Genes, p53. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Neoplasm Transplantation. Neoplasms, Experimental. Paraffin Embedding. Photography. Time Factors. Vimentin / metabolism

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  • (PMID = 19289902.001).
  • [ISSN] 1648-9144
  • [Journal-full-title] Medicina (Kaunas, Lithuania)
  • [ISO-abbreviation] Medicina (Kaunas)
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Lithuania
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
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68. Korshunov A, Sycheva R, Gorelyshev S, Golanov A: Clinical utility of fluorescence in situ hybridization (FISH) in nonbrainstem glioblastomas of childhood. Mod Pathol; 2005 Sep;18(9):1258-63
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  • Astrocytic gliomas are the most common pediatric brain tumors; however, nonbrainstem glioblastomas are extremely rare compared with their adult counterparts.
  • Little information is available on the clinical significance of various molecular markers in pediatric grade IV astrocytomas.
  • The current study was focused on the molecular analysis and clinico-pathological correlations in a set of 44 tumor samples obtained from pediatric patients with nonbrainstem glioblastomas.

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  • (PMID = 15832192.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 3.1.3.67 / PTEN Phosphohydrolase
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69. van den Boom J, Wolter M, Blaschke B, Knobbe CB, Reifenberger G: Identification of novel genes associated with astrocytoma progression using suppression subtractive hybridization and real-time reverse transcription-polymerase chain reaction. Int J Cancer; 2006 Nov 15;119(10):2330-8
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  • [Title] Identification of novel genes associated with astrocytoma progression using suppression subtractive hybridization and real-time reverse transcription-polymerase chain reaction.
  • To identify novel genes involved in glioma progression we performed suppression subtractive hybridization combined with cDNA array analysis on 4 patients with primary low-grade gliomas of World Health Organization (WHO) grade II that recurred as secondary glioblastomas (WHO grade IV).
  • Eight genes showing differential expression between primary and recurrent tumors in 3 of the 4 patients were selected for further analysis using real-time reverse transcription-PCR on a series of 10 pairs of primary low-grade and recurrent high-grade gliomas as well as 42 astrocytic gliomas of different WHO grades.
  • These analyses revealed that 5 genes, i.e., AMOG (ATP1B2, 17p13.1), APOD (3q26.2-qter), DMXL1 (5q23.1) DRR1 (TU3A, 3p14.2) and PSD3 (KIAA09428/HCA67/EFA6R, 8p22), were expressed at significantly lower levels in secondary glioblastomas as compared to diffuse astrocytomas of WHO grade II.
  • In addition, AMOG, DRR1 and PSD3 transcript levels were significantly lower in primary glioblastomas than in diffuse astrocytomas.
  • Treatment of glioma cell lines with 5-aza-2'-deoxycytidine and trichostatin A resulted in increased expression of AMOG and APOD transcripts.
  • Sequencing of sodium bisulfite-modified DNA demonstrated AMOG promoter hypermethylation in the glioma cell lines and 1 primary anaplastic astrocytoma with low AMOG expression.
  • Taken together, we identified interesting novel candidate genes that likely contribute to glioma progression and provide first evidence for a role of epigenetic silencing of AMOG in malignant glioma cells.
  • [MeSH-major] Adenosine Triphosphatases / genetics. Astrocytoma / genetics. Brain Neoplasms / genetics. Cation Transport Proteins / genetics. Cell Adhesion Molecules, Neuronal / genetics. Gene Silencing. Nucleic Acid Hybridization. Reverse Transcriptase Polymerase Chain Reaction
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Apolipoproteins / genetics. Apolipoproteins D. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Biomarkers, Tumor / genetics. DNA Methylation. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Glycoproteins / genetics. Histone Deacetylases / genetics. Humans. Hydroxamic Acids / pharmacology. Membrane Transport Proteins / genetics. Nerve Tissue Proteins / genetics. Nuclear Proteins / genetics. Oligonucleotide Array Sequence Analysis. Protein Synthesis Inhibitors / pharmacology. Proteins / genetics

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  • (PMID = 16865689.001).
  • [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 / APOD protein, human; 0 / ATP1B2 protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Apolipoproteins; 0 / Apolipoproteins D; 0 / Biomarkers, Tumor; 0 / Cation Transport Proteins; 0 / Cell Adhesion Molecules, Neuronal; 0 / DMXL1 protein, human; 0 / FAM107A protein, human; 0 / Glycoproteins; 0 / Hydroxamic Acids; 0 / Membrane Transport Proteins; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / PSD protein, human; 0 / Protein Synthesis Inhibitors; 0 / Proteins; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3; EC 3.6.1.- / Adenosine Triphosphatases; M801H13NRU / Azacitidine
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70. Ernst A, Campos B, Meier J, Devens F, Liesenberg F, Wolter M, Reifenberger G, Herold-Mende C, Lichter P, Radlwimmer B: De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures. Oncogene; 2010 Jun 10;29(23):3411-22
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  • [Title] De-repression of CTGF via the miR-17-92 cluster upon differentiation of human glioblastoma spheroid cultures.
  • Glioblastoma spheroid cultures are enriched in tumor-initiating cells, and provide a model to test new treatment options in vitro.
  • In primary astrocytic gliomas (n=82), expression of several members of miR-17-92 was significantly higher relative to those of normal brain (n=8) and significantly increased with tumor grade progression (P<0.05).

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  • (PMID = 20305691.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / MIRN17 microRNA, human; 0 / Membrane Proteins; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins; 139568-91-5 / Connective Tissue Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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71. Elias A, Siegelin MD, Steinmüller A, von Deimling A, Lass U, Korn B, Mueller W: Epigenetic silencing of death receptor 4 mediates tumor necrosis factor-related apoptosis-inducing ligand resistance in gliomas. Clin Cancer Res; 2009 Sep 1;15(17):5457-65
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  • [Title] Epigenetic silencing of death receptor 4 mediates tumor necrosis factor-related apoptosis-inducing ligand resistance in gliomas.
  • PURPOSE: To identify and characterize epigenetically regulated genes able to predict sensitivity or resistance to currently tested chemotherapeutic agents in glioma therapy.
  • EXPERIMENTAL DESIGN: We used methylation-sensitive BeadArray technology to identify novel epigenetically regulated genes associated with apoptosis and with potential therapeutic targets in glioma therapy.
  • To elucidate the functional consequences of promoter methylation in the identified target death receptor 4 (DR4), we investigated tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated and anti-DR4-mediated apoptosis in glioma cell lines (U373 and A172) with loss of DR4 and one glioma cell line (LN18) with robust DR4 expression.
  • RESULTS: In human astrocytic tumors, we detected DR4 promoter hypermethylation in 60% (n = 5) of diffuse astrocytomas WHO grade 2, in 75% (n = 8) of anaplastic astrocytomas WHO grade 3, and in 70% of glioblastomas WHO grade 4 (n = 33).
  • DR4 is a cell surface protein restricted to glioma cells and is targeted by TRAIL.
  • Glioma cell lines U373 and A172 harbored heavily methylated DR4 promoters, and 5-aza-2-deoxycytidine-mediated demethylation reconstituted DR4 expression in these cell lines.
  • Functional knockdown of DR4 by DR4-specific small interfering RNA in TRAIL-sensitive glioma cell line LN18 significantly mitigated apoptosis induced by an agonistic anti-DR4 antibody.
  • 5-Aza-2-deoxycytidine-mediated demethylation resulted in a functional reconstitution of DR4 on the cell surface of TRAIL-resistant glioma cell line U373 and sensitized U373 to TRAIL-mediated apoptosis.
  • CONCLUSIONS: DR4 promoter methylation is frequent in human astrocytic gliomas, and epigenetic silencing of DR4 mediates resistance to TRAIL/DR4-based glioma therapies.
  • [MeSH-major] Apoptosis. Drug Resistance, Neoplasm / genetics. Gene Silencing. Glioma / drug therapy. Receptors, Tumor Necrosis Factor / genetics. TNF-Related Apoptosis-Inducing Ligand / therapeutic use
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line, Tumor. DNA Methylation / drug effects. DNA Methylation / physiology. Humans. Promoter Regions, Genetic / drug effects. Promoter Regions, Genetic / physiology. RNA, Small Interfering / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 19706813.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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72. 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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73. Giannopoulou E, Ravazoula P, Kalofonos H, Makatsoris T, Kardamakis D: Expression of HIF-1alpha and iNOS in astrocytic gliomas: a clinicopathological study. In Vivo; 2006 May-Jun;20(3):421-5

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  • [Title] Expression of HIF-1alpha and iNOS in astrocytic gliomas: a clinicopathological study.
  • BACKGROUND: Hypoxia-inducible-factor-1 (HIF-1) is present at high levels in human tumors and plays a crucial role in tumor promotion by up-regulating several target genes.
  • PATIENTS AND METHODS: Sixty-three human astrocytic gliomas were analyzed by immunohistochemistry for HIF-1alpha and iNOS using formalin-fixed paraffin-embedded material.
  • RESULTS: HIF-1alpha was detected only in astrocytic gliomas grades III and IV, both in the nucleus and in the cytoplasm.
  • The iNOS expression was increased in astrocytic gliomas grades I, II and III and was statistically significantly decreased in astrocytic gliomas grade IV. iNOS was localized round the capillary vessels as well.
  • CONCLUSION: We believe that HIF-1alpha and iNOS expressions merit further investigations in order to understand the biology of astrocytic gliomas.
  • [MeSH-major] Astrocytoma / enzymology. Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Nitric Oxide Synthase Type II / biosynthesis

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  • (PMID = 16724682.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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74. 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

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  • [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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75. Massi D, Landriscina M, Piscazzi A, Cosci E, Kirov A, Paglierani M, Di Serio C, Mourmouras V, Fumagalli S, Biagioli M, Prudovsky I, Miracco C, Santucci M, Marchionni N, Tarantini F: S100A13 is a new angiogenic marker in human melanoma. Mod Pathol; 2010 Jun;23(6):804-13
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  • S100A13 is upregulated in astrocytic gliomas, in which it correlates with VEGF-A expression, microvessel density and tumor grading, and promotes a more aggressive, invasive phenotype in lung cancer-derived cell lines.
  • The level of expression of S100A13 mRNA also significantly increased with progression of disease, from radial growth phase (0.7+/-0.7) to vertical growth phase (3.6+/-3.1) to metastases (7.0+/-7.0) (P<0.001).
  • In conclusion, S100A13 is expressed in melanocytic lesions when the angiogenic switch occurs and it may cooperate with VEGF-A in supporting the formation of new blood vessels, favoring the shift from radial to vertical tumor growth.
  • [MeSH-major] Biomarkers, Tumor / analysis. Capillaries / chemistry. Melanoma / blood supply. Melanoma / chemistry. Neovascularization, Pathologic / metabolism. S100 Proteins / analysis. Skin Neoplasms / blood supply. Skin Neoplasms / chemistry
  • [MeSH-minor] Aged. Antigens, CD / analysis. Female. Fibroblast Growth Factor 1 / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Predictive Value of Tests. Prognosis. RNA, Messenger / analysis. Receptors, Cell Surface / analysis. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 20208480.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL035627; United States / NHLBI NIH HHS / HL / R01 HL035627; United States / NHLBI NIH HHS / HL / R01 HL035627-23
  • [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 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / ENG protein, human; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / S100 Proteins; 0 / S100A13 protein, human; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 104781-85-3 / Fibroblast Growth Factor 1
  • [Other-IDs] NLM/ NIHMS204422; NLM/ PMC2882157
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76. Juhász C, Chugani DC, Muzik O, Wu D, Sloan AE, Barger G, Watson C, Shah AK, Sood S, Ergun EL, Mangner TJ, Chakraborty PK, Kupsky WJ, Chugani HT: In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors. J Cereb Blood Flow Metab; 2006 Mar;26(3):345-57
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  • Abnormal metabolism of tryptophan has been implicated in modulation of tumor cell proliferation and immunoresistance. alpha-[(11)C]Methyl-L-tryptophan (AMT) is a PET tracer to measure cerebral tryptophan metabolism in vivo.
  • In the present study, we have measured tumor tryptophan uptake in 40 patients with primary brain tumors using AMT PET and standard uptake values (SUV).
  • All grade II to IV gliomas and glioneuronal tumors showed increased AMT SUV, including all recurrent/residual tumors.
  • Low-grade astrocytic gliomas showed increased tryptophan metabolism, as measured by k(3)'.
  • In astrocytic tumors, low grade was associated with high k(3)' and lower VD', while high-grade tumors showed the reverse pattern.
  • The findings show high AMT uptake in primary and residual/recurrent gliomas and glioneuronal tumors.
  • Increased AMT uptake can be due to increased metabolism of tryptophan and/or high volume of distribution, depending on tumor type and grade.
  • High tryptophan metabolic rates in low-grade tumors may indicate activation of the kynurenine pathway, a mechanism regulating tumor cell growth.
  • AMT PET might be a useful molecular imaging method to guide therapeutic approaches aimed at controlling tumor cell proliferation by acting on tryptophan metabolism.
  • [MeSH-minor] Adolescent. Adult. Aged. Carbon Radioisotopes. Child. Child, Preschool. Electroencephalography / methods. Electroencephalography / standards. Female. Gadolinium. Glucose / metabolism. Humans. Infant. Magnetic Resonance Imaging / methods. Magnetic Resonance Imaging / standards. Male. Middle Aged. Neoplasm Staging. Positron-Emission Tomography / methods. Positron-Emission Tomography / standards. Seizures / metabolism. Sensitivity and Specificity

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  • (PMID = 16079785.001).
  • [ISSN] 0271-678X
  • [Journal-full-title] Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • [ISO-abbreviation] J. Cereb. Blood Flow Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan; AU0V1LM3JT / Gadolinium; IY9XDZ35W2 / Glucose
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77. 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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78. Haapasalo J, Mennander A, Helen P, Haapasalo H, Isola J: Ultrarapid Ki-67 immunostaining in frozen section interpretation of gliomas. J Clin Pathol; 2005 Mar;58(3):263-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultrarapid Ki-67 immunostaining in frozen section interpretation of gliomas.
  • BACKGROUND: Astrocytic tumours, the most common gliomas, are often classified intraoperatively using standard morphological staining.
  • The final diagnosis and grading of gliomas on paraffin wax sections is often assisted by Ki-67 immunohistochemistry, but standard immunostaining protocols take too long to be used intraoperatively.
  • Thirty four pilocytic and diffuse astrocytomas were immunostained by rapid Ki-67 and results were compared with corresponding MIB-1 staining, histological grading, and prognosis.
  • A comparison of Ultrarapid-Ki67 and MIB-1 immunostaining of paraffin wax sections showed almost identical quantitative correlation in astrocytic gliomas (r = 0.916; p<0.001).
  • The Ultrarapid-Ki67 indices (percentage of positive cells) of low grade (I/II) astrocytomas ranged from 0% to 6.1%, whereas those of representative high grade (III/IV) tumours were significantly higher (range, 5.6-45%; p<0.001).
  • The best prognostic cutoff point for Ultrarapid-Ki67 was 7.5%, which divided diffuse grade II-IV astrocytomas into significantly differing subsets (p = 0.0008).
  • CONCLUSION: Ultrarapid-Ki67 immunostaining is a useful adjunct to morphological diagnosis and grading of astrocytic tumours, and as a fast test (approximately 10 minutes for staining plus three to four minutes for scoring), it could be used in routine intraoperative diagnosis of gliomas and other neoplastic diseases.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Ki-67 Antigen / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Antinuclear / immunology. Antibodies, Monoclonal / immunology. Child. Child, Preschool. Diagnosis, Differential. Female. Frozen Sections. Humans. Immunoenzyme Techniques. Intraoperative Care / methods. Male. Middle Aged. Neoplasm Proteins / analysis. Prognosis. Time Factors

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  • (PMID = 15735157.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Ki-67 Antigen; 0 / MIB-1 antibody; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC1770597
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79. 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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80. Krafft C, Sobottka SB, Geiger KD, Schackert G, Salzer R: Classification of malignant gliomas by infrared spectroscopic imaging and linear discriminant analysis. Anal Bioanal Chem; 2007 Mar;387(5):1669-77
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classification of malignant gliomas by infrared spectroscopic imaging and linear discriminant analysis.
  • Supervised classification models can be trained to identify the tissue type based on the spectroscopic fingerprint.
  • An approach is described to apply this methodology to human astrocytic gliomas, which are graded according to their malignancy from one to four.
  • Multiple IR images of three tissue sections from one patient with a malignant glioma are acquired and assigned to the six classes normal brain tissue, astrocytoma grade II, astrocytoma grade III, glioblastoma multiforme grade IV, hemorrhage, and other tissue by a linear discriminant analysis model which was trained by data from a single-channel detector.
  • The first specimen contained approximately 95% malignant glioma regions, that means astrocytoma grade III or glioblastoma.
  • The smaller percentage of 12-34% malignant glioma in the second specimen is consistent with its location at the tumor periphery.
  • The detection of less than 0.2% malignant glioma in the third specimen points to a location outside the tumor.

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  • (PMID = 17103151.001).
  • [ISSN] 1618-2642
  • [Journal-full-title] Analytical and bioanalytical chemistry
  • [ISO-abbreviation] Anal Bioanal Chem
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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81. Hartmann C, Hentschel B, Wick W, Capper D, Felsberg J, Simon M, Westphal M, Schackert G, Meyermann R, Pietsch T, Reifenberger G, Weller M, Loeffler M, von Deimling A: Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas. Acta Neuropathol; 2010 Dec;120(6):707-18
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  • [Title] Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas.
  • WHO grading of human brain tumors extends beyond a strictly histological grading system by providing a basis predictive for the clinical behavior of the respective neoplasm.
  • For example, patients with glioblastoma WHO grade IV usually show a less favorable clinical course and receive more aggressive first-line treatment than patients with anaplastic astrocytoma WHO grade III.
  • Here we provide evidence that the IDH1 status is more prognostic for overall survival than standard histological criteria that differentiate high-grade astrocytomas.
  • We sequenced the isocitrate dehydrogenase 1 gene (IDH1) at codon 132 in 382 patients with anaplastic astrocytoma and glioblastoma from the NOA-04 trial and from a prospective translational cohort study of the German Glioma Network.
  • Patients with anaplastic astrocytomas carried IDH1 mutations in 60%, and patients with glioblastomas in 7.2%.
  • The sequence from more favorable to poorer outcome was (1) anaplastic astrocytoma with IDH1 mutation, (2) glioblastoma with IDH1 mutation, (3) anaplastic astrocytoma without IDH1 mutation and (4) glioblastoma without IDH1 mutation (p < 0.0001).
  • In this combined set of anaplastic astrocytomas and glioblastomas both, IDH1 mutation and IDH1 expression status were of greater prognostic relevance than histological diagnosis according to the current WHO classification system.
  • We propose to complement the current WHO classification and grading of high-grade astrocytic gliomas by the IDH1 mutation status and to use this combined histological and molecular classification in future clinical trials.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Glioma / classification. Glioma / genetics. Isocitrate Dehydrogenase / genetics. Mutation / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Cohort Studies. Female. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Young Adult


82. Robe PA, Martin DH, Nguyen-Khac MT, Artesi M, Deprez M, Albert A, Vanbelle S, Califice S, Bredel M, Bours V: Early termination of ISRCTN45828668, a phase 1/2 prospective, randomized study of sulfasalazine for the treatment of progressing malignant gliomas in adults. BMC Cancer; 2009;9:372
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  • [Title] Early termination of ISRCTN45828668, a phase 1/2 prospective, randomized study of sulfasalazine for the treatment of progressing malignant gliomas in adults.
  • BACKGROUND: Sulfasalazine, a NF-kappaB and x(c)-cystine/glutamate antiport inhibitor, has demonstrated a strong antitumoral potential in preclinical models of malignant gliomas.
  • As it presents an excellent safety profile, we initiated a phase 1/2 clinical study of this anti-inflammatory drug for the treatment of recurrent WHO grade 3 and 4 astrocytic gliomas in adults.
  • METHODS: 10 patients with advanced recurrent anaplastic astrocytoma (n = 2) or glioblastoma (n = 8) aged 32-62 years were recruited prior to the planned interim analysis of the study.
  • Subjects were randomly assigned to daily doses of 1.5, 3, 4.5, or 6 grams of oral sulfasalazine, and treated until clinical or radiological evidence of disease progression or the development of serious or unbearable side effects.
  • Primary endpoints were the evaluation of toxicities according to the CTCAE v.3.0, and the observation of radiological tumor responses based on MacDonald criteria.
  • One tumor remained stable for 2 months with sulfasalazine treatment, at the lowest daily dose of the drug.
  • CONCLUSION: Although the proper influence of sulfasalazine treatment on patient outcome was difficult to ascertain in these debilitated patients with a large tumor burden (median KPS = 50), ISRCTN45828668 was terminated after its interim analysis.
  • This study urges to exert cautiousness in future trials of Sulfasalazine for the treatment of malignant gliomas.
  • [MeSH-major] Early Termination of Clinical Trials. Glioma / drug therapy. Sulfasalazine / administration & dosage
  • [MeSH-minor] Adult. Disease Progression. Female. Humans. Male. Middle Aged. Prospective Studies. Treatment Failure

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  • (PMID = 19840379.001).
  • [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] 3XC8GUZ6CB / Sulfasalazine
  • [Other-IDs] NLM/ PMC2771045
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83. 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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84. Ohgaki H, Kleihues P: Epidemiology and etiology of gliomas. Acta Neuropathol; 2005 Jan;109(1):93-108
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidemiology and etiology of gliomas.
  • Gliomas of astrocytic, oligodendroglial and ependymal origin account for more than 70% of all brain tumors.
  • With the exception of pilocytic astrocytomas, the prognosis of glioma patients is still poor.
  • Brain tumors are a component of several inherited tumor syndromes, but the prevalence of these syndromes is very low.
  • Several occupations, environmental carcinogens, and diet (N-nitroso compounds) have been reported to be associated with an elevated glioma risk, but the only environmental factor unequivocally associated with an increased risk of brain tumors, including gliomas, is therapeutic X-irradiation.
  • In particular, children treated with X-irradiation for acute lymphoblastic leukemia show a significantly elevated risk of developing gliomas and primitive neuroectodermal tumor (PNET), often within 10 years after therapy.
  • TP53 mutations are frequent in low-grade gliomas and secondary glioblastomas derived therefrom.
  • TP53 mutations are significantly more frequent in low-grade astrocytomas with promoter methylation of the O(6)-methylguanine-DNA methyltransferase repair gene, suggesting that, in addition to deamination of 5-methylcytosine, exogenous or endogenous alkylation in the O(6) position of guanine may contribute to the formation of these mutations.
  • [MeSH-major] Glioma / epidemiology. Glioma / etiology. Risk Factors
  • [MeSH-minor] Age Factors. Central Nervous System Viral Diseases / complications. Craniocerebral Trauma / complications. Educational Status. Electromagnetic Fields / adverse effects. Humans. Hypersensitivity / complications. Incidence. Models, Biological. Mortality. Mutation / genetics. Occupational Exposure. Radiation, Ionizing. Sex Factors. Smoking / adverse effects. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 15685439.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 153
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85. Belda-Iniesta C, de Castro Carpeño J, Casado Sáenz E, Cejas Guerrero P, Perona R, González Barón M: Molecular biology of malignant gliomas. Clin Transl Oncol; 2006 Sep;8(9):635-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular biology of malignant gliomas.
  • Gliomas are the most common primary brain tumours.
  • In keeping with the degree of aggressiveness, gliomas are divided into four grades, with different biological behaviour.
  • Furthermore, as different gliomas share a predominant histological appearance, the final classification includes both, histological features and degree of malignancy.
  • For example, gliomas of astrocytic origin (astrocytomas) are classified into pilocytic astrocytoma (grade I), astrocytoma (grade II), anaplastic astrocytoma (grade III) and glioblastoma multiforme (GMB) (grade IV).
  • Each subtype has a specific prognosis that dictates the clinical management.
  • Obviously, prognosis and biological behaviour of malignant gliomas are closely related and supported by the different molecular background that possesses each type of glioma.
  • Furthermore, the ability that allows several low-grade gliomas to progress into more aggressive tumors has allowed cancer researchers to elucidate several pathways implicated in molecular biology of these devastating tumors.
  • In this review, we describe classical pathways involved in human malignant gliomas with special focus with recent advances, such as glioma stem-like cells and expression patterns from microarray studies.
  • [MeSH-major] Central Nervous System Neoplasms / genetics. Glioma / genetics

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  • (PMID = 17005465.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Number-of-references] 36
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86. Ohgaki H, Kleihues P: Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas. J Neuropathol Exp Neurol; 2005 Jun;64(6):479-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.
  • Published data on prognostic and predictive factors in patients with gliomas are largely based on clinical trials and hospital-based studies.
  • This review summarizes data on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland (approximately 1.16 million inhabitants).
  • While survival rates for pilocytic astrocytomas were excellent (96% at 10 years), the prognosis of diffusely infiltrating gliomas was poorer, with median survival times (MST) of 5.6 years for low-grade astrocytoma WHO grade II, 1.6 years for anaplastic astrocytoma grade III, and 0.4 years for glioblastoma.
  • TP53 mutations were most frequent in gemistocytic astrocytomas (88%), followed by fibrillary astrocytomas (53%) and oligoastrocytomas (44%), but infrequent (13%) in oligodendrogliomas.
  • LOH 1p/19q typically occurred in tumors without TP53 mutations and were most frequent in oligodendrogliomas (69%), followed by oligoastrocytomas (45%), but were rare in fibrillary astrocytomas (7%) and absent in gemistocytic astrocytomas.
  • Primary (de novo) glioblastomas prevailed (95%), while secondary glioblastomas that progressed from low-grade or anaplastic gliomas were rare (5%).
  • [MeSH-major] Astrocytoma. Brain Neoplasms. Loss of Heterozygosity. Oligodendroglioma. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Age Distribution. Chromosomes, Human, Pair 10. Disease Progression. Humans. Incidence. Mutation. Predictive Value of Tests. Recurrence. Sex Factors. Survival Rate. Switzerland / epidemiology


87. 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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88. Abou-Ghazal M, Yang DS, Qiao W, Reina-Ortiz C, Wei J, Kong LY, Fuller GN, Hiraoka N, Priebe W, Sawaya R, Heimberger AB: The incidence, correlation with tumor-infiltrating inflammation, and prognosis of phosphorylated STAT3 expression in human gliomas. Clin Cancer Res; 2008 Dec 15;14(24):8228-35
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  • [Title] The incidence, correlation with tumor-infiltrating inflammation, and prognosis of phosphorylated STAT3 expression in human gliomas.
  • We sought to determine the incidence of phosphorylated STAT3 (p-STAT3) expression in malignant gliomas of different pathologic types, whether p-STAT3 expression is a negative prognostic factor, and whether p-STAT3 expression influences the inflammatory response within gliomas.
  • METHODS: Using immunohistochemical analysis, we measured the incidence of p-STAT3 expression in 129 patients with gliomas of various pathologic types in a glioma tissue microarray.
  • We categorized our results according to the total number of p-STAT3-expressing cells within the gliomas and correlated this number with the number of infiltrating T cells and T regulatory cells.
  • RESULTS: We did not detect p-STAT3 expression in normal brain tissues or low-grade astrocytomas.
  • We observed significant differences in the incidence of p-STAT3 expression between the different grades of astrocytomas and different pathologic glioma types. p-STAT3 expression was associated with the population of tumor-infiltrating immune cells but not with that of T regulatory cells.
  • On univariate analysis, we found that p-STAT3 expression within anaplastic astrocytomas was a negative prognostic factor.
  • CONCLUSIONS: p-STAT3 expression is common within gliomas of both the astrocytic and oligodendroglial lineages and portends poor survival in patients with anaplastic astrocytomas. p-STAT3 expression differs significantly between gliomas of different pathologic types and grades and correlated with the degree of immune infiltration.

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  • (PMID = 19088040.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120813-01A1; United States / NCI NIH HHS / CA / R01 CA120813; United States / NCI NIH HHS / CA / R01 CA120813-01A1
  • [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 / STAT3 Transcription Factor; 0 / STAT3 protein, human
  • [Other-IDs] NLM/ NIHMS78715; NLM/ PMC2605668
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89. Pfister S, Witt O: Pediatric gliomas. Recent Results Cancer Res; 2009;171:67-81
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  • [Title] Pediatric gliomas.
  • Pediatric gliomas comprise a clinically, histologically, and molecularly very heterogeneous group of CNS tumors.
  • In addition, these tumors are largely different from their counterparts occurring in adults, although they are histologically indistinguishable and uniformly classified by the current WHO classification for CNS tumors.
  • Pilocytic astrocytoma (WHO grade I), mainly arising in the posterior fossa, is the most common representative in children, whereas glioblastoma multiforme (WHO grade IV) predominates in adults.
  • When radical surgical resection is possible in low-grade gliomas, it will likely cure the patient.
  • If complete surgical resection is not possible, however, for example in brainstem gliomas, which are defined by their anatomic localization rather than by their histological or molecular features, therapeutic options are limited and prognosis is usually poor.
  • Mitogen-activated protein kinase (MAPK) and PI3K/AKT signaling were identified as prominent oncogenic pathways in astrocytic tumors in several studies, whereas NOTCH signaling was implicated in the pathogenesis of a subset of intracranial ependymomas.
  • Future therapeutic strategies targeting these (and other) pathways or conferring epigenetic modifications in the tumor might contribute to a better treatment outcome of patients with unresectable or disseminated tumors at diagnosis.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics

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  • (PMID = 19322538.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 59
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90. Figarella-Branger D, Colin C, Coulibaly B, Quilichini B, Maues De Paula A, Fernandez C, Bouvier C: [Histological and molecular classification of gliomas]. Rev Neurol (Paris); 2008 Jun-Jul;164(6-7):505-15
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  • [Title] [Histological and molecular classification of gliomas].
  • [Transliterated title] Classification histologique et moléculaire des gliomes.
  • Gliomas are the most frequent tumors of the central nervous system.
  • The WHO classification, based on the presumed cell origin, distinguishes astrocytic, oligodendrocytic and mixed gliomas.
  • The main histological subtype of grade I gliomas are pilocytic astrocytomas, which are benign.
  • Diffuse astrocytomas, oligodendrogliomas and oligoastrocytomas are low-grade (II) or high-grade (III and IV) tumors.
  • Glioblastomas correspond to grade IV astrocytomas. C.
  • Daumas-Duport et al. have proposed another classification based on histology and imaging data, which distinguishes oligodendrogliomas and mixed gliomas of grade A (without endothelial proliferation and/or contrast enhancement), oligodendrogliomas and mixed gliomas of grade B (with endothelial proliferation or contrast enhancement), glioblastomas and glioneuronal malignant tumors.
  • Many studies have searched for a molecular classification.
  • Recurrent abnormalities in gliomas have been found.
  • De novo glioblastomas, which occur in young patients without of a prior history of brain tumor and harbor frequent amplification of EGFR, deletion of p16 and mutation of PTEN while mutation of p53 is infrequent.
  • Secondary glioblastomas occur in the context of a preexisting low-grade glioma and are characterized by more frequent mutation of p53.
  • However, some concerns exist for the method of detection of this abnormality.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Animals. Astrocytoma / classification. Astrocytoma / pathology. Chromosomes / genetics. Humans. Oligodendroglioma / classification. Oligodendroglioma / pathology. Signal Transduction / physiology


91. Burzynski SR: Treatments for astrocytic tumors in children: current and emerging strategies. Paediatr Drugs; 2006;8(3):167-78
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  • [Title] Treatments for astrocytic tumors in children: current and emerging strategies.
  • Despite these accomplishments, CNS tumors remain the leading cause of death in pediatric oncology.
  • Astrocytic tumors form the most common histologic group among childhood brain tumors.
  • They are a heterogeneous group that from a practical therapeutic point of view can be subdivided into low-grade astrocytomas (LGA), optic pathway gliomas (OPG), high-grade astrocytomas (HGA), and brainstem gliomas (BSG).
  • Careful follow-up without any treatment is indicated for a small percentage of patients diagnosed with LGA with an indolent course including children with neurofibromatosis type 1 (NF1).
  • Radiation therapy is generally recommended for children with progressive LGA, or after failure of chemotherapy, accomplishing tumor control at 10 years in over 60% of patients.
  • OPG is the most common type of brain tumor associated with NF1.
  • Tumor growth in some of these patients is slow with no treatment recommended for an extended period of time.
  • The prognosis for children with the remaining types of astrocytomas remains poor.
  • Careful evaluation of histology, location of the tumor, patient age, and consideration of treatment-related morbidity play an important part in selecting between clinical observation, surgery, radiation, chemotherapy, or investigational agents.
  • The goals of treatment for astrocytic tumors should extend well beyond objective responses and increased survival.
  • [MeSH-major] Astrocytoma / therapy. Central Nervous System Neoplasms / therapy

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  • (PMID = 16774296.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Number-of-references] 155
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92. Piekutowska-Abramczuk D, Ciara E, Popowska E, Grajkowska W, Dembowska-Bagińska B, Kowalewska E, Czajńska A, Perek-Polnik M, Roszkowski M, Syczewska M, Krajewska-Walasek M, Perek D, Chrzanowska KH: The frequency of NBN molecular variants in pediatric astrocytic tumors. J Neurooncol; 2010 Jan;96(2):161-8
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  • [Title] The frequency of NBN molecular variants in pediatric astrocytic tumors.
  • Gliomas, particularly those of astrocytic origin, are the most frequent primary central nervous system tumors that develop in children.
  • Several genomic and gene alterations are known to be involved in astrocytoma development, but the precise mechanisms remain poorly understood.
  • The NBN gene, which participates in DNA double-strand break repair and maintenance of genome stability, has been postulated to be a susceptibility factor for a number of cancers.
  • Here we report the results of NBN gene analyses performed in 127 children with various astrocytic tumors.
  • The common Slavic deletion c.657_661del5 (p.K219fsX19) was detected in a patient with pilocytic astrocytoma; a known mutation, c.643C>T (p.R215W), and a new substitution, c.565C>G (p.Q189E), were identified in two patients with primary glioblastoma.
  • The risk of developing astrocytic malignancies is estimated to be 1.33 times higher for c.657_661del5 and 3.2 times higher for c.643C>T than in the general Polish population (P > 0.05).
  • Because of the low frequency of the mutations identified in the studied group, we were unable to determine the exact role of NBN in the development of astrocytoma in children.
  • The presence of two potentially pathogenic NBN molecular variants among 16 glioblastoma cases (12.5%) could be a remarkable finding in our study.
  • We thus cannot exclude a possible role of NBN in the tumorigenesis of a certain type of astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Cell Cycle Proteins / genetics. Central Nervous System Neoplasms / genetics. Mutation / genetics. Nuclear Proteins / genetics

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  • (PMID = 19629396.001).
  • [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 / Cell Cycle Proteins; 0 / NBN protein, human; 0 / Nuclear Proteins
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93. Schlierf B, Friedrich RP, Roerig P, Felsberg J, Reifenberger G, Wegner M: Expression of SoxE and SoxD genes in human gliomas. Neuropathol Appl Neurobiol; 2007 Dec;33(6):621-30
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  • [Title] Expression of SoxE and SoxD genes in human gliomas.
  • Here, we have examined Sox gene expression in 60 human primary gliomas.
  • Transcripts from each of the six group E and group D genes were expressed in gliomas of various types and malignancy grades, but with significant differences.
  • Low-grade astrocytomas, but not glioblastomas, also showed elevated SOX8 transcript levels.
  • Taken together, the expression pattern of Sox genes in gliomas is heterogeneous and overall compatible with the less differentiated state of glioma cells as compared with their normal adult counterparts.
  • Despite their restricted expression in astrocytes and oligodendrocytes during normal development, none of the Sox genes was selectively expressed in tumours of the oligodendroglial or astrocytic lineage.
  • This is compatible with an origin of gliomas from neuroepithelial stem or precursor cells.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression. Glioma / metabolism. Sex-Determining Region Y Protein / biosynthesis

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  • (PMID = 17961134.001).
  • [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; 0 / Sex-Determining Region Y Protein
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94. 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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95. 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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96. Jin YH, Jung S, Jin SG, Jung TY, Moon KS, Kim IY: GRIM-19 Expression and Function in Human Gliomas. J Korean Neurosurg Soc; 2010 Jul;48(1):20-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GRIM-19 Expression and Function in Human Gliomas.
  • OBJECTIVE: We determined whether the expression of GRIM-19 is correlated with pathologic types and malignant grades in gliomas, and determined the function of GRIM-19 in human gliomas.
  • METHODS: Tumor tissues were isolated and frozen at -80 just after surgery.
  • The tissues consisted of normal brain tissue (4), astrocytomas (2), anaplastic astrocytomas (2), oligodendrogliomas (13), anaplastic oligodendrogliomas (11), and glioblastomas (16).
  • To profile tumor-related genes, we applied RNA differential display using a Genefishing DEG kit, and validated the tumor-related genes by reverse transcription polymerase chain reaction (RT-PCR).
  • The morphologic and cytoskeletal changes were examined via light and confocal microscopy.
  • RESULTS: Based on RT-PCR analysis, the expression of GRIM-19 was higher in astrocytic tumors than oligodendroglial tumors.
  • CONCLUSION: GRIM-19 may be one of the gene profiles which regulate cell death via apoptosis in human gliomas.

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  • (PMID = 20717508.001).
  • [ISSN] 1598-7876
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2916144
  • [Keywords] NOTNLM ; Cell line / GRIM-19 / Gene Fishing / Glioblastoma / Human glioma
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97. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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98. Miwa T, Hirose Y, Sasaki H, Ikeda E, Yoshida K, Kawase T: Genetic characterization of adult infratentorial gliomas. J Neurooncol; 2009 Feb;91(3):251-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic characterization of adult infratentorial gliomas.
  • Adult infratentorial gliomas are rare and have not been well studied.
  • Nineteen adult infratentorial gliomas were analyzed for chromosomal aberration by comparative genomic hybridization, and for expression of p53 and epidermal growth factor receptor (EGFR) by immunohistochemistry.
  • The most frequent chromosomal aberration was the gain of 7p, and five of the seven cerebellar or fourth ventricle malignant gliomas had that aberration.
  • However, the gain of 7q, the characteristic abnormality of supratentorial astrocytomas commonly associated with the gaining of 7p, was observed only in 1 of 11 adult infratentorial astrocytic tumors.
  • Results of immunohistochemistry of p53 and EGFR were comparable to those reported in supratentorial gliomas.
  • Our findings might suggest the presence of distinct tumorigenic pathway in adult infratentorial gliomas.
  • [MeSH-major] Brain Neoplasms / genetics. Frontal Lobe / pathology. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18941867.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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99. Ohgaki H, Kleihues P: Genetic alterations and signaling pathways in the evolution of gliomas. Cancer Sci; 2009 Dec;100(12):2235-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic alterations and signaling pathways in the evolution of gliomas.
  • Gliomas are the most common primary brain tumors.
  • The vast majority (>90%) develops rapidly after a short clinical history and without evidence of a less malignant precursor lesion (primary or de novo glioblastoma).
  • Secondary glioblastomas develop more slowly through progression from low-grade or anaplastic astrocytoma.
  • These glioblastoma subtypes constitute distinct disease entities that affect patients of different age, develop through distinct genetic pathways, show different RNA and protein expression profiles, and may differ in their response to radio- and chemotherapy.
  • Recently, isocitrate dehydrogenase 1 (IDH1) mutations have been identified as a very early and frequent genetic alteration in the pathway to secondary glioblastomas as well as that in oligodendroglial tumors, providing the first evidence that low-grade astrocytomas and oligodendrogliomas may share common cells of origin.
  • In this review, we summarize the current status of genetic alterations and signaling pathways operative in the evolution of astrocytic and oligodendroglial tumors.
  • [MeSH-major] Glioma / etiology. Mutation. Signal Transduction
  • [MeSH-minor] Animals. Cyclin-Dependent Kinase Inhibitor p16 / physiology. Gene Expression Profiling. Humans. Isocitrate Dehydrogenase / physiology. Loss of Heterozygosity. PTEN Phosphohydrolase / physiology. Phosphatidylinositol 3-Kinases / physiology. Tumor Suppressor Protein p14ARF / physiology. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 19737147.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Number-of-references] 92
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100. Scarabino T, Giannatempo GM, Nemore F, Popolizio T, Stranieri A: Supratentorial low-grade gliomas. Neuroradiology. J Neurosurg Sci; 2005 Sep;49(3):73-6
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  • [Title] Supratentorial low-grade gliomas. Neuroradiology.
  • A brain tumors can be reliably ruled out, if the standard magnetic resonance examination is performed properly and experts interpret the results as negative for tumor.
  • In this paper we will illustrate morphological aspects of low-grade supratentorial neoplasms, including tumors of neuroepithelial tissue, such as low-grade diffuse fibrillary astrocytomas, and circumscribed astrocytic lesions (pilocytic astrocytoma, pleomorphic xantoastrocytoma and subependymal giant cell astrocytoma).
  • [MeSH-major] Glioma / diagnostic imaging. Glioma / pathology. Magnetic Resonance Imaging. Supratentorial Neoplasms / diagnostic imaging. Supratentorial Neoplasms / pathology

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  • (PMID = 16288189.001).
  • [ISSN] 0390-5616
  • [Journal-full-title] Journal of neurosurgical sciences
  • [ISO-abbreviation] J Neurosurg Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 14
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