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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuregulin-1 enhances survival of human astrocytic glioma cells.
  • Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.
  • In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.
  • Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.
  • We then verify receptor expression in a panel of human glioma cell lines.
  • Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.
  • Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.
  • Moreover, Nrg-1beta activates an inhibitor of apoptosis, Akt, implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas.
  • This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

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

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  • (PMID = 19847810.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NKD1 protein, human; 0 / NKD2 protein, human; 0 / Proto-Oncogene Proteins; 0 / SFRP1 protein, human; 0 / SFRP2 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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4. Komotar RJ, Carson BS, Rao C, Chaffee S, Goldthwaite PT, Tihan T: Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases. Neurosurgery; 2005 Jan 01;56(1):E206-E210

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  • [Title] Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases.

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  • (PMID = 28184642.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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5. Lamoral-Theys D, Le Mercier M, Le Calvé B, Rynkowski MA, Bruyère C, Decaestecker C, Haibe-Kains B, Bontempi G, Dubois J, Lefranc F, Kiss R: Long-term temozolomide treatment induces marked amino metabolism modifications and an increase in TMZ sensitivity in Hs683 oligodendroglioma cells. Neoplasia; 2010 Jan;12(1):69-79
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  • Gliomas account for more than 50% of all primary brain tumors.
  • The worst prognosis is associated with gliomas of astrocytic origin, whereas gliomas with an oligodendroglial origin offer higher sensitivity to chemotherapy, especially when oligodendroglioma cells display 1p19q deletions.
  • Temozolomide (TMZ) provides therapeutic benefits and is commonly used with radiotherapy in highly malignant astrocytic tumors, including glioblastomas.
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / pharmacology. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Genomics / methods. HT29 Cells. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Proteomics / methods. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Xenograft Model Antitumor Assays

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  • (PMID = 20072655.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Other-IDs] NLM/ PMC2805885
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6. Figarella-Branger D, Bouvier C: [Histological classification of human gliomas: state of art and controversies]. Bull Cancer; 2005 Apr;92(4):301-9
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  • [Title] [Histological classification of human gliomas: state of art and controversies].
  • [Transliterated title] Classification anatomopathologique des gliomes: faits et controverses.
  • The histological classification of human gliomas remains in 2005 a challenge.
  • The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.
  • Although the standard remains the WHO classification, this classification suffered from lack of reproducibility among pathologists.
  • In particular this classification does not take into account the intrinsic morphological heterogeneity of infiltrative gliomas and does not discriminate the tumour cells from the residual brain parenchyma.
  • According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).
  • Circumscribed gliomas mainly corresponds to pilocytic astrocytomas (grade I).
  • In contrast, the Sainte Anne classification takes into account the macroscopic informations provided by imaging techniques and the tumour growth patterns.
  • Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.
  • According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).
  • In the future the glioma classification has to be unique and should take into account clinical data, neuroradiological and histological features and results of molecular biology.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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  • (PMID = 15888386.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
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7. 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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8. 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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9. Khattab AZ, Ahmed MI, Fouad MA, Essa WA: Significance of p53 and CD31 in astrogliomas. Med Oncol; 2009;26(1):86-92
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  • [Title] Significance of p53 and CD31 in astrogliomas.
  • BACKGROUND: Astrogliomas are the most common primary brain tumor.
  • Its progression is the result of activation of oncogenes, inactivation of tumor suppressor genes (TSGs), and expression of various growth factors.
  • The angiogenesis and p53 in astrogliomas play an important role in its grading, treatment strategies, and hence its clinical outcome.
  • OBJECTIVES: To analyze the frequency of presentation and the possible co-expression of p53 and angiogenesis marker (CD31) and their clinical implications in astrogliomas.
  • MATERIAL AND METHODS: This retrograde study included 45 cases with astrocytomas in the form of paraffin blocks.
  • Sections were stained with hematoxylin and eosin to determine the type and histological grade according to WHO (2007) classification of CNS tumors.
  • RESULTS: Both p53 and CD31 expressions were correlated well with the histopathological grades of different subtypes of astrogliomas with good discrimination between low and high grades.
  • Overall, a highly significant statistical correlation was observed between the grades of astrocytomas and the p53 and CD31 labeling indices.
  • Obviously, these observations demonstrate that the co-expression and increased levels of p53 and CD31 in astrogliomas are increasing as the tumor grade is increasing.
  • Thus, the two markers can be used as adjunct to the diagnosis and stratification of the high grade from the low-grade intrinsic brain astrogliomas.
  • [MeSH-major] Antigens, CD31 / biosynthesis. Astrocytoma / metabolism. Biomarkers, Tumor. Brain Neoplasms / metabolism. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 18821037.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53
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10. Mizoguchi M, Betensky RA, Batchelor TT, Bernay DC, Louis DN, Nutt CL: Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival. J Neuropathol Exp Neurol; 2006 Dec;65(12):1181-8
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  • [Title] Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival.
  • Diffuse astrocytic gliomas are the most common human glial tumors with glioblastoma being the most malignant form.
  • In this study, we investigated the activation status of these 3 signaling molecules as well as wild-type (EGFRwt) and mutant (EGFRvIII) EGFR in 82 malignant astrocytic gliomas (55 glioblastomas and 27 anaplastic astrocytomas) using immunohistochemistry.
  • The distribution of these 3 activated molecules varied significantly with tumor grade; although activation of STAT3 was essentially identical between anaplastic astrocytomas and glioblastomas, an increase in the activation of MAPK and AKT appeared to correlate with the progression of anaplastic astrocytoma to glioblastoma.
  • Taken together, these findings begin to elucidate the interrelationship between these signaling pathways in astrocytic gliomas in vivo.
  • [MeSH-major] Astrocytoma / enzymology. Brain Neoplasms / enzymology. Glioblastoma / enzymology. Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / biosynthesis. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Disease Progression. Enzyme Activation / genetics. Genetic Predisposition to Disease / genetics. Humans. Immunohistochemistry. Mutation / genetics. Predictive Value of Tests. Prognosis. Signal Transduction / physiology. Survival Rate / trends. Transcriptional Activation / genetics

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  • (PMID = 17146292.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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11. 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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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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13. Lin Y, Jiang T, Li G: MGMT expression in low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13001

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  • [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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14. 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

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  • [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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15. 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

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  • [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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16. 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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17. 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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18. 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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19. 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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20. Witt H, Korshunov A, Remke M, Janzarik WG, Gnekow A, Scheurlen W, Kulozik AE, Lichter P, Pfister S: DNA methylation pattern of brain stem pilocytic astrocytomas in children. J Clin Oncol; 2009 May 20;27(15_suppl):10021

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

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  • (PMID = 27962622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. 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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22. 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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23. 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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24. 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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25. 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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26. Tosoni A, Franceschi E, Ermani M, Bacci A, Volpin L, Lombardo L, Ravenna G, Pinna G, Poggi R, Brandes AA: MGMT methylation status as a prognostic factor in anaplastic astrocytomas. J Clin Oncol; 2009 May 20;27(15_suppl):2052

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

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  • (PMID = 27964674.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Korkolopoulou P, Perdiki M, Thymara I, Boviatsis E, Agrogiannis G, Kotsiakis X, Angelidakis D, Rologis D, Diamantopoulou K, Thomas-Tsagli E, Kaklamanis L, Gatter K, Patsouris E: Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX. Hum Pathol; 2007 Apr;38(4):629-38

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

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  • (PMID = 17367605.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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28. Elsir T, Eriksson A, Orrego A, Lindström MS, Nistér M: Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas. J Neuropathol Exp Neurol; 2010 Feb;69(2):129-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas.
  • PROX1 is a prospero-related transcription factor that plays a critical role in the development of various organs including the mammalian lymphatic and central nervous systems; it controls cell proliferation and differentiation through different transcription pathwaysand has both oncogenic and tumor-suppressive functions.
  • We investigated PROX1 expression patterns in 56 human astrocytic gliomas of different grades using immunohistochemistry.
  • An average of 79% of cells in World Health Organization Grade IV (glioblastoma, n = 15) and 57% of cells in World Health Organization Grade III (anaplastic astrocytoma, n = 13) were strongly PROX1 positive; low-grade diffuse astrocytomas (Grade II, n = 13) had 21% of cells that were strongly positive; Grade I tumors (n = 15) had 1.5%; and non-neoplastic brain tissue (n = 15) had 3.7% of cells that were PROX1 positive.
  • Analyses of coexpression with proliferation markers suggest that PROX1+ cells have a marginally lower rate of proliferation than other tumor cells but are still mitotically active.
  • We conclude that PROX1 may constitute a useful tool for the diagnosis and grading ofastrocytic gliomas and for distinguishing Grade III and Grade IV tumors from Grade I and Grade II tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Homeodomain Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Antigens, Nuclear / metabolism. Biomarkers / metabolism. Brain Diseases / metabolism. Cell Proliferation. Humans. Immunohistochemistry. Microtubule-Associated Proteins / metabolism. Microvessels / metabolism. Mitosis. Nerve Tissue Proteins / metabolism. Tubulin / metabolism

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  • (PMID = 20084020.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / neuronal nuclear antigen NeuN, human; 0 / prospero-related homeobox 1 protein
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29. 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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30. Pareés I, Alonso J, Rovira A, Martínez E, Montalban X: [Diffuse astrocytoma presenting as an optic-spinal syndrome]. Rev Neurol; 2009 Apr 1-15;48(7):354-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diffuse astrocytoma presenting as an optic-spinal syndrome].
  • [Transliterated title] Síndrome opticomedular como forma de presentación de un astrocitoma difuso.
  • INTRODUCTION: Spinal cord involvement is a rare presentation of grade II astrocytomas.
  • Nevertheless, differentiation from inflammatory demyelinating diseases of the central nervous system can be challenging in some clinical situations.
  • A patient with an optic-spinal syndrome due to a fibrillary astrocytoma is described.
  • CASE REPORT: A 32 years-old man was admitted to the hospital because of a subacute spinal cord syndrome.
  • A new MRI with spectroscopy revealed an infiltrative lesion involving the right frontal lobe, optic chiasm, internal capsule, brainstem and cervical spinal cord, which was suggestive of low-grade astrocytoma.
  • Brain biopsy confirmed the diagnosis of diffuse fibrillary astrocytoma.
  • Brain biopsy is often necessary for a definite diagnosis.
  • [MeSH-major] Astrocytoma. Demyelinating Diseases. Optic Neuritis. Spinal Cord / pathology

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  • (PMID = 19319816.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Oligoclonal Bands
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31. 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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32. Aguilar Moliner I, Costa Orvay JA, Juma K, Costa Clara JM, Cruz Martínez O, Pou Fernández J: [Optic pathway astrocytoma: an unusual cause of failure to thrive in infants]. An Pediatr (Barc); 2007 Jun;66(6):622-4
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  • [Title] [Optic pathway astrocytoma: an unusual cause of failure to thrive in infants].
  • [Transliterated title] Astrocitoma de vías ópticas: una causa infrecuente de retraso ponderal en el lactante.
  • We report a case of low-grade astrocytoma of the optic pathway in a 2-month-old child whose main symptoms at diagnosis were failure to thrive and anorexia.
  • Unfortunately, despite therapeutic efforts, the tumor showed local and metastatic progression refractory to chemotherapy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Failure to Thrive / etiology. Optic Nerve Glioma / diagnosis

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  • (PMID = 17583627.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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33. Perdiki M, Korkolopoulou P, Thymara I, Agrogiannis G, Piperi C, Boviatsis E, Kotsiakis X, Angelidakis D, Diamantopoulou K, Thomas-Tsagli E, Patsouris E: Cyclooxygenase-2 expression in astrocytomas. Relationship with microvascular parameters, angiogenic factors expression and survival. Mol Cell Biochem; 2007 Jan;295(1-2):75-83

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

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  • (PMID = 16868662.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / Membrane Proteins; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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34. Xu P, Qiu M, Zhang Z, Kang C, Jiang R, Jia Z, Wang G, Jiang H, Pu P: The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo. J Neurooncol; 2010 Mar;97(1):41-51
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  • [Title] The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo.
  • Deregulation of Notch signaling has been implicated in some genetic diseases and tumorigenesis.
  • The function of Notch signaling in a variety of tumors can be either oncogenic or tumor-suppressive, depending on the cellular context.
  • In this study, Notch1 overexpression was observed in the majority of 45 astrocytic gliomas with different grades and in U251MG glioma cells.
  • Meanwhile, tumor growth was delayed in established subcutaneous gliomas in nude mice treated with Notch1 siRNA in vivo.
  • These results suggest that Notch1 plays an important oncogenic role in the development and progression of astrocytic gliomas.
  • [MeSH-major] Astrocytoma / genetics. Gene Expression Regulation, Neoplastic / physiology. Receptor, Notch1 / genetics
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Disease Models, Animal. Flow Cytometry / methods. Humans. In Situ Nick-End Labeling / methods. Matrix Metalloproteinase 9 / metabolism. Mice. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Transfection / methods

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  • (PMID = 19771395.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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35. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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36. Freitas MR, de Muzio SD, Pessoa RC, Stávale JN, Borges LR, Malheiros SM: [Diffuse bone marrow metastasis in cerebellar high-grade astrocytoma. A case report]. Rev Neurol; 2009 Mar 1-15;48(5):242-4
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  • [Title] [Diffuse bone marrow metastasis in cerebellar high-grade astrocytoma. A case report].
  • [Transliterated title] Metastasis difusa de la medula osea en un astrocitoma cerebeloso de alto grado. Un caso clinico.
  • INTRODUCTION: Cerebellar high-grade astrocytoma is uncommon.
  • Although more prone to present cerebrospinal fluid dissemination, the cerebellar location is not particularly related to the occurrence of extra-cranial metastases, which are also unusual in supratentorial malignant gliomas.
  • CASE REPORT: A 46 year-old man with cerebellar anaplastic astrocytoma who developed pancytopenia due to extensive bone marrow metastases.
  • CONCLUSION: Extraneural metastases of brain gliomas are rare and the spread to the bone marrow confers an extremely poor prognosis for these patients.
  • The expected improvement in glioma patients' survival due to the combination of more efficient therapies may lead to an increased incidence of this uncommon presentation, justifying a more rigorous follow-up of systemic manifestations.
  • [MeSH-major] Astrocytoma / pathology. Bone Marrow Neoplasms / secondary. Cerebellar Neoplasms / pathology

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  • (PMID = 19263392.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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37. 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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  • [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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38. 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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  • [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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39. Fisher PG, Tihan T, Goldthwaite PT, Wharam MD, Carson BS, Weingart JD, Repka MX, Cohen KJ, Burger PC: Outcome analysis of childhood low-grade astrocytomas. Pediatr Blood Cancer; 2008 Aug;51(2):245-50
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  • [Title] Outcome analysis of childhood low-grade astrocytomas.
  • BACKGROUND: We aimed to determine the long-term natural history of low-grade astrocytomas (LGA) in children, with respect to pathology, and to evaluate influence of treatment on survival.
  • RESULTS: Two hundred seventy-eight children (160 males; mean age 9.1 years; tumor location: 77 cerebrum, 62 cerebellum, 51 hypothalamic, 30 thalamus, 9 ventricle, 40 brainstem, and 9 spine) were assessed.
  • Among 246 specimens reviewed, diagnoses were 135 pilocytic astrocytoma (PA), 27 diffuse astrocytoma (DA), 75 unclassifiable well-differentiated astrocytoma (NOS), and 9 subependymal giant cell astrocytoma.
  • Reviewed diagnoses were highly associated with OS (P < 0.0001), with 5-year OS for PA 96%, DA 48%, and NOS 86%; these differences remained significant when stratified by location or extent of resection.
  • Among patients with residual tumor after surgery, 5-year PFS was 48% with observation alone (n = 114), no different (P = 0.32) from that achieved with immediate irradiation (n = 86).
  • While tumor location and resection extent affect outcome, pathologic diagnosis when carefully interpreted significantly influences long-term survival.
  • [MeSH-major] Astrocytoma / mortality. Brain Neoplasms / mortality

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  • (PMID = 18386785.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Knizetova P, Darling JL, Bartek J: Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy. J Cell Mol Med; 2008 Jan-Feb;12(1):111-25
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  • [Title] Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy.
  • Malignant astrogliomas are among the most aggressive, highly vascular and infiltrating tumours bearing a dismal prognosis, mainly due to their resistance to current radiation treatment and chemotherapy.
  • Efforts to identify and target the mechanisms that underlie astroglioma resistance have recently focused on candidate cancer stem cells, their biological properties, interplay with their local microenvironment or 'niche', and their role in tumour progression and recurrence.
  • Both paracrine and autocrine regulation of astroglioma cell behaviour by locally produced cytokines such as the vascular endothelial growth factor (VEGF) are emerging as key factors that determine astroglioma cell fate.
  • Here, we review these recent rapid advances in astroglioma research, with emphasis on the significance of VEGF in astroglioma stem-like cell biology.
  • Furthermore, we highlight the unique DNA damage checkpoint properties of the CD133-marker-positive astroglioma stem-like cells, discuss their potential involvement in astroglioma radioresistance, and consider the implications of this new knowledge for designing combinatorial, more efficient therapeutic strategies.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / therapy. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Neoplastic Stem Cells / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18031298.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 129
  • [Other-IDs] NLM/ PMC3823475
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41. 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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42. Rodríguez-Francia P, Sánchez-Tocino H, García-Cantera M, Martín-Castillo J: [Optic nerve pilocytic astrocytoma with retinal involvement]. Arch Soc Esp Oftalmol; 2005 Dec;80(12):733-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Optic nerve pilocytic astrocytoma with retinal involvement].
  • [Transliterated title] Astrocitoma pilocítico de nervio óptico con afectación de retina.
  • INTRODUCTION: This is an atypical case of a pilocytic astrocytoma that involved the optic nerve (ON) and the retina.
  • CLINICAL CASE: The patient was a 30-year-old male, who had attended ONCE since his early childhood because of the suspicion of an intraocular tumor.
  • The ophthalmology exploration showed an ON and retinal coloboma in the right eye and microphthalmy, shutting of the pupil, retinal detachment and proof of an intraocular tumor in the left eye.
  • The MR revealed an ON tumor that involved the retina.
  • The histopathological study after enucleation was pilocytic astrocytoma.
  • [MeSH-major] Optic Nerve Glioma / secondary. Optic Nerve Neoplasms / pathology. Retinal Neoplasms / secondary

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  • (PMID = 16372218.001).
  • [ISSN] 0365-6691
  • [Journal-full-title] Archivos de la Sociedad Española de Oftalmología
  • [ISO-abbreviation] Arch Soc Esp Oftalmol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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43. Shostak KO, Dmitrenko VV, Vudmaska MI, Naidenov VG, Beletskii AV, Malisheva TA, Semenova VM, Zozulya YP, Demotes-Mainard J, Kavsan VM: Patterns of expression of TSC-22 protein in astrocytic gliomas. Exp Oncol; 2005 Dec;27(4):314-8
MedlinePlus Health Information. consumer health - Brain Tumors.

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

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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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44. Takata K, Gasparetto EL, Leite Cda C, Lucato LT, Reed UC, Matushita H, Aguiar PH, Rosemberg S: [Subependymal giant cell astrocytoma in patients with tuberous sclerosis: magnetic resonance imaging findings in ten cases]. Arq Neuropsiquiatr; 2007 Jun;65(2A):313-6
MedlinePlus Health Information. consumer health - Tuberous Sclerosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Subependymal giant cell astrocytoma in patients with tuberous sclerosis: magnetic resonance imaging findings in ten cases].
  • [Transliterated title] Astrocitoma subependimário de células gigantes em pacientes com esclerose tuberosa: achados em ressonância magnética de dez casos.
  • OBJECTIVE: To report the magnetic resonance imaging (MRI) findings in 10 patients with subependimal giant cell astrocytoma (SGCA) and tuberous sclerosis (TS).
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cerebral Ventricles / pathology. Tuberous Sclerosis / pathology


45. Azad S, Kudesia S, Chawla N, Azad R, Singhal M, Rai SM, Arora P: Pilomyxoid astrocytoma. Indian J Pathol Microbiol; 2010 Apr-Jun;53(2):294-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilomyxoid astrocytoma.
  • Pilomyxoid astrocytoma (PMA) is a recently described brain tumor.
  • PMA shares similar features with pilocytic astrocytoma (PA), the most common central nervous system (CNS) tumor in the pediatric population, yet displays subtle histologic differences.
  • The histological findings revealed a tumor composed of a monotonous population of loosely arranged cells with delicate piloid like processes, within a prominent myxoid background.
  • The tumor lacked biphasic appearance, Rosenthal fibers, eosinophilic granular bodies and calcification that are commonly observed in classical PA.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / pathology. Brain Neoplasms / diagnosis. Brain Neoplasms / pathology

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  • (PMID = 20551536.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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46. 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


47. 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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48. 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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  • [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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49. Faria AV, Azevedo GC, Zanardi VA, Ghizoni E, Queiroz LS: Dissemination patterns of pilocytic astrocytoma. Clin Neurol Neurosurg; 2006 Sep;108(6):568-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dissemination patterns of pilocytic astrocytoma.
  • Two patients with multifocal pilocytic astrocytoma diagnosed by magnetic resonance imaging (MRI) and confirmed by histopathological examination are reported.
  • They presented distinct sites and mechanisms of metastasis: to distant ventricles through the cerebral spinal fluid (CSF) in patient 1 and to contralateral parenchyma, possibly through white matter tracts, in patient 2, a pathway not so far reported in pilocytic astrocytoma.
  • Early detection of multifocal pilocytic astrocytoma by MRI may change treatment strategies and improve prognosis.
  • [MeSH-major] Astrocytoma / secondary. Brain Neoplasms / pathology


50. 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


51. 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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52. Bongiorni L, Arroyo HA, Lubienicki F: [Subependymal nodules-sudependymal giant cell astrocytoma complex in children with tuberous sclerosis]. Medicina (B Aires); 2009;69(1 Pt 1):8-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Subependymal nodules-sudependymal giant cell astrocytoma complex in children with tuberous sclerosis].
  • [Transliterated title] Complejo nódulo subependimario-astrocitoma subependimario gigantocelular en niños con esclerosis tuberosa.
  • The object of this paper is to describe the imaging and clinical characteristics of subependymal nodule (SN) - subependymal giant cell astrocytoma (SGCA) complex in tuberous sclerosis and analyze its evolution in order to attempt early detection and the prevention of intracranial hypertension.
  • Six patients presented visual deficit and in these, the average diameter of the tumor was 31.5 mm, a high value when compared to 18.7 mm in the patients without visual deficit.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cerebral Ventricles / pathology. Tuberous Sclerosis / pathology


53. Misra A, Chattopadhyay P, Chosdol K, Sarkar C, Mahapatra AK, Sinha S: Clonal mutations in primary human glial tumors: evidence in support of the mutator hypothesis. BMC Cancer; 2007;7:190
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: A verifiable consequence of the mutator hypothesis is that even low grade neoplasms would accumulate a large number of mutations that do not influence the tumor phenotype (clonal mutations).
  • In this study, we have attempted to quantify the number of clonal mutations in primary human gliomas of astrocytic cell origin.
  • These alterations were identified in tumor tissue, microscopically confirmed to have over 70% neoplastic cells.
  • METHODS: Random Amplified Polymorphic DNA (RAPD) analysis was performed using a set of fifteen 10-mer primers of arbitrary but definite sequences in 17 WHO grade II astrocytomas (low grade diffuse astrocytoma or DA) and 16 WHO grade IV astrocytomas (Glioblastoma Multiforme or GBM).
  • The RAPD profile of the tumor tissue was compared with that of the leucocyte DNA of the same patient and alteration(s) scored.
  • CONCLUSION: This study demonstrates the presence of extensive clonal mutations in gliomas, more in lower grade.
  • This is consistent with our earlier work demonstrating that technique like RAPD analysis, unbiased for locus, is able to demonstrate more intra-tumor genetic heterogeneity in lower grade gliomas compared to higher grade.
  • [MeSH-minor] Cell Line, Tumor. Cloning, Molecular. DNA / metabolism. DNA Primers / chemistry. Data Interpretation, Statistical. Glioma / genetics. Humans. Leukocytes / metabolism. Models, Genetic. Models, Theoretical. Polymerase Chain Reaction. Polymorphism, Genetic. Reproducibility of Results

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  • (PMID = 17925012.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2190769
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54. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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55. Yang Z, Wang Y, Fang J, Chen F, Liu J, Wu J, Wang Y, Song T, Zeng F, Rao Y: Downregulation of WIF-1 by hypermethylation in astrocytomas. Acta Biochim Biophys Sin (Shanghai); 2010 Jun 15;42(6):418-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of WIF-1 by hypermethylation in astrocytomas.
  • Wnt inhibitory factor-1 (WIF-1) acts as a Wnt antagonist and tumor suppressor, but hypermethylation of WIF-1 gene promoter and low expression of WIF-1 activate Wnt signaling aberrantly and induce the development of several human tumors.
  • By using RT-PCR, immunohistochemistry and methylation-specific PCR, we analyzed the expression and methylation of WIF-1 in 4 normal brain tissues, 35 freshly resected astrocytoma tissues and 4 glioblastoma-derived cell lines.
  • Significant downregulation of WIF-1 mRNA and protein expression levels was observed in astrocytoma tissues compared with normal brain tissues.
  • Significant association between WIF-1 downregulation and pathological grade of astrocytomas was found.
  • WIF-1 gene aberrant methylation was observed in 19 of 35 (54.29%) tumor samples.
  • Our results suggested that the WIF-1 gene is frequently silenced in astrocytoma by aberrant promoter methylation.
  • This may be an important mechanism in astrocytoma carcinogenesis.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Astrocytoma / genetics. DNA Methylation. Repressor Proteins / genetics
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / metabolism. Cell Line, Tumor. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Promoter Regions, Genetic. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Wnt Proteins / genetics. beta Catenin / genetics

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  • (PMID = 20539942.001).
  • [ISSN] 1745-7270
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / WIF1 protein, human; 0 / Wnt Proteins; 0 / beta Catenin; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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56. Ohgaki H, Kleihues P: Epidemiology and etiology of gliomas. Acta Neuropathol; 2005 Jan;109(1):93-108
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  • [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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57. 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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58. Rush SZ, Abel TW, Valadez JG, Pearson M, Cooper MK: Activation of the Hedgehog pathway in pilocytic astrocytomas. Neuro Oncol; 2010 Aug;12(8):790-8
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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 the Hedgehog pathway in pilocytic astrocytomas.
  • Pilocytic astrocytoma is commonly viewed as a benign lesion.
  • However, disease onset is most prevalent in the first two decades of life, and children are often left with residual or recurrent disease and significant morbidity.
  • The Hedgehog (Hh) pathway regulates the growth of higher WHO grade gliomas, and in this study, we have evaluated the activation and operational status of this regulatory pathway in pilocytic astrocytomas.
  • Expression levels of the Hh pathway transcriptional target PTCH were elevated in 45% of tumor specimens analyzed (ages 1-22 years) and correlated inversely with patient age.
  • Evaluation of a tissue array revealed oligodendroglioma-like features, pilomyxoid features, infiltration, and necrosis more commonly in specimens from younger patients (below the median patient age of 10 years).
  • Taken together, these findings suggest that Hh pathway activation is common in pediatric pilocytic astrocytomas and may be associated with younger age at diagnosis and tumor growth.

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  • (PMID = 20223881.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA068485; United States / NINDS NIH HHS / NS / K02NS053614
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Transcription Factors; 0 / patched receptors
  • [Other-IDs] NLM/ PMC2940682
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59. Lefranc F, Rynkowski M, DeWitte O, Kiss R: Present and potential future adjuvant issues in high-grade astrocytic glioma treatment. Adv Tech Stand Neurosurg; 2009;34:3-35
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  • [Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.
  • Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.
  • Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.
  • Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.
  • Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.
  • Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.
  • Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells.
  • The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy


60. Hillmann P, Köse M, Söhl K, Müller CE: Ammonium-induced calcium mobilization in 1321N1 astrocytoma cells. Toxicol Appl Pharmacol; 2008 Feb 15;227(1):36-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ammonium-induced calcium mobilization in 1321N1 astrocytoma cells.
  • In the present study, an astrocytoma cell line 1321N1 and a neuroblastoma glioma hybrid cell line NG108-15 were used as model systems for astrocytes and neuronal cells, respectively.
  • Ammonium salts evoked a transient increase in intracellular calcium concentrations ([Ca(2+)](i)) in astrocytoma (EC(50)=6.38 mM), but not in NG108-15 cells.
  • Ammonium (5 mM) also significantly inhibited the proliferation of 1321N1 astrocytoma cells.
  • While mRNA for the mammalian ammonium transporters RhBG and RhCG could not be detected in 1321N1 astrocytoma cells, both transporters were expressed in NG108-15 cells.
  • Human 1321N1 astrocytoma cells appear to be an excellent, easily accessible human model for studying HE, which can substitute animal studies, while NG108-15 cells may be useful for investigating the role of the recently discovered Rhesus family type ammonium transporters in neuronal cells.
  • [MeSH-major] Astrocytoma / metabolism. Calcium / metabolism. Quaternary Ammonium Compounds / pharmacology
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. DNA Primers. Humans. Potassium Chloride / pharmacology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18061226.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Quaternary Ammonium Compounds; 660YQ98I10 / Potassium Chloride; SY7Q814VUP / Calcium
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61. Villarejo F, de Diego JM, de la Riva AG: Prognosis of cerebellar astrocytomas in children. Childs Nerv Syst; 2008 Feb;24(2):203-10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognosis of cerebellar astrocytomas in children.
  • OBJECTIVE: Our main objective is to review a large series of cerebellar astrocytomas in children and evaluate the outcome of the patients depending on astrocytoma class.
  • The effect of astrocytoma characteristics on the children's prognosis was determined by grouping a series of cerebellar astrocytomas by their location, radiological aspect, size, and histology and determining whether this was related with outcome.
  • MATERIALS AND METHODS: Two hundred and three children with cerebellar astrocytomas were retrospectively reviewed, and their tumors were classified by location, macroscopic radiological appearance, size, and histology.
  • RESULTS: Our patients' results were classified according to the Lapras scale/classification as normal, with some neurological deficit but able to lead a normal life, and those with severe post surgical deficits.
  • There were six recurrences and 22 deaths because of the disease.
  • One was whether the tumor was completely resected or not; this was the treatment in most cases in this series.
  • The second factor was the location, size, and macroscopic appearance of the tumor.
  • [MeSH-major] Astrocytoma / pathology. Cerebellar Neoplasms / pathology

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  • (PMID = 17710415.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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62. Hamlat A, Saikali S, Diabira S, Messerer M, Riffaud L: Diagnosis of childhood astrocytomas. Expert Opin Med Diagn; 2009 Sep;3(5):501-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of childhood astrocytomas.
  • BACKGROUND: Astrocytomas are the most common brain tumours, accounting for 28 - 50% of all primary CNS tumours.
  • Objectives/method: The clinical presentations of CNS astrocytomas vary with their sites of location; therefore, a period of uncertainty often precedes diagnosis, and approximately 42% of patients with an intracranial process make several visits to various physicians between the onset and diagnosis.
  • However, on clinical suspicion of a brain tumour, a wide range of neuroimaging techniques may be used to assess the diagnosis of paediatric brain lesions.
  • In this review the authors, for ease of presentation, describe the clinical presentations of supratentorial, infratentorial and spinal cord astrocytomas as well as their radiological and pathological features, and discuss their differential diagnoses.
  • RESULTS/CONCLUSIONS: Understanding and mastering the numerous imaging features of several subtypes of primary brain tumours affecting children, in addition to radiological features of non-tumoural disorders, remains a significant challenge and demands increased awareness of the paediatric brain diseases.

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  • (PMID = 23495981.001).
  • [ISSN] 1753-0059
  • [Journal-full-title] Expert opinion on medical diagnostics
  • [ISO-abbreviation] Expert Opin Med Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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63. Nakamura M, Tsuji O, Fujiyoshi K, Watanabe K, Tsuji T, Ishii K, Matsumoto M, Toyama Y, Chiba K: Cordotomy for patients with thoracic malignant astrocytoma. J Neurosurg Spine; 2010 Oct;13(4):418-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cordotomy for patients with thoracic malignant astrocytoma.
  • OBJECT: The optimal management of malignant astrocytomas remains controversial, and the prognosis of these lesions has been dismal regardless of the administered treatment.
  • In this study the authors investigated the surgical outcomes of cordotomy in patients with thoracic malignant astrocytomas to determine the effectiveness of this procedure.
  • METHODS: Cordotomy was performed in 5 patients with glioblastoma multiforme (GBM) and 2 with anaplastic astrocytoma (AA).
  • In the 2 patients with GBM, cordotomy was performed 2 and 3 weeks after a partial tumor resection.
  • In the 2 patients with AA, the initial treatment consisted of partial tumor resection and subtotal resection combined with radiotherapy, and rostral tumor growth and progressive paralysis necessitated cordotomy 2 and 28 months later.
  • One patient with a secondary GBM underwent cordotomy; the GBM developed 1 year after subtotal resection and radiotherapy for a WHO Grade II astrocytoma.
  • In patients with thoracic GBM, even if paralysis is incomplete, cordotomy should be performed before the tumor disseminates through the CSF.
  • If the tumor persists, radiotherapy and chemotherapy are indicated, and cordotomy should be reserved for lesions growing progressively after such second-line treatments.
  • [MeSH-major] Astrocytoma / surgery. Cordotomy. Thoracic Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Disease Progression. Encephalitis / etiology. Female. Glioblastoma / complications. Glioblastoma / pathology. Glioblastoma / surgery. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Pain, Postoperative. Paraplegia / etiology. Paraplegia / surgery. Prognosis. Radiotherapy, Adjuvant. Treatment Outcome. Young Adult

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  • (PMID = 20887138.001).
  • [ISSN] 1547-5646
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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64. Niculescu CE, Stănescu L, Popescu M, Niculescu D: Supratentorial pilocytic astrocytoma in children. Rom J Morphol Embryol; 2010;51(3):577-80
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  • [Title] Supratentorial pilocytic astrocytoma in children.
  • The authors describe the case of a child aged 2 years and 4 months with increased intracranial pressure, symptomatology accompanied by rapid deterioration of general condition.
  • Histopathological examination revealed the typical grade I pilocytic astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Supratentorial Neoplasms / pathology

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  • (PMID = 20809042.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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65. Maris C, Rorive S, Sandras F, D'Haene N, Sadeghi N, Bièche I, Vidaud M, Decaestecker C, Salmon I: Tenascin-C expression relates to clinicopathological features in pilocytic and diffuse astrocytomas. Neuropathol Appl Neurobiol; 2008 Jun;34(3):316-29
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  • [Title] Tenascin-C expression relates to clinicopathological features in pilocytic and diffuse astrocytomas.
  • AIMS: Tenascin-C (TN-C) is an extracellular matrix brain glycoprotein for which conflicting in vitro and in vivo results are reported in the literature dealing with its involvement in astrocytoma aggressiveness, in particular astrocytoma invasion.
  • In view of these conflicting results and the lack of data available on low-grade astrocytomas, the present study focuses on pilocytic World Health Organization (WHO) grade I, and diffuse WHO grade II astrocytomas, that is, two histological entities associated with very different invasive abilities.
  • METHODS: Using real-time reverse transcription polymerase chain reaction and immunohistochemistry, we analysed the TN-C expression in normal brain tissue as well as in a series of 54 pilocytic and 53 grade II astrocytomas.
  • Paralleling these observations, we showed that TN-C expression in low-grade astrocytomas similarly varies according to tumour site.
  • Cox regression analysis evidenced that TN-C provided an independent prognostic value which is enhanced in the case of grade II astrocytomas for which positive TN-C expression is associated with a higher risk of recurrence.
  • We also analysed TN-C expression specifically in vascular areas of low-grade astrocytomas without demonstrating any prognostic value for this additional feature.
  • RESULTS: Similarly to normal brain, low-grade astrocytomas exhibit variations in TN-C expression with site, and this expression is associated with an independent prognostic value in terms of recurrence.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Tenascin / biosynthesis
  • [MeSH-minor] Adult. Age Factors. Biomarkers, Tumor / analysis. Child. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Neoplasm Recurrence, Local / pathology. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Spinal Cord Neoplasms / metabolism. Spinal Cord Neoplasms / mortality. Spinal Cord Neoplasms / pathology

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  • (PMID = 17983425.001).
  • [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 / Biomarkers, Tumor; 0 / Tenascin
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66. Matsuda K, Sakurada K, Mouri W, Saino M, Sato S, Saito S, Kayama T, Nakazato Y: [Operative case of isomorphic astrocytoma]. Brain Nerve; 2007 Aug;59(8):881-6
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  • [Title] [Operative case of isomorphic astrocytoma].
  • Diffuse astrocytomas are classified as WHO Grade II tumors.
  • Recently, a subtype presenting with better prognosis has been proposed, and it is known as "isomorphic astrocytoma."
  • A clinical case that we encountered was believed to be categorized as this subtype; it has been presented in this report.
  • The tumor was resected under awake surgery.
  • The pathological diagnosis was diffuse astrocytoma, but this tumor was considered to be the isomorphic subtype.
  • Some parts of the tumor showed a relatively high MIB-1 labeling index (LI) of 9.2%, and additional 50-Gy radiotherapy was performed.
  • Isomorphic astrocytoma is characterized by prolonged epileptic seizures, a low MIB-1 LI, and better prognosis.
  • In our case, since the MIB-1 LI was higher in some parts of the tumor, the appropriate therapy for WHO Grade II tumors was performed.
  • However, this case was considered representative of isomorphic astrocytoma.
  • No reports of this tumor subtype have been previously described in Japan.
  • Therefore, this report is the first case of isomorphic astrocytoma reported to Japanese literature.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery

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  • (PMID = 17713125.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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67. Zajdel A, Wilczok A, Slowinski J, Orchel J, Mazurek U: Aldehydic lipid peroxidation products in human brain astrocytomas. J Neurooncol; 2007 Sep;84(2):167-73
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  • [Title] Aldehydic lipid peroxidation products in human brain astrocytomas.
  • We explored whether these aldehydes and histone H3 mRNA levels could serve as biomarkers of malignancy and predictive factor in human brain astrocytomas.
  • Aldehydic lipid peroxidation products were determined as their dinitrophenylhydrazone derivatives in specimens obtained from 26 adult patients with brain astrocytomas.
  • H3 mRNA, 2-hydroxyhexanal, and 4-hydroxynonenal levels were higher in high-grade astrocytomas compared to low-grade astrocytomas and showed negative correlation with survival.
  • Higher levels of 2-hydroxyhexanal and 4-hydroxynonenal, and lower levels of n-hexanal were associated with poorer patient prognosis.
  • Our data suggest that tissue concentrations of aldehydic lipid peroxidation products can assist grading and predicting the clinical outcome in patients with astrocytic brain tumors.
  • Possibly, this parameter will enhance optimal selection of patients for individualized treatment protocols, tailored to unique biochemical and molecular profile of the tumor.
  • [MeSH-major] Aldehydes / analysis. Astrocytoma / metabolism. Brain Chemistry / physiology. Brain Neoplasms / metabolism. Lipid Peroxidation / physiology

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  • (PMID = 17487452.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Histones; 0 / RNA, Messenger
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68. Foehr ED, Lorente G, Vincent V, Nikolich K, Urfer R: FAS associated phosphatase (FAP-1) blocks apoptosis of astrocytomas through dephosphorylation of FAS. J Neurooncol; 2005 Sep;74(3):241-8
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  • [Title] FAS associated phosphatase (FAP-1) blocks apoptosis of astrocytomas through dephosphorylation of FAS.
  • Astrocytomas are the most common primary tumor of the adult human central nervous system.
  • Despite efforts to develop more effective clinical treatment strategies, median survival time for patients with the most severe form of astrocytoma, glioblastoma multiforme (GBM), remains about one year.
  • Astrocytomas are resistant to cytotoxic therapy in general and radiation therapy in particular, greatly limiting treatment options.
  • We have characterized the role of the tyrosine phosphatase FAP-1 (FAS-associated phosphatase 1) in astrocytomas.
  • Our studies demonstrate that FAP-1 is overexpressed in astrocytomas and this contributes to the resistance of the tumor cells to FAS-mediated apoptosis.
  • We demonstrate that knockdown of FAP-1 by RNA interference leads to increased apoptosis and increased sensitivity of astrocytoma cells to FAS-induced cell death.
  • FAP-1 binds to FAS in a ligand-dependent manner and forms a signaling complex that modulates the ability of astrocytoma cells to undergo FAS ligand (FASL)-mediated cell death.
  • In astrocytoma cells, FASL treatment induces tyrosine phosphorylation of FAS.
  • This is the first direct evidence that FAS activity can be regulated by reversible phosphorylation and suggests a mechanism for astrocytoma resistance to apoptosis.
  • [MeSH-major] Antigens, CD95 / metabolism. Apoptosis / physiology. Astrocytoma / pathology. Brain Neoplasms / pathology. Protein Tyrosine Phosphatases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Gene Expression. Gene Expression Profiling. Humans. Immunoblotting. Immunohistochemistry. Phosphorylation. Protein Phosphatase 1. Protein Tyrosine Phosphatase, Non-Receptor Type 13. RNA Interference. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16187021.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / RNA, Messenger; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / PTPN13 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 13; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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69. Santhosh K, Kesavadas C, Radhakrishnan VV, Abraham M, Gupta AK: Multifocal desmoplastic noninfantile astrocytoma. J Neuroradiol; 2008 Dec;35(5):286-91
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  • [Title] Multifocal desmoplastic noninfantile astrocytoma.
  • This is a report of a case of multifocal desmoplastic astrocytoma in an 11-year-old child in which we describe the MRI findings and discuss the possible mechanism of its development.
  • The MRI appearances in our case support the view that the tumor is primarily of leptomeningeal or superficial cortical origin, with cystic formation secondary to entrapment of cerebrospinal fluid.
  • Desmoplastic astrocytoma at a noninfantile age is extremely rare: only four cases have been reported in the literature so far.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Imaging / methods

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  • (PMID = 18538396.001).
  • [ISSN] 0150-9861
  • [Journal-full-title] Journal of neuroradiology. Journal de neuroradiologie
  • [ISO-abbreviation] J Neuroradiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Contrast Media
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70. Pascual-Castroviejo I, Pascual-Pascual SI, Velázquez-Fragua R, Viaño J, Carceller F, Hernández-Moneo JL, Gutiérrez-Molina M, Morales C: [Subependymal giant cell astrocytoma in tuberous sclerosis complex. A presentation of eight paediatric patients]. Neurologia; 2010 Jun;25(5):314-21
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  • [Title] [Subependymal giant cell astrocytoma in tuberous sclerosis complex. A presentation of eight paediatric patients].
  • [Transliterated title] Astrocitoma subependimario de células gigantes en el complejo de esclerosis tuberosa. Presentación de ocho pacientes infantiles.
  • OBJECTIVE: Presentation of 8 patients with subependymal giant-cell astrocytomas (SGCA) associated with tuberous sclerosis complex (TSC).
  • [MeSH-major] Astrocytoma / etiology. Astrocytoma / pathology. Brain Neoplasms / etiology. Brain Neoplasms / pathology. Tuberous Sclerosis


71. Yue WY, Chen ZP: Does vasculogenic mimicry exist in astrocytoma? J Histochem Cytochem; 2005 Aug;53(8):997-1002
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  • [Title] Does vasculogenic mimicry exist in astrocytoma?
  • Vasculogenic mimicry (VM) has been observed in melanoma and in some nonmelanoma tumor types.
  • It is unknown whether a similar VM phenomenon exists in astrocytoma.
  • The present study was to examine 45 astrocytomas (including World Health Organization grade II 15 cases, grade III 15 cases, and grade IV 15 cases) by CD34 endothelial marker periodic acid-Schiff (PAS) dual staining to see if VM existing in these tumors.
  • The results demonstrated that endothelium-lined vessels dominated the tumor microvasculature and stained positively for PAS, laminin, and endothelial marker.
  • PAS-positive pattern of VM was found in two grade IV astrocytomas.
  • Channels stained positively for PAS, laminin, and negatively for CD34 of the VM entrapped in the tumor tissue.
  • Furthermore, in astrocytoma, especially glioblastoma, focus of anaplastic tumor cells appeared with CD34 expression, whereas some tumor cells lost glial fibrillary acid protein expression.
  • It is assumed that genetically deregulated tumor cells in astrocytoma could lose the astrocyte-specific protein and express inappropriate markers not expected in cells of astrocyte lineage.
  • The present results suggest that VM phenomenon exists in some malignant astrocytoma.
  • [MeSH-major] Astrocytoma / blood supply. Brain Neoplasms / blood supply
  • [MeSH-minor] Antigens, CD34 / metabolism. Biomarkers / metabolism. Coloring Agents. Endothelium, Vascular / metabolism. Humans. Microcirculation. Neoplasm Staging. Periodic Acid. Schiff Bases

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  • (PMID = 15923371.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers; 0 / Coloring Agents; 0 / Schiff Bases; 10450-60-9 / Periodic Acid
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72. 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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  • (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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73. 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

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  • [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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74. Khan MA, Hashmi S: Low-grade astrocytoma causing calvarial scalloping. Pediatr Neurosurg; 2007;43(2):155-7
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  • [Title] Low-grade astrocytoma causing calvarial scalloping.
  • Gliomas are tumors of the white matter.
  • Only 1 case of low-grade astrocytoma causing calvarial erosion has been reported in the literature of the CT era.
  • We report the first case of a low-grade astrocytoma causing calvarial erosion in an adolescent.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / surgery. Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Osteolysis / pathology. Osteolysis / surgery. Parietal Lobe / pathology. Parietal Lobe / surgery. Skull / pathology. Skull / surgery

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 17337932.001).
  • [ISSN] 1016-2291
  • [Journal-full-title] Pediatric neurosurgery
  • [ISO-abbreviation] Pediatr Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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75. 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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76. 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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77. Kim SH, Kang SS, Jung TY, Jung S: Juvenile pilomyxoid astrocytoma in the opticohypothalamus. J Korean Neurosurg Soc; 2010 Nov;48(5):445-7

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  • [Title] Juvenile pilomyxoid astrocytoma in the opticohypothalamus.
  • Pilomyxoid astrocytoma (PMA) is a newly recognized variant of a pilocytic astrocytoma.
  • This report describes a case of a pilomyxoid astrocytoma that occurred in the opticohypothalamus.
  • Magnetic resonance imaging (MRI) showed an irregular lobulated tumor with heterogeneous enhancement at the suprasellar region involving the hypothalamus.
  • Adjuvant chemotherapy with cisplatin and vincristine was started following tumor resection.
  • Although long-term outcome is yet to be determined, the administration of combined cisplatin and vincristine treatment seems to be an effective regimen for a pilomyxoid astrocytoma.

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  • [Cites] Anticancer Res. 2009 Mar;29(3):919-26 [19414328.001]
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  • (PMID = 21286484.001).
  • [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/ PMC3030087
  • [Keywords] NOTNLM ; Adjuvant chemotherapy / Opticohypothalamus / Pilomyxoid astrocytoma
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78. Guan Y, Mizoguchi M, Yoshimoto K, Hata N, Shono T, Suzuki SO, Araki Y, Kuga D, Nakamizo A, Amano T, Ma X, Hayashi K, Sasaki T: MiRNA-196 is upregulated in glioblastoma but not in anaplastic astrocytoma and has prognostic significance. Clin Cancer Res; 2010 Aug 15;16(16):4289-97
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  • [Title] MiRNA-196 is upregulated in glioblastoma but not in anaplastic astrocytoma and has prognostic significance.
  • They are implicated in tumorigenesis and function both as tumor suppressors and as oncogenes.
  • The clinical significance of miRNA expression profiles in malignant gliomas remains unclear.
  • EXPERIMENTAL DESIGN: In this study, we examined the expression levels of 365 mature human miRNAs in 12 malignant gliomas, including 8 glioblastomas and 4 anaplastic astrocytomas, using TaqMan real-time quantitative PCR arrays.
  • A validation study was done to corroborate a subset of the results, including expression levels of miR-196a, -196b, -21, and -15b, by analyzing 92 malignant gliomas by conventional real-time PCR.
  • RESULTS: Expression profiles in glioblastomas and anaplastic astrocytomas suggested that 16 miRNAs were candidate markers associated with the malignant progression of gliomas.
  • Both miRNAs showed increased expression levels in glioblastomas relative to both anaplastic astrocytomas and normal brains in the validation study.
  • CONCLUSIONS: Our results suggest that miR-196 may play a role in the malignant progression of gliomas and may be a prognostic predictor in glioblastomas.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioblastoma / genetics. MicroRNAs / genetics

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  • (PMID = 20601442.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MIRN196 microRNA, human; 0 / MicroRNAs
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79. Li B, Qi XQ, Chen X, Huang X, Liu GY, Chen HR, Huang CG, Luo C, Lu YC: Expression of targeting protein for Xenopus kinesin-like protein 2 is associated with progression of human malignant astrocytoma. Brain Res; 2010 Sep 17;1352:200-7
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  • [Title] Expression of targeting protein for Xenopus kinesin-like protein 2 is associated with progression of human malignant astrocytoma.
  • However, the contribution of TPX2 expression to astrocytoma progression is unclear.
  • The aim of this study was to investigate TPX2 expression in human astrocytoma samples and cell lines.
  • TPX2 protein expression was detected in the nucleus of astrocytoma tissues by immunohistochemistry and immunofluorescence staining.
  • Real-time PCR and Western blot analysis showed that the expression levels of TPX2 were higher in high-grade astrocytoma tissues and cell lines than that in low-grade astrocytoma tissues and normal cell lines.
  • Immunohistochemical analysis of tumor tissues from 52 patients with astrocytoma showed that TPX2 over-expression was significantly associated with decreased patient survival.
  • These data suggest that TPX2 expression is associated with the progression of malignant astrocytoma.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Cell Cycle Proteins / genetics. Microtubule-Associated Proteins / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Apoptosis. Aurora Kinases. Brain / metabolism. Cell Division. Cell Line, Tumor. Cyclin B1 / genetics. Cyclin D1 / genetics. Disease Progression. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Protein-Serine-Threonine Kinases / genetics. Proto-Oncogene Proteins c-myc / genetics. Survival Rate. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 20599806.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Microtubule-Associated Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / TPX2 protein, human; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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80. Holland H, Koschny T, Ahnert P, Meixensberger J, Koschny R: WHO grade-specific comparative genomic hybridization pattern of astrocytoma - a meta-analysis. Pathol Res Pract; 2010 Oct 15;206(10):663-8
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  • [Title] WHO grade-specific comparative genomic hybridization pattern of astrocytoma - a meta-analysis.
  • To detect novel genetic alterations, many astrocytomas have been investigated by comparative genomic hybridization (CGH).
  • To identify aberration profiles characteristic of World Health Organization (WHO) grade I, II, III, and IV astrocytoma, we performed a meta-analysis of detailed genome wide CGH data of all 467 cases published so far.
  • Low-grade astrocytoma has already demonstrated one characteristic of glioblastoma multiforme, gain of chromosome 7 with a hot spot at 7q32, but without loss of chromosome 10.
  • In anaplastic astrocytoma, a more complex aberration pattern emerges from diffuse genetic imbalances.
  • In contrast to lower tumor grades, glioblastoma multiforme demonstrates +7p12 as the most frequently affected band on chromosome 7.
  • To quantify the gradual transition from WHO grade II-IV astrocytoma, we calculated the relative increase and decrease in frequency for each detected aberration of the tumor genome.
  • The most pronounced and diverse changes of genetic material occur at the virtual transition from low-grade to anaplastic astrocytoma.
  • Summing up, the expansion of the CGH results to the 850 GTG-band resolution enabled a meta-analysis to visualize WHO grade-specific aberration profiles in astrocytoma.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Aberrations. Comparative Genomic Hybridization. Glioblastoma / genetics. World Health Organization
  • [MeSH-minor] Gene Expression Regulation, Neoplastic. Genotype. Humans. Neoplasm Staging. Phenotype. Prognosis

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  • [Copyright] Copyright © 2010 Elsevier GmbH. All rights reserved.
  • (PMID = 20570053.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis
  • [Publication-country] Germany
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81. Fu JB, Parsons HA, Shin KY, Guo Y, Konzen BS, Yadav RR, Smith DW: Comparison of functional outcomes in low- and high-grade astrocytoma rehabilitation inpatients. Am J Phys Med Rehabil; 2010 Mar;89(3):205-12
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  • [Title] Comparison of functional outcomes in low- and high-grade astrocytoma rehabilitation inpatients.
  • OBJECTIVES: To compare inpatient rehabilitation outcomes between patients with low- and high-grade astrocytoma.
  • A high-grade (21 of 443 patients) and low-grade astrocytoma (21 of 24 patients) group were matched on three of five criteria in the order of importance: area of brain involvement (divided into left cerebral, right cerebral, midline and/or bilateral cerebral, and infratentorial), single vs. multiple intracranial neurosurgical procedures, age (within 10 yrs), period of rehabilitation admission (within 3 yrs), and sex.
  • The high-grade group had significantly (P < 0.05) higher total gain and longer stay in inpatient rehabilitation (mean +/- standard deviation, 21.7 +/- 10.1 vs. 13.0 +/- 9.3 and 13 +/- 7.1 day vs. 9 +/- 6.2 days, respectively) than did the low-grade astrocytoma group.
  • CONCLUSIONS: Compared with patients with low-grade astrocytoma, patients with high-grade astrocytoma had higher total functional independence measure gain but also longer lengths of stay.

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  • (PMID = 20068429.001).
  • [ISSN] 1537-7385
  • [Journal-full-title] American journal of physical medicine & rehabilitation
  • [ISO-abbreviation] Am J Phys Med Rehabil
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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82. Chatley A, Jaiswal AK, Jain M, Behari S: Congenital irreducible atlantoaxial dislocation associated with cervical intramedullary astrocytoma causing progressive spastic quadriparesis. Neurol India; 2008 Oct-Dec;56(4):477-9
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  • [Title] Congenital irreducible atlantoaxial dislocation associated with cervical intramedullary astrocytoma causing progressive spastic quadriparesis.
  • Simultaneous presence of congenital irreducible atlantoaxial dislocation (AAD) and cervical intramedullary astrocytoma has not been previously described and may cause disabling myelopathy.
  • Lateral radiographs and magnetic resonance imaging showed irreducible AAD, occipitalized atlas, C2-3 fusion, and,an intramedullary tumor from C2-5 level iso-to-hypointense, non-enhancing, except in a small segment in the dorsal C2 level.
  • A suboccipital craniectomy with C2-5 laminectomy revealed a greyish-white tenacious tumor.
  • The tumor was decompressed using a C2-5 midline myelotomy and duroplasty.
  • Histopathology revealed a low-grade astrocytoma.
  • Thus, the suboccipital craniectomy and laminectomy with midline myelotomy and duroplasty facilitated space for progressively expanding intramedullary astrocytoma with irreducible AAD; the lateral mass fixation provided stability at the craniovertebral junction.
  • [MeSH-major] Astrocytoma / complications. Atlanto-Axial Joint. Dislocations / complications. Dislocations / congenital. Quadriplegia / etiology. Spinal Neoplasms / complications

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  • (PMID = 19127046.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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83. Wong VC, Ma J, Hawkins CE: Telomerase inhibition induces acute ATM-dependent growth arrest in human astrocytomas. Cancer Lett; 2009 Feb 8;274(1):151-9
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  • [Title] Telomerase inhibition induces acute ATM-dependent growth arrest in human astrocytomas.
  • The purpose of the study was to examine the degree of hTERT, the catalytic subunit of telomerase, expression in paediatric high-grade astrocytoma and to explore the potential of telomerase inhibition as a therapy for these tumours. hTERT was expressed at high levels in 36 of 44 paediatric astrocytomas.
  • Telomerase inhibition induced acute DNA damage and ATM-pathway-dependent G2/M cell cycle arrest in astrocytomas in vitro, both occurring prior to telomere shortening itself.
  • Our data suggest that telomerase inhibition could be a useful adjuvant therapy for high-grade astrocytomas, potentially inducing tumour growth arrest following short-term treatment.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Cycle Proteins / metabolism. Cell Proliferation. DNA-Binding Proteins / metabolism. Protein-Serine-Threonine Kinases / metabolism. Telomerase / antagonists & inhibitors. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Cell Cycle / physiology. Child. DNA Damage. Flow Cytometry. Humans. Immunoenzyme Techniques. Telomere / physiology. Tumor Cells, Cultured

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  • (PMID = 18945545.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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84. Eskelin S, Tommila P, Palosaari T, Kivelä T: Photodynamic therapy with verteporfin to induce regression of aggressive retinal astrocytomas. Acta Ophthalmol; 2008 Nov;86(7):794-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photodynamic therapy with verteporfin to induce regression of aggressive retinal astrocytomas.
  • PURPOSE: To evaluate the effect of photodynamic therapy (PDT) with verteporfin on symptomatic, aggressive retinal astrocytomas.
  • Two patients were treated with a single session of PDT using the standard parameters of the Verteporfin in Photodynamic Therapy (VIP) study: a 34-year-old man whose previously stationary juxtapapillary retinal astrocytoma, secondary to tuberous sclerosis, progressed within 7 months to involve the foveola; and a 68-year-old man whose acquired retinal astrocytoma progressed over 18 months in spite of standard photocoagulation.
  • RESULTS: The progressing, vascularized part of both retinal astrocytomas regressed, with little change in the poorly vascularized, stationary part of the congenital hamartoma.
  • CONCLUSION: PDT with verteporfin can induce regression of progressive, vascularized, aggressive retinal astrocytomas and may prevent typical progression to total retinal detachment and enucleation, whether the astrocytoma is associated with tuberous sclerosis or not.
  • PDT may be considered a first-line treatment for aggressive retinal astrocytomas.
  • [MeSH-major] Astrocytoma / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use. Porphyrins / therapeutic use. Retinal Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Disease Progression. Humans. Light Coagulation. Male. Neoplasm Invasiveness. Prospective Studies. Retinal Detachment / etiology. Treatment Outcome. Tuberous Sclerosis / complications

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  • (PMID = 18759802.001).
  • [ISSN] 1755-3768
  • [Journal-full-title] Acta ophthalmologica
  • [ISO-abbreviation] Acta Ophthalmol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Porphyrins; 129497-78-5 / verteporfin
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85. Cuadrado-Pereira M, Rodriguez-Saenz J, Andujar-Felix J: Spinal cord high grade astrocytoma. Bol Asoc Med P R; 2007 Jan-Mar;99(1):60-3

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  • [Title] Spinal cord high grade astrocytoma.
  • OBJECTIVES: To describe the medical history, psychosocial aspects and the rehabilitation management of a patient with a high-grade astrocytoma of the spinal cord.
  • To review the literature regarding the epidemiology, classification, treatment, prognosis, and outcomes of astrocytomas involving the spinal cord.
  • To discuss issues and controversies in the rehabilitation management of spinal cord high-grade astrocytomas.
  • RESULTS: Aggressive multimodality treatment including acute inpatient interdisciplinary rehabilitation approach provided excellent results exceeding survival time and functional expectations for a patientwith high-grade astrocytoma.
  • (1) the survival time of more than three years, which exceeded the expected survival time of ten months for a patient diagnosed with spinal cord high grade astrocytoma and (2) for the outcomes achieved through an intensive comprehensive acute inpatient interdisci-plinary rehabilitation program which helped the patient achieve previous premorbid functional goals.
  • [MeSH-major] Astrocytoma. Spinal Cord Neoplasms

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  • (PMID = 17616049.001).
  • [ISSN] 0004-4849
  • [Journal-full-title] Boletín de la Asociación Médica de Puerto Rico
  • [ISO-abbreviation] Bol Asoc Med P R
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Puerto Rico
  • [Number-of-references] 18
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86. 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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87. Oka F, Yamashita Y, Kumabe T, Tominaga T: Total resection of a hemorrhagic tectal pilocytic astrocytoma--case report. Neurol Med Chir (Tokyo); 2007 May;47(5):219-21
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  • [Title] Total resection of a hemorrhagic tectal pilocytic astrocytoma--case report.
  • A 21-year-old man presented with a hemorrhagic pilocytic astrocytoma of the tectal plate manifesting as sudden onset of severe headache, vertigo, nausea, and vomiting.
  • Magnetic resonance (MR) imaging revealed a dorsally exophytic tectal tumor as hypointense on the T(1)-weighted image and hyperintense on the T(2)-weighted image with contrast enhancement.
  • Radical resection of the tumor was selected because of the unusual aggressive clinical course with hemorrhage and suspicion of malignant components.
  • The tumor was totally resected via an occipital transtentorial approach using a neuronavigation system without surgical complications.
  • The histological diagnosis was pilocytic astrocytoma.
  • Tectal plate pilocytic astrocytoma is rarely associated with hemorrhage but should be considered in the differential diagnosis of intracranial hemorrhage with acute presentation.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery. Intracranial Hemorrhages / etiology. Tectum Mesencephali

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  • (PMID = 17527049.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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88. Britto R, Umesh S, Hegde AS, Hegde S, Santosh V, Chandramouli BA, Somasundaram K: Shift in AP-2alpha localization characterizes astrocytoma progression. Cancer Biol Ther; 2007 Mar;6(3):413-8
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  • [Title] Shift in AP-2alpha localization characterizes astrocytoma progression.
  • Activator protein 2alpha (AP-2alpha) has been shown to be lost in the advanced stages of many cancers, including gliomas.
  • In this study, we wanted to analyze the expression of AP-2alpha in astrocytoma samples of different grades both at the RNA level, by real-time qPCR and at the protein level, by immunohistochemistry, and to examine its correlation, if any, with patient outcome.
  • We did not find any clear pattern of regulation at the RNA level with tumor grade.
  • Interestingly, we found cytoplasmic AP-2alpha expression in a majority of higher grade astrocytomas (Grade IV-85%; 33/39 and Grade III-74%; 14/19) in comparison to lower grades (Grade I-0%; 0/5 and Grade II-37.5%; 3/8) suggesting that the translocation of this protein from the nucleus to the cytoplasm may be responsible for the increased malignancy.
  • Within GBMs, we found that decreased nuclear expression was indicative of a better prognosis.
  • The striking observation was the shift in localization of this protein from the nucleus to the cytoplasm with increasing tumor grade, pointing to a crucial role for this transcription factor in the progression of astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Transcription Factor AP-2 / analysis
  • [MeSH-minor] Cell Nucleus / chemistry. Cell Nucleus / metabolism. Cytoplasm / chemistry. Cytoplasm / metabolism. Disease Progression. Humans. Prognosis. Protein Transport. RNA, Messenger / analysis. RNA, Messenger / metabolism

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  • (PMID = 17471019.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Transcription Factor AP-2
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89. Raju GP, Urion DK, Sahin M: Neonatal subependymal giant cell astrocytoma: new case and review of literature. Pediatr Neurol; 2007 Feb;36(2):128-31
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  • [Title] Neonatal subependymal giant cell astrocytoma: new case and review of literature.
  • Subependymal giant cell astrocytomas are one of the three major intracranial lesions found in tuberous sclerosis complex.
  • Subependymal giant cell astrocytomas are typically slow-growing tumors of mixed glioneuronal lineage which can become aggressive and cause obstructive hydrocephalus usually in older children and adolescents.
  • Neonatal subependymal giant cell astrocytomas are extremely rare, and their natural history and prognosis are poorly understood.
  • This report investigates an extremely large neonatal subependymal giant cell astrocytoma which was initially identified in utero at 19 weeks of gestation in a high-risk pregnancy with no family history of tuberous sclerosis complex.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Imaging

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  • (PMID = 17275668.001).
  • [ISSN] 0887-8994
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 16
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90. Xiao A, Yin C, Yang C, Di Cristofano A, Pandolfi PP, Van Dyke T: Somatic induction of Pten loss in a preclinical astrocytoma model reveals major roles in disease progression and avenues for target discovery and validation. Cancer Res; 2005 Jun 15;65(12):5172-80
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  • [Title] Somatic induction of Pten loss in a preclinical astrocytoma model reveals major roles in disease progression and avenues for target discovery and validation.
  • High-grade astrocytomas are invariably deadly and minimally responsive to therapy.
  • Pten is frequently mutated in aggressive astrocytoma but not in low-grade astrocytoma.
  • However, the Pten astrocytoma suppression mechanisms are unknown.
  • Here we introduced conditional null alleles of Pten (Pten(loxp/loxp)) into a genetically engineered mouse astrocytoma model [TgG(deltaZ)T121] in which the pRb family proteins are inactivated specifically in astrocytes.
  • Depletion of Pten function in adult astrocytoma cells alleviated the apoptosis evoked by pRb family protein inactivation and also induced tumor cell invasion.
  • Thus, we show that Pten deficiency in pRb-deficient astrocytoma cells contributes to tumor progression via multiple mechanisms, including suppression of apoptosis, increased cell invasion, and angiogenesis, all of which are hallmarks of high-grade astrocytoma.
  • These studies not only provide mechanistic insight into the role of Pten in astrocytoma suppression but also describe a valuable animal model for preclinical testing that is coupled with a primary cell-based system for target discovery and drug screening.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Protein Tyrosine Phosphatases / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Alleles. Animals. Apoptosis / genetics. Disease Models, Animal. Disease Progression. Female. Genes, Tumor Suppressor. Male. Mice. Mice, Transgenic. Neoplasm Invasiveness. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / pathology. PTEN Phosphohydrolase. Retinoblastoma Protein / deficiency. Retinoblastoma Protein / physiology

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  • (PMID = 15958561.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01-CA84314
  • [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 / Retinoblastoma Protein; 0 / Tumor Suppressor Proteins; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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91. Dashti SR, Robinson S, Rodgers M, Cohen AR: Pineal region giant cell astrocytoma associated with tuberous sclerosis: case report. J Neurosurg; 2005 Apr;102(3 Suppl):322-5
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  • [Title] Pineal region giant cell astrocytoma associated with tuberous sclerosis: case report.
  • Tuberous sclerosis complex is a genetic disorder characterized by the development of hamartomas in multiple organs including the brain, skin, eye, kidney, and heart.
  • Subependymal giant cell astrocytomas, typically located adjacent to the foramen of Monro, can enlarge and cause symptomatic ventricular obstruction.
  • The authors describe the case of a 3-year-old boy with a history of tuberous sclerosis and retinal lesions who presented with an enlarging enhancing pineal region mass.
  • Pathological examination showed a giant cell astrocytoma.
  • To the authors' knowledge, this is the first reported case of tuberous sclerosis associated with a giant cell astrocytoma of the pineal region.
  • [MeSH-major] Astrocytoma / complications. Astrocytoma / surgery. Pinealoma / complications. Pinealoma / surgery. Tuberous Sclerosis / complications

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  • (PMID = 15881760.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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92. Stupp R, Reni M, Gatta G, Mazza E, Vecht C: Anaplastic astrocytoma in adults. Crit Rev Oncol Hematol; 2007 Jul;63(1):72-80
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  • [Title] Anaplastic astrocytoma in adults.
  • Anaplastic astrocytoma is an uncommon disease in the adult population.
  • Based on randomized data available, chemotherapy has consistently failed to improve the outcome of patients with anaplastic astrocytoma, while a meta-analysis showed a small, but significant improvement in survival favouring the use of chemotherapy.
  • In recurrent disease, chemotherapy with temozolomide has been proven to be active and well-tolerated in phase II trials, but no comparative phase III trials of other cytotoxic drugs have been conducted.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Aged. Clinical Trials as Topic. Clinical Trials, Phase II as Topic. Female. Humans. Incidence. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Prognosis. Risk Factors. Survival Analysis

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  • (PMID = 17478095.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 69
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93. Brehar FM, Ciurea AV, Zarnescu O, Bleotu C, Gorgan RM, Dragu D, Matei L: Infiltrating growing pattern xenografts induced by glioblastoma and anaplastic astrocytoma derived tumor stem cells. Chirurgia (Bucur); 2010 Sep-Oct;105(5):685-94
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  • [Title] Infiltrating growing pattern xenografts induced by glioblastoma and anaplastic astrocytoma derived tumor stem cells.
  • OBJECTIVE: The number of evidences regarding the role of tumor stem cells (TSC) in the initiation and progression of high-grade astrocytomas became more and more numerous in the last years.
  • This issue has been intensively tested in glioblastoma, but little attention has been paid for anaplastic astrocytoma.
  • The main objective of this paper was to study the morphological characteristics of the xenografts developed from glioblastoma and anaplastic astrocytoma derived cancer stem cells.
  • METHODS: The authors of this study successfully isolated and partial characterized primary cultures of glioblastoma and anaplastic astrocytoma derived TSC.
  • RESULTS: The tumor xenografts which have been established in nude mice using TSC had different characteristics when compared with U87 xenografts previously developed by our group, and depend of the origin type of the tumors (glioblastoma versus anaplastic astrocytoma).
  • The diffuse growing pattern and cells infiltration have been more pronounced in both anaplastic astrocytoma and glioblastoma derived TSC xenografts compared with U87 line xenografts.
  • CONCLUSION: Our results support the hypothesis regarding the role of TSC in the infiltration process of glioblastoma and anaplastic astrocytoma.
  • The extensive infiltration growing patterns of these types of xenografts make them useful models for studying the invasion mechanisms in gliomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Neoplastic Stem Cells / pathology. Transplantation, Heterologous

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  • (PMID = 21141095.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
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94. Rao SA, Santosh V, Somasundaram K: Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma. Mod Pathol; 2010 Oct;23(10):1404-17
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  • [Title] Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma.
  • Malignant astrocytoma includes anaplastic astrocytoma (grade III) and glioblastoma (grade IV).
  • Among them, glioblastoma is the most common primary brain tumor with dismal responses to all therapeutic modalities.
  • We performed a large-scale, genome-wide microRNA (miRNA) (n=756) expression profiling of 26 glioblastoma, 13 anaplastic astrocytoma and 7 normal brain samples with an aim to find deregulated miRNA in malignant astrocytoma.
  • We identified several differentially regulated miRNAs between these groups, which could differentiate glioma grades and normal brain as recognized by PCA.
  • More importantly, we identified a most discriminatory 23-miRNA expression signature, by using PAM, which precisely distinguished glioblastoma from anaplastic astrocytoma with an accuracy of 95%.
  • The differential expression pattern of nine miRNAs was further validated by real-time RT-PCR on an independent set of malignant astrocytomas (n=72) and normal samples (n=7).
  • Thus we have identified the miRNA expression signature for malignant astrocytoma, in particular glioblastoma, and showed the miRNA involvement and their importance in astrocytoma development.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. MicroRNAs / genetics

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  • (PMID = 20711171.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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95. Bender AM, Collier LS, Rodriguez FJ, Tieu C, Larson JD, Halder C, Mahlum E, Kollmeyer TM, Akagi K, Sarkar G, Largaespada DA, Jenkins RB: Sleeping beauty-mediated somatic mutagenesis implicates CSF1 in the formation of high-grade astrocytomas. Cancer Res; 2010 May 1;70(9):3557-65
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  • [Title] Sleeping beauty-mediated somatic mutagenesis implicates CSF1 in the formation of high-grade astrocytomas.
  • To identify glioma-associated genes, we evaluated tumor formation in the brain tissue from 117 transgenic mice that had undergone constitutive SB-mediated transposition.
  • Upon analysis, 21 samples (18%) contained neoplastic tissue with features of high-grade astrocytomas.
  • These tumors expressed glial markers and were histologically similar to human glioma.
  • Genomic DNA from SB-induced astrocytoma tissue was extracted and transposon insertion sites were identified.
  • Using reverse transcription-PCR, we documented increased Csf1 RNAs in tumor versus adjacent normal tissue, with the identification of transposon-terminated Csf1 mRNAs in astrocytomas with SB insertions in intron 8.
  • Together, these results indicate that SB-insertional mutagenesis can identify high-grade astrocytoma-associated genes and they imply an important role for CSF1 in the development of these tumors.

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20388773.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113636-02; United States / NCI NIH HHS / CA / CA113636-03; United States / NCI NIH HHS / CA / R01CA113636; United States / NCI NIH HHS / CA / R01 CA113636-03; United States / NCI NIH HHS / CA / K01CA122183; United States / NCI NIH HHS / CA / T32 CA009138; United States / NCI NIH HHS / CA / R01 CA113636-05; United States / NCI NIH HHS / CA / R01 CA113636-01A1; United States / NCI NIH HHS / CA / CA113636-01A1; United States / NCI NIH HHS / CA / R01 CA113636; United States / NCI NIH HHS / CA / CA113636-05; United States / NCI NIH HHS / CA / R01 CA113636-04; United States / NCI NIH HHS / CA / CA113636-02; United States / NCI NIH HHS / CA / K01 CA122183; United States / NCI NIH HHS / CA / CA113636-04
  • [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 / DNA Transposable Elements; 0 / RNA, Messenger; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.7.- / Transposases
  • [Other-IDs] NLM/ NIHMS185042; NLM/ PMC2862088
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96. Akaishi K, Nakayama J, Sakai K, Kobayashi T, Rutka JT: Antigen p57/Kip2 as a potential negative regulator of human astrocytoma growth. J Clin Neurosci; 2009 Dec;16(12):1615-8
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  • [Title] Antigen p57/Kip2 as a potential negative regulator of human astrocytoma growth.
  • This study was performed to determine the relationship between p57/Kip2 and the growth of human astrocytomas.
  • Immunohistochemical staining for p57/Kip2, p53, p16, and Ki67 antigen was performed on paraffin-embedded tissue specimens obtained from 36 patients with astrocytoma.
  • Expression of p57/Kip2, p53, p16, and Ki67 antigen was generally increased in association with the astrocytoma tumor grade.
  • Expression of p16 was higher in patients whose tumors express p57/Kip2 in greater than 10% of tumor cells (p<0.05).
  • Expression of p53 also tended to be higher, but not to a statistically significant extent, in patients whose tumors express p57/Kip2 in greater than 10% of tumor cells.
  • These findings suggest that p57/Kip2 inhibits the growth of human astrocytomas, and may function in parallel with p16 and p53.
  • However, p57/Kip2 is, by itself, insufficient to arrest the cellular proliferation of human astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p57 / metabolism. Gene Expression Regulation, Neoplastic / physiology
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Proteins / metabolism. Retrospective Studies. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19822429.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1C protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p57; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / P16 protein, human; 0 / Tumor Suppressor Protein p53
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97. Zakrzewski K, Biernat W, Liberski PP, Polis L, Nowoslawska E: Pilocytic astrocytoma as a predominant component of a recurrent complex type DNT. Folia Neuropathol; 2009;47(3):284-8
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  • [Title] Pilocytic astrocytoma as a predominant component of a recurrent complex type DNT.
  • We report an unusual case of a 7-year-old girl with a temporal lobe DNT, which recurred four years after subtotal resection of the tumour.
  • In the recurrent lesion we identified pilocytic astrocytoma (PA) as a predominant component of the tumour.
  • In rare cases development of a secondary, histologically different neoplasm may also occur.

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  • (PMID = 19813149.001).
  • [ISSN] 1641-4640
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
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98. Yu J, Deshmukh H, Gutmann RJ, Emnett RJ, Rodriguez FJ, Watson MA, Nagarajan R, Gutmann DH: Alterations of BRAF and HIPK2 loci predominate in sporadic pilocytic astrocytoma. Neurology; 2009 Nov 10;73(19):1526-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alterations of BRAF and HIPK2 loci predominate in sporadic pilocytic astrocytoma.
  • OBJECTIVE: Independent studies have previously demonstrated that both the HIPK2 and BRAF genes are amplified and rearranged, respectively, in pilocytic astrocytomas (PAs).
  • CONCLUSIONS: BRAF rearrangement represents the most common genetic alteration in sporadic, but not neurofibromatosis type 1-associated, pilocytic astrocytomas (PAs).
  • These findings implicate BRAF in the pathogenesis of these common low-grade astrocytomas in children, and suggest that PAs arise either from NF1 inactivation or BRAF gain of function.

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  • (PMID = 19794125.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NCI NIH HHS / CA / P30 CA91842
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / DNA, Neoplasm; EC 2.7.1.- / HIPK2 protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  • [Other-IDs] NLM/ PMC2777068
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99. Ooba H, Abe T, Kamida T, Anan M, Momii Y, Tokuuye K, Fujiki M: Malignant fibrous histiocytosis after high-dose proton radiation therapy for anaplastic astrocytoma. J Clin Neurosci; 2009 Dec;16(12):1641-3
Genetic Alliance. consumer health - Anaplastic Astrocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant fibrous histiocytosis after high-dose proton radiation therapy for anaplastic astrocytoma.
  • This report presents a 70-year-old male who presented with a rare malignant fibrous histiocytosis after high-dose proton radiation therapy for anaplastic astrocytoma.
  • [MeSH-minor] Aged. Astrocytoma / radiotherapy. Brain Neoplasms / radiotherapy. Humans. Magnetic Resonance Imaging / methods. Male

  • Genetic Alliance. consumer health - Histiocytosis.
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  • (PMID = 19766005.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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100. Bence M, Kereszturi E, Mozes V, Sasvari-Szekely M, Keszler G: Hypoxia-induced transcription of dopamine D3 and D4 receptors in human neuroblastoma and astrocytoma cells. BMC Neurosci; 2009;10:92
Genetic Alliance. consumer health - Neuroblastoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia-induced transcription of dopamine D3 and D4 receptors in human neuroblastoma and astrocytoma cells.
  • In order to clarify the hypoxic sensitivity of key dopaminergic genes, we aimed to study their transcriptional regulation in the context of neuroblastoma and astrocytoma cell lines exposed to 1% hypoxia.
  • [MeSH-minor] Astrocytoma. Blotting, Western. Cell Line, Tumor. Gene Transfer Techniques. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunohistochemistry. Neuroblastoma. Reverse Transcriptase Polymerase Chain Reaction. Transcriptional Activation

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  • (PMID = 19653907.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DRD3 protein, human; 0 / DRD4 protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Receptors, Dopamine D3; 137750-34-6 / Receptors, Dopamine D4
  • [Other-IDs] NLM/ PMC3224682
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