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1. Onguru O, Celasun B, Gunhan O: Desmoplastic non-infantile ganglioglioma. Neuropathology; 2005 Jun;25(2):150-2
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  • [Title] Desmoplastic non-infantile ganglioglioma.
  • Desmoplastic ganglioglioma is a rare, markedly desmoplastic variant of ganglioglioma that usually presents in the first year of life.
  • It is a mixed glial and neuronal cerebral tumor.
  • A few cases of desmoplastic ganglioglioma have been reported in non-infantile patients.
  • We report a case of desmoplastic ganglioglioma in a 14-year-old boy.
  • Histopathological examination revealed a low-grade glial tumor with prominent desmoplasia including hypocellular collagenous areas.
  • The tumor was well demarcated with respect to the surrounding brain.
  • Ganglion cells with dysplastic features were present in the tumor and clustered in some areas.
  • Immunohistochemistry revealed glial fibrillary acidic protein positivity in the astrocytic cells hidden in the desmoplastic tissue.
  • This present case confirms that desmoplastic ganglioglioma can be present in young adult patients with its characteristic radiologic features.
  • [MeSH-major] Brain Neoplasms / pathology. Ganglioglioma / pathology


2. Haapasalo JA, Nordfors KM, Hilvo M, Rantala IJ, Soini Y, Parkkila AK, Pastoreková S, Pastorek J, Parkkila SM, Haapasalo HK: Expression of carbonic anhydrase IX in astrocytic tumors predicts poor prognosis. Clin Cancer Res; 2006 Jan 15;12(2):473-7
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  • [Title] Expression of carbonic anhydrase IX in astrocytic tumors predicts poor prognosis.
  • PURPOSE: Carbonic anhydrase IX (CA IX) is a hypoxia-inducible enzyme, which is associated with neoplastic growth.
  • Ectopic CA IX expression has been observed in several tumors, whose normal counterparts do not express this enzyme.
  • Normal human brain tissue shows only slight or no expression of CA IX.
  • EXPERIMENTAL DESIGN: We describe CA IX expression in human diffusely infiltrating astrocytomas.
  • The association of CA IX is evaluated with clinicopathologic and molecular factors including cell proliferation and apoptosis as well as the expression of p53 and epidermal growth factor receptor.
  • RESULTS: CA IX immunopositivity was observed in 284 cases of 362 (78%) tumors.
  • The CA IX immunoreactivity showed strong association with tumor malignancy grades (P < 0.0001).
  • CA IX showed no association with p53 expression nor did it correlate with epidermal growth factor receptor-amplification, apoptosis, or cell proliferation.
  • CA IX intensity had significant prognostic value in univariate (P=0.0011, log-rank test) and multivariate survival analysis (P = 0.038, Cox analysis).
  • Our results suggest that CA IX is a useful biomarker for predicting poor prognosis of astrocytic tumors.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Astrocytoma / enzymology. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Carbonic Anhydrases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Apoptosis. Cell Proliferation. Female. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Recurrence, Local / enzymology. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / pathology. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / metabolism. Survival Rate. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16428489.001).
  • [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 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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3. Kitai R, Horita R, Sato K, Yoshida K, Arishima H, Higashino Y, Hashimoto N, Takeuchi H, Kubota T, Kikuta K: Nestin expression in astrocytic tumors delineates tumor infiltration. Brain Tumor Pathol; 2010 Apr;27(1):17-21
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  • [Title] Nestin expression in astrocytic tumors delineates tumor infiltration.
  • Nestin is an intermediate filament protein expressed in undifferentiated cells during central nervous system development, and glioma is known to be a highly infiltrative tumor.
  • We determined whether nestin was expressed in astrocytic tumors and could identify infiltrating tumor cells.
  • We screened 65 archival, paraffin-embedded adult astrocytic tumors using immunohistochemical staining and computerized overlaid photographs.
  • Normal biopsied brains and metastatic brain tumors were also examined.
  • The intensity of nestin expression corresponded to the tumor grade.
  • Overlaid images showed that nestin immunostaining delineated tumor invasion into adjacent gray and white matter.
  • Nestin is a useful marker for examining the infiltration of malignant cells into surrounding tissue.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Intermediate Filament Proteins / metabolism. Intermediate Filament Proteins / physiology. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Child. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Nestin. Young Adult

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  • (PMID = 20425043.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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4. 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.
  • Carbonic anhydrase XII (CA XII) is a transmembrane enzyme that is associated with neoplastic growth.
  • 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.
  • [MeSH-major] Astrocytoma / enzymology. Biomarkers, Tumor / analysis. Brain Neoplasms / enzymology. Carbonic Anhydrases / genetics. Carbonic Anhydrases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Alternative Splicing. Amino Acid Sequence. Blotting, Western. Child. Child, Preschool. Humans. Immunohistochemistry. Isoenzymes / chemistry. Isoenzymes / genetics. Isoenzymes / metabolism. Kaplan-Meier Estimate. Middle Aged. Molecular Sequence Data. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] J Mol Biol. 2000 Feb 25;296(3):921-36 [10677292.001]
  • [Cites] Neuro Oncol. 2007 Jul;9(3):308-13 [17435181.001]
  • [Cites] Histochem Cell Biol. 2000 Sep;114(3):197-204 [11083462.001]
  • [Cites] J Histochem Cytochem. 2000 Dec;48(12):1601-8 [11101628.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7075-83 [11156414.001]
  • [Cites] Am J Pathol. 2001 Mar;158(3):905-19 [11238039.001]
  • [Cites] Bioorg Med Chem. 2001 Mar;9(3):703-14 [11310605.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9545-50 [11493685.001]
  • [Cites] Br J Cancer. 2003 Apr 7;88(7):1065-70 [12671706.001]
  • [Cites] J Neurosurg. 2003 Sep;99(3):467-73 [12959431.001]
  • [Cites] Hum Pathol. 2003 Aug;34(8):756-63 [14506635.001]
  • [Cites] Virology. 1992 Apr;187(2):620-6 [1312272.001]
  • [Cites] Histochemistry. 1993 Jan;99(1):37-41 [8468192.001]
  • [Cites] Am J Pathol. 1993 May;142(5):1347-51 [7684193.001]
  • [Cites] Anal Quant Cytol Histol. 1994 Aug;16(4):261-8 [7524516.001]
  • [Cites] J Pathol. 1994 Dec;174(4):275-82 [7884589.001]
  • [Cites] Mol Hum Reprod. 2000 Jan;6(1):68-74 [10611263.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):577-84 [10666387.001]
  • [Cites] J Mol Biol. 2000 Feb 25;296(3):911-9 [10677291.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7608-13 [9636197.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12596-601 [9770531.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):151-60 [9892097.001]
  • [Cites] World J Gastroenterol. 2005 Jan 14;11(2):155-63 [15633208.001]
  • [Cites] Cancer. 2005 Mar 15;103(6):1234-44 [15666327.001]
  • [Cites] Surg Neurol. 2005 Oct;64(4):286-94; discussion 294 [16229087.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):473-7 [16428489.001]
  • [Cites] Bioessays. 2006 Apr;28(4):378-86 [16547952.001]
  • [Cites] Neurosurg Focus. 2006;20(4):E5 [16709036.001]
  • [Cites] J Cell Sci. 2006 Jul 1;119(Pt 13):2635-41 [16787944.001]
  • [Cites] Neuropathol Appl Neurobiol. 2006 Aug;32(4):441-50 [16866989.001]
  • [Cites] Curr Opin Oncol. 2006 Nov;18(6):644-7 [16988588.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2220-4 [10688890.001]
  • (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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5. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • 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


6. Allerstorfer S, Sonvilla G, Fischer H, Spiegl-Kreinecker S, Gauglhofer C, Setinek U, Czech T, Marosi C, Buchroithner J, Pichler J, Silye R, Mohr T, Holzmann K, Grasl-Kraupp B, Marian B, Grusch M, Fischer J, Micksche M, Berger W: FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities. Oncogene; 2008 Jul 10;27(30):4180-90
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  • [Title] FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities.
  • Fibroblast growth factor 5 (FGF5) is widely expressed in embryonic but scarcely in adult tissues.
  • Here we report simultaneous overexpression of FGF5 and its predominant high-affinity receptor (FGFR1 IIIc) in astrocytic brain tumour specimens (N=49) and cell cultures (N=49).
  • Moreover, tumour cell migration was distinctly stimulated by rFGF5 but attenuated by FGF5 siRNA.
  • Moreover, rFGF5 and supernatants of highly FGF5-positive GBM cell lines specifically stimulated proliferation, migration and tube formation of human umbilical vein endothelial cells.
  • In summary, we demonstrate for the first time that FGF5 contributes to the malignant progression of human astrocytic brain tumours by both autocrine and paracrine effects.
  • [MeSH-major] Autocrine Communication / physiology. Brain Neoplasms / genetics. Fibroblast Growth Factor 5 / physiology. Glioblastoma / genetics. Oncogenes. Paracrine Communication / physiology
  • [MeSH-minor] Cell Death / drug effects. Cell Movement / drug effects. Cell Proliferation / drug effects. Culture Media, Conditioned / pharmacology. Disease Progression. Genes, Dominant / physiology. Humans. Mutant Proteins / genetics. Mutant Proteins / physiology. Neovascularization, Pathologic / chemically induced. Neovascularization, Pathologic / genetics. Recombinant Proteins / pharmacology. Transfection. Tumor Cells, Cultured

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  • [Cites] Brain Res Mol Brain Res. 1996 May;38(1):161-5 [8737680.001]
  • [Cites] J Biol Chem. 1996 Jun 21;271(25):15292-7 [8663044.001]
  • [Cites] Vet Pathol. 1997 May;34(3):171-9 [9163872.001]
  • [Cites] Oncogene. 1997 Sep 18;15(12):1417-24 [9333017.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1998;59:135-76 [9427842.001]
  • [Cites] Cancer Res. 1998 Jan 15;58(2):352-61 [9443417.001]
  • [Cites] Surg Neurol. 1998 Feb;49(2):189-95; discussion 196 [9457270.001]
  • [Cites] Biochem Cell Biol. 1997;75(6):669-85 [9599656.001]
  • [Cites] J Pharmacol Exp Ther. 1998 Jul;286(1):569-77 [9655904.001]
  • [Cites] Neurosurgery. 1998 Aug;43(2):337-46 [9696088.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):29262-71 [9786939.001]
  • [Cites] Cancer Res. 1998 Dec 1;58(23):5285-90 [9850049.001]
  • [Cites] J Invest Dermatol. 1998 Dec;111(6):963-72 [9856803.001]
  • [Cites] Int J Cancer. 1999 Oct 29;83(3):415-23 [10495436.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Jun;131(6):355-63 [15856298.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):139-49 [15863030.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):179-86 [15863033.001]
  • [Cites] Growth Factors. 2005 Jun;23(2):87-95 [16019430.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11011-6 [16046538.001]
  • [Cites] Biochem Pharmacol. 2006 Feb 14;71(4):426-40 [16343446.001]
  • [Cites] J Cell Sci. 2006 Feb 1;119(Pt 3):459-69 [16418217.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3584-92 [16585183.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):281-93 [16554966.001]
  • [Cites] Mol Cancer Res. 2006 Dec;4(12):927-34 [17189383.001]
  • [Cites] Br J Cancer. 2007 Mar 26;96(6):960-9 [17342095.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4055-63 [17720881.001]
  • [Cites] J Neurosci. 2003 Jul 23;23(16):6404-12 [12878680.001]
  • [Cites] Cell Tissue Res. 2003 Aug;313(2):139-57 [12845521.001]
  • [Cites] J Clin Invest. 1973 Nov;52(11):2745-56 [4355998.001]
  • [Cites] Mol Cell Biol. 1988 Aug;8(8):3487-95 [3211147.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(20):8022-6 [1700424.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):1840-5 [2005884.001]
  • [Cites] Development. 1991 Jun;112(2):397-406 [1794310.001]
  • [Cites] J Invest Dermatol. 2000 Mar;114(3):456-63 [10692103.001]
  • [Cites] Glia. 2000 May;30(3):231-41 [10756073.001]
  • [Cites] Nat Cell Biol. 2001 Jul;3(7):650-7 [11433297.001]
  • [Cites] Cancer Res. 2001 Jul 15;61(14):5511-6 [11454700.001]
  • [Cites] J Cell Sci. 2002 Jan 15;115(Pt 2):329-39 [11839785.001]
  • [Cites] Int J Pancreatol. 2001;29(2):85-92 [11876253.001]
  • [Cites] Neurol Res. 2002 Apr;24(3):244-8 [11958417.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Feb;88(2):773-80 [12574212.001]
  • [Cites] Int J Cancer. 1993 Jan 21;53(2):209-14 [8381111.001]
  • [Cites] Neuron. 1993 Mar;10(3):369-77 [8461132.001]
  • [Cites] Brain Res. 1993 Mar 19;606(1):79-86 [8462006.001]
  • [Cites] Eur J Neurosci. 1994 Feb 1;6(2):244-52 [8167846.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2794-9 [8168112.001]
  • [Cites] Cell. 1994 Sep 23;78(6):1017-25 [7923352.001]
  • [Cites] J Neurooncol. 1994;18(3):207-16 [7964981.001]
  • [Cites] Oncogene. 1997 Jan 16;14(2):171-83 [9010219.001]
  • (PMID = 18362893.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 19920
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / FGF5 protein, human; 0 / Mutant Proteins; 0 / Recombinant Proteins; 129653-64-1 / Fibroblast Growth Factor 5
  • [Other-IDs] NLM/ PMC2879862; NLM/ UKMS30927
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7. Beetz C, Bergner S, Brodoehl S, Brodhun M, Ewald C, Kalff R, Krüger J, Patt S, Kiehntopf M, Deufel T: Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology. Int J Oncol; 2006 Nov;29(5):1183-91
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  • [Title] Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology.
  • Astrocytomas are intracranial malignancies for which invasive growth and high motility of tumour cells preclude total resection; the tumours usually recur in a more aggressive and, eventually, lethal form.
  • In order to identify novel molecular markers for prognosis we obtained expression profiles of: i) tumours associated with particularly long recurrence-free intervals, ii) tumours which led to rapid patient death, and iii) tumour-free control brain.
  • An extended set of tumours was then investigated by RT-PCR targeting 12 selected genes.
  • Data from these experiments were summarised into a sample-specific index which assigns tumours to high- and low-risk groups as successfully as does morphology-based grading.
  • Our finding of cell-specificity for some of these outcome-determining genes relates global expression data to the presence of morphological correlates of tumour behaviour and, thus, provides a link between morphology-based and molecular pathology.
  • Our identification of expression signatures that are associated individually with clinical outcome confirms the prognostic relevance of gene expression data and, thus, represents a step towards eventually implementing molecular diagnosis into clinical practice in neuro-oncology.
  • [MeSH-major] Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / mortality. Gene Expression Profiling. Genes, Neoplasm / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17016650.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Neoplasm
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8. Benatiya AI, Bouayed MA, Touiza E, Daoudi K, Mernissi FZ, Tahri H: [Bourneville's tuberous sclerosis. A case report]. J Fr Ophtalmol; 2005 Dec;28(10):e11
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  • [Transliterated title] La sclérose tubéreuse de Bourneville. A propos d'un cas.
  • INTRODUCTION: Bourneville's tuberous sclerosis (BTS) is an autosomal dominant phakomatosis characterized by the development of a benign hamartoma-like tumor, which is usually located in the skin, kidney, heart, brain, and eyes.
  • OBSERVATION: A 28-year-old man was a known BTS patient followed in the dermatology clinic.
  • The ophthalmologic exam and the angiography with fluorescein revealed retinal astrocytic hamartomas bilaterally.
  • The chest X-ray, renal scan, heart scan and a CT scan of the brain failed to show any other localizations of the disease.
  • The lesions described had remained unchanged over a period of 6 years.
  • CONCLUSION: Retinal lesions during BTS are dominated by the presence of astrocytic hamartomas essentially around the papillae.
  • [MeSH-major] Retinal Neoplasms / diagnosis. Tuberous Sclerosis / diagnosis
  • [MeSH-minor] Adult. Humans. Male

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  • (PMID = 16395191.001).
  • [ISSN] 1773-0597
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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9. Mendonça R, Lima LG, Fernandes LN, Ferreira NP, De Napoli G: [Primary connus medullaris glioblastoma: case report]. Arq Neuropsiquiatr; 2005 Jun;63(2B):539-42
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  • [Transliterated title] Glioblastoma primário de cone medula: relato de caso.
  • Glioblastomas are the most common type of brain tumors; astrocytic in their origin, they are anaplastic tumors, and are located mainly in the cerebral hemispheres.
  • Primary growth in the conus medullaris is very rare, and the assessment and prognosis of this kind of tumor are distinct and unique.
  • We present here the case of a 39 years-old man with an intramedullary tumor of the spinal cord, with an histo pathological diagnosis of glioblastoma, along with some therapeutic considerations.
  • [MeSH-major] Glioblastoma / diagnosis. Spinal Cord Neoplasms / diagnosis
  • [MeSH-minor] Adult. Humans. Male

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  • (PMID = 16059615.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
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10. Capper D, Mittelbronn M, Meyermann R, Schittenhelm J: Pitfalls in the assessment of MGMT expression and in its correlation with survival in diffuse astrocytomas: proposal of a feasible immunohistochemical approach. Acta Neuropathol; 2008 Feb;115(2):249-59
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  • Implementation of this data in routine clinical diagnostics is limited due to often inappropriate study designs, e.g. pooling of tumor entities, WHO grades or primary and secondary glioblastomas, disregard concerning the infiltration zone or various epidemiological factors.
  • The aim of our study was to evaluate MGMT expression and its prognostic value taking into consideration the aforementioned deficiencies.
  • For this, 162 astrocytic tumors WHO II-IV (36 diffuse astrocytomas WHO II, 51 anaplastic astrocytomas, 75 primary glioblastomas) as well as 25 glioblastoma infiltration zones and 19 glioblastoma relapses were analyzed for immunohistochemical MGMT protein expression using tissue microarray technique.
  • Expression of MGMT significantly decreased from WHO grade II (25.6%) to glioblastoma (16.8%, p = 0.01) with lowest levels in grade III tumors (10.2%, II/III p < 0.0001).
  • The optimal cut-off value of MGMT positive nuclei in primary glioblastomas discriminating patients with significantly different survival rates was at 15% (Log-Rank p = 0.0002).
  • Individual relapse tumors showed changes of MGMT expression to a varying degree.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neurosurgical Procedures. Prognosis. Radiotherapy. Tissue Array Analysis

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  • (PMID = 17965865.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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11. Takaya S, Hashikawa K, Turkheimer FE, Mottram N, Deprez M, Ishizu K, Kawashima H, Akiyama H, Fukuyama H, Banati RB, Roncaroli F: The lack of expression of the peripheral benzodiazepine receptor characterises microglial response in anaplastic astrocytomas. J Neurooncol; 2007 Oct;85(1):95-103
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  • We examined two anaplastic astrocytomas showing minimal contrast-enhancement and therefore little damage of the blood brain barrier to minimise the presence of blood borne macrophages within tumour tissue.
  • The two lesions were studied in vivo using positron emission tomography (PET) with the specific PBR ligand [(11)C](R)-PK11195 and the corresponding tumour tissue was investigated with an anti-PBR antibody.
  • As comparison, PBR was investigated in three brains with multiple sclerosis (MS) and three with Parkinson's disease (PD).
  • PET studies showed that [(11)C](R)-PK11195 binding was markedly lower in tumours than in the contralateral grey matter.
  • Our results demonstrated PBR suppression in glioma-infiltrating microglia and suggested that PBR may have a relevant role in modulating the anti-tumour inflammatory response in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Microglia / metabolism. Microglia / pathology. Receptors, GABA-A / biosynthesis
  • [MeSH-minor] Adult. Antibodies, Monoclonal. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Isoquinolines. Magnetic Resonance Imaging. Male. Middle Aged. Multiple Sclerosis / pathology. Oligonucleotide Array Sequence Analysis. Parkinson Disease / pathology. Peripheral Nerves / metabolism. Positron-Emission Tomography. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Radiopharmaceuticals

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  • [Cites] BMC Bioinformatics. 2006 Dec 01;7:526 [17140431.001]
  • [Cites] Glia. 2002 Nov;40(2):206-17 [12379908.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Dev Neurosci. 2004 Jan-Feb;26(1):30-7 [15509896.001]
  • [Cites] Ann Neurol. 1988 Dec;24(6):708-12 [2849920.001]
  • [Cites] Acta Neuropathol. 1996 Sep;92(3):288-93 [8870831.001]
  • [Cites] J Neurochem. 2000 Apr;74(4):1694-704 [10737628.001]
  • [Cites] Neurobiol Dis. 2003 Dec;14 (3):417-24 [14678758.001]
  • [Cites] J Neurooncol. 1998 May;38(1):19-26 [9540054.001]
  • [Cites] Lab Invest. 1994 Jan;70(1):23-8 [8302015.001]
  • [Cites] Neuropathol Appl Neurobiol. 1998 Aug;24(4):293-301 [9775395.001]
  • [Cites] Trends Pharmacol Sci. 2006 Aug;27(8):402-9 [16822554.001]
  • [Cites] Acta Neurochir (Wien). 1992;119(1-4):146-52 [1336303.001]
  • [Cites] Brain. 2004 Jun;127(Pt 6):1379-92 [15069023.001]
  • [Cites] Cancer Res. 1988 Oct 15;48(20):5837-41 [3262414.001]
  • [Cites] J Histochem Cytochem. 2004 Jan;52(1):19-28 [14688214.001]
  • [Cites] Mol Med. 2006 Jul-Aug;12(7-8):161-70 [17088948.001]
  • [Cites] Acta Neuropathol. 2004 Jul;108(1):43-8 [15088099.001]
  • [Cites] J Neurosci Res. 2005 Aug 1;81(3):447-55 [15959903.001]
  • [Cites] J Nucl Med. 2007 Jan;48(1):158-67 [17204713.001]
  • [Cites] Science. 2005 May 27;308(5726):1314-8 [15831717.001]
  • [Cites] Neurogenetics. 2004 Jun;5(2):95-108 [15042428.001]
  • [Cites] J Neurosci Res. 2005 Aug 1;81(3):327-41 [15948185.001]
  • [Cites] J Neurosci Res. 2006 May 15;83(7):1293-8 [16547968.001]
  • [Cites] Brain Res. 1990 Jun 4;518(1-2):199-208 [2167748.001]
  • [Cites] Ann Neurol. 1989 Dec;26(6):752-8 [2557794.001]
  • [Cites] Cancer Lett. 2000 Aug 11;156(2):125-32 [10880761.001]
  • [Cites] J Nucl Med. 1991 Aug;32(8):1608-10 [1651383.001]
  • [Cites] J Neurooncol. 2007 Jan;81(1):1-7 [16868661.001]
  • [Cites] Trends Neurosci. 2006 Feb;29(2):68-74 [16406093.001]
  • [Cites] Pharmacol Ther. 2006 Jun;110(3):503-24 [16337685.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4375-81 [11389063.001]
  • [Cites] J Neurochem. 2002 Nov;83(3):546-55 [12390516.001]
  • [Cites] Eur J Pharmacol. 1992 Sep 1;228(2-3):131-9 [1332878.001]
  • [Cites] J Recept Signal Transduct Res. 2003;23(2-3):225-38 [14626449.001]
  • [Cites] J Neuroinflammation. 2005 Oct 31;2:24 [16259628.001]
  • [Cites] J Neurocytol. 1997 Feb;26(2):77-82 [9181482.001]
  • [Cites] Trends Neurosci. 1996 Aug;19(8):312-8 [8843599.001]
  • [Cites] Pharmacol Rev. 1999 Dec;51(4):629-50 [10581326.001]
  • [Cites] Cytometry. 1996 May 1;24(1):39-48 [8723901.001]
  • [Cites] Cancer Res. 1995 Jun 15;55(12):2691-5 [7780986.001]
  • [Cites] Neuro Oncol. 2006 Jul;8(3):261-79 [16775224.001]
  • [Cites] IEEE Trans Med Imaging. 2003 Mar;22(3):289-301 [12760547.001]
  • [Cites] Life Sci. 2004 Jan 30;74(11):1387-95 [14706569.001]
  • [Cites] Ann Neurol. 1989 Oct;26(4):564-8 [2554790.001]
  • [Cites] Glia. 2005 Sep;51(4):279-85 [15818597.001]
  • [Cites] J Cereb Blood Flow Metab. 1996 Sep;16(5):834-40 [8784228.001]
  • [Cites] Brain. 2000 Nov;123 ( Pt 11):2321-37 [11050032.001]
  • [Cites] Cancer. 1990 Jan 1;65(1):93-7 [2152852.001]
  • (PMID = 17520179.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U120085814
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Isoquinolines; 0 / RNA, Messenger; 0 / Radiopharmaceuticals; 0 / Receptors, GABA-A; YNF83VN1RL / PK 11195
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12. Mittelbronn M, Simon P, Löffler C, Capper D, Bunz B, Harter P, Schlaszus H, Schleich A, Tabatabai G, Goeppert B, Meyermann R, Weller M, Wischhusen J: Elevated HLA-E levels in human glioblastomas but not in grade I to III astrocytomas correlate with infiltrating CD8+ cells. J Neuroimmunol; 2007 Sep;189(1-2):50-8
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  • [Title] Elevated HLA-E levels in human glioblastomas but not in grade I to III astrocytomas correlate with infiltrating CD8+ cells.
  • To investigate HLA-E expression and immune cell infiltration in human astrocytic tumors in vivo, we analyzed normal CNS controls and astrocytomas of all WHO grades by immunohistochemistry.
  • Both, CD8(+) immune cell infiltration and HLA-E expression were significantly higher in astrocytic tumors than in normal brain.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. CD8-Positive T-Lymphocytes / physiology. Gene Expression Regulation, Neoplastic / physiology. Glioblastoma / metabolism. HLA Antigens / metabolism. Histocompatibility Antigens Class I / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged

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  • (PMID = 17675252.001).
  • [ISSN] 0165-5728
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-E antigen; 0 / Histocompatibility Antigens Class I
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13. Andreiuolo F, Junier MP, Hol EM, Miquel C, Chimelli L, Leonard N, Chneiweiss H, Daumas-Duport C, Varlet P: GFAPdelta immunostaining improves visualization of normal and pathologic astrocytic heterogeneity. Neuropathology; 2009 Feb;29(1):31-9
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  • [Title] GFAPdelta immunostaining improves visualization of normal and pathologic astrocytic heterogeneity.
  • Neuropathological analysis of cellular mechanisms underlying gliosis and brain tumors is slowed by the lack of markers allowing to distinguish glial subpopulations in normal or pathological human brains.
  • [MeSH-major] Astrocytes / cytology. Astrocytes / pathology. Brain Diseases / pathology. Brain Neoplasms / pathology. Glial Fibrillary Acidic Protein / analysis. Glioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Brain / cytology. Brain / pathology. Brain Chemistry. Epilepsy / metabolism. Epilepsy / pathology. Female. Gliosis / metabolism. Gliosis / pathology. Hippocampus / chemistry. Hippocampus / pathology. Humans. Immunohistochemistry / methods. Male. Microscopy, Confocal. Middle Aged. Sclerosis / metabolism. Sclerosis / pathology. Vimentin / analysis. Young Adult

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  • (PMID = 18564099.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
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14. Kato Y, Hayatsu N, Kaneko MK, Ogasawara S, Hamano T, Takahashi S, Nishikawa R, Matsutani M, Mishima K, Narimatsu H: Increased expression of highly sulfated keratan sulfate synthesized in malignant astrocytic tumors. Biochem Biophys Res Commun; 2008 May 16;369(4):1041-6
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  • [Title] Increased expression of highly sulfated keratan sulfate synthesized in malignant astrocytic tumors.
  • Keratan sulfate (KS) proteoglycans are expressed on a subpopulation of microglia in normal adult brain.
  • However, it has not been clarified whether KS is expressed in brain tumors and is involved in their malignancy.
  • In this study, 54 astrocytic tumors were investigated about KS-expression using Western-blot with 5D4.
  • KS was hardly detected by 5D4 in diffuse astrocytoma, suggesting that KS-expression is significantly expressed in malignant astrocytic tumors.
  • In immunohistochemistry, KS is highly expressed in cell surface of malignant astrocytic tumors.
  • Taken together, KS might be associated with the malignancy of astrocytic tumors, and be useful for a prognostic factor of astrocytic tumors.
  • [MeSH-major] Astrocytoma / pathology. Central Nervous System Neoplasms / pathology. Keratan Sulfate / metabolism

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  • (PMID = 18329383.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9056-36-4 / Keratan Sulfate
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15. Yamasaki F, Kurisu K, Satoh K, Arita K, Sugiyama K, Ohtaki M, Takaba J, Tominaga A, Hanaya R, Yoshioka H, Hama S, Ito Y, Kajiwara Y, Yahara K, Saito T, Thohar MA: Apparent diffusion coefficient of human brain tumors at MR imaging. Radiology; 2005 Jun;235(3):985-91
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  • [Title] Apparent diffusion coefficient of human brain tumors at MR imaging.
  • PURPOSE: To determine if apparent diffusion coefficient (ADC) can be used to differentiate brain tumors at magnetic resonance (MR) imaging.
  • MR images were reviewed retrospectively in 275 patients with brain tumors: 147 males and 128 females 1-81 years old, treated between September 1997 and July 2003.
  • Regions of interest were placed manually in tumor regions on MR images, and ADC was calculated with a five-point regression method at b values of 0, 250, 500, 750, and 1000 sec/mm2.
  • ADC values were average values in tumor.
  • All brain tumor subgroups were analyzed.
  • Logistic discriminant analysis was performed by using ADC, age, and patient sex as independent variables to discriminate among tumor groups.
  • RESULTS: A significant negative correlation existed between ADC and astrocytic tumors of World Health Organization grades 2-4 (grade 2 vs grades 3 and 4, accuracy of 91.3% [P < .01]; grade 3 vs 4, accuracy of 82.4% [P < .01]).
  • ADC of dysembryoplastic neuroepithelial tumors (DNTs) was higher than that of astrocytic grade 2 tumors (accuracy, 100%) and other glioneuronal tumors.
  • ADC of malignant lymphomas was lower than that of glioblastomas and metastatic tumors (accuracy, 83.6%; P < .01).
  • ADC of primitive neuroectodermal tumors (PNETs) was lower than that of ependymomas (accuracy, 100%).
  • ADC of epidermoid tumors was lower than that of chordomas (accuracy, 100%).
  • CONCLUSION: ADC is useful for differentiation of some human brain tumors, particularly DNT, malignant lymphomas versus glioblastomas and metastatic tumors, and ependymomas versus PNETs.
  • [MeSH-major] Brain Neoplasms / pathology. Magnetic Resonance Imaging
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Male. Middle Aged. Retrospective Studies

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  • [Copyright] Copyright RSNA, 2005.
  • (PMID = 15833979.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Li X, Wang Y, Wang Y, Zhen H, Yang H, Fei Z, Zhang J, Liu W, Wang Y, Zhang X: Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis. Tumour Biol; 2007;28(3):165-72
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  • [Title] Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis.
  • A high expression of EphA2 has been detected in many non-central nervous system tumors; however, the EphA2 expression in brain astrocytic tumors remains unclear.
  • In this study, we investigated the expression of EphA2 mRNA and protein in 90 cases of human astrocytic tumors by reverse transcription polymerase chain reaction and immunohistochemistry, respectively.
  • The proliferative index (PI) of tumor cells was evaluated by Ki-67 immunohistochemistry, and the apoptotic index (AI) was determined by TdT-mediated dUTP nick end labeling assay.
  • The correlation between EphA2 expression, pathologic grade, proliferation and apoptosis of astrocytic tumors was further analyzed.
  • Therefore, EphA2 may be a new biomarker for astrocytic tumors.
  • It may also affect the proliferation and apoptosis of tumor cells and be an attractive therapy target for astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Receptor, EphA2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Cell Division. Child. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / genetics


17. Schittenhelm J, Mittelbronn M, Nguyen TD, Meyermann R, Beschorner R: WT1 expression distinguishes astrocytic tumor cells from normal and reactive astrocytes. Brain Pathol; 2008 Jul;18(3):344-53
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  • [Title] WT1 expression distinguishes astrocytic tumor cells from normal and reactive astrocytes.
  • Recently, the over-expression of Wilms' tumor gene product WT1 was reported in astrocytic tumor cells.
  • In astrocytomas, WT1-positive tumor cells were found in pilocytic astrocytomas (66.7% of cases), diffuse astrocytomas (52.7%) WHO grade II (52.7%), anaplastic astrocytomas (83.4%) and glioblastomas (98.1%).
  • Overall, the majority of all astrocytic neoplasms (84.5%) expressed WT1.
  • Establishing a cut-off value of 0% immunoreactive tumor cells served to recognize neoplastic astrocytes with 100% specificity and 68% sensitivity and was associated with positive and negative predictive values of 1 and 0.68, respectively.
  • Therefore, WT1 expression in astrocytes indicates a neoplastic origin and might represent an important diagnostic tool to differentiate reactive from neoplastic astrocytes by immunohistochemistry.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gliosis / metabolism. WT1 Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Endothelial Cells / metabolism. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 18371184.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / WT1 Proteins
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18. Hede SM, Hansson I, Afink GB, Eriksson A, Nazarenko I, Andrae J, Genove G, Westermark B, Nistér M: GFAP promoter driven transgenic expression of PDGFB in the mouse brain leads to glioblastoma in a Trp53 null background. Glia; 2009 Aug 15;57(11):1143-53
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  • Glioblastomas are the most common and malignant astrocytic brain tumors in human adults.
  • The tumor suppressor gene TP53 is commonly mutated and/or lost in astrocytic brain tumors and the TP53 alterations are often found in combination with excessive growth factor signaling via PDGF/PDGFRalpha.
  • Here, we have generated transgenic mice over-expressing human PDGFB in brain, under control of the human GFAP promoter.
  • These mice showed no phenotype, but on a Trp53 null background a majority of them developed brain tumors.
  • This occurred at 2-6 months of age and tumors displayed human glioblastoma-like features with integrated development of Pdgfralpha+ tumor cells and Pdgfrbeta+/Nestin+ vasculature.
  • The transgene was expressed in subependymal astrocytic cells, in glia limitans, and in astrocytes throughout the brain substance, and subsequently, microscopic tumor lesions were initiated equally in all these areas.
  • With tumor size, there was an increase in Nestin positivity and variability in lineage markers.
  • These results indicate an unexpected plasticity of all astrocytic cells in the adult brain, not only of SVZ cells.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / genetics. Genes, p53. Glial Fibrillary Acidic Protein / genetics. Glioblastoma / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins c-sis / metabolism
  • [MeSH-minor] Animals. Astrocytes / metabolism. Disease Models, Animal. Gene Expression. Humans. Intermediate Filament Proteins / metabolism. Mice. Mice, Transgenic. Nerve Tissue Proteins / metabolism. Nestin. Neuroglia / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism

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  • (PMID = 19115382.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Proto-Oncogene Proteins c-sis; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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19. Fu YJ, Miyahara H, Uzuka T, Natsumeda M, Okamoto K, Hirose T, Fujii Y, Takahashi H: Intraventricular pleomorphic xanthoastrocytoma with anaplastic features. Neuropathology; 2010 Aug;30(4):443-8
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  • Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic tumor that usually occurs in the superficial cerebral hemispheres of children and young adults and has a relatively favorable prognosis.
  • We report an unusual case of supratentorial, intraventricular tumor in a 52-year-old man.
  • The tumor was composed of pleomorphic cells, including giant cells, most of which were multinucleated, and small cells.
  • In addition, frequent xanthic changes in the cytoplasm of the tumor cells, and widespread reticulin deposits and lymphocytic infiltrates in the stroma were characteristic features.
  • Many tumor cells were positive for GFAP, and a number were positive for neurofilament protein and synaptophysin, indicating their neuronal differentiation.
  • In addition, occasional tumor cells were positive for CD34. p53 protein was entirely negative in the tumor cells.
  • In diagnosing this tumor histopathologically, differentiation between PXA and giant cell glioblastoma (GCG), a rare variant of glioblastoma, was problematic.
  • The present case indicates that PXA can occur as an intraventricular tumor, and suggests that in some instances, it would be very difficult to differentiate PXA and GCG histopathologically.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology

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  • (PMID = 20051018.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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20. Biernat W, Zawrocki A: Molecular alterations in ependymomas. Folia Neuropathol; 2007;45(4):155-63
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  • Ependymal tumours are uncommon neoplasms of the central nervous system.
  • Basic molecular alterations underlying their development are not so well defined in contrast to the astrocytic tumours.

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  • (PMID = 18176888.001).
  • [ISSN] 1641-4640
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Number-of-references] 82
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26. Idbaih A, Marie Y, Lucchesi C, Pierron G, Manié E, Raynal V, Mosseri V, Hoang-Xuan K, Kujas M, Brito I, Mokhtari K, Sanson M, Barillot E, Aurias A, Delattre JY, Delattre O: BAC array CGH distinguishes mutually exclusive alterations that define clinicogenetic subtypes of gliomas. Int J Cancer; 2008 Apr 15;122(8):1778-86
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  • Whole chromosomes (chrs) 1p and 19q losses with centromeric breakpoints and EGFR high level amplification were found to be mutually exclusive, permitting identification of 3 distinct, nonoverlapping groups of tumors with striking clinicopathological differences.
  • Type A tumors with chrs 1p and 19q co-deletion exhibited an oligodendroglial phenotype and a longer patient survival.
  • Type B tumors were characterized by EGFR amplification.
  • They harbored a WHO high grade of malignancy and a short patient survival.
  • Finally, type C tumors displayed none of the previous patterns but the presence of chr 7 gain, chr 9p deletion and/or chr 10 loss.
  • It included astrocytic tumors in patients younger than in type B and whose prognosis was highly dependent upon the number of alterations.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosome Deletion. Glioma / genetics. Glioma / pathology. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Astrocytoma / genetics. Astrocytoma / pathology. Chromosomes, Artificial, Bacterial. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9. Disease-Free Survival. Female. Humans. Loss of Heterozygosity. Male. Middle Aged. Multivariate Analysis. Nucleic Acid Hybridization. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Oligonucleotides. Predictive Value of Tests. Prognosis. Proportional Hazards Models. Survival Analysis. World Health Organization

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  • (PMID = 18076069.001).
  • [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 / Oligonucleotides; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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27. Järvelä S, Helin H, Haapasalo J, Järvelä T, Junttila TT, Elenius K, Tanner M, Haapasalo H, Isola J: Amplification of the epidermal growth factor receptor in astrocytic tumours by chromogenic in situ hybridization: association with clinicopathological features and patient survival. Neuropathol Appl Neurobiol; 2006 Aug;32(4):441-50
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  • [Title] Amplification of the epidermal growth factor receptor in astrocytic tumours by chromogenic in situ hybridization: association with clinicopathological features and patient survival.
  • Chromogenic in situ hybridization (CISH) was used to detect amplification of the epidermal growth factor receptor (EGFR) gene in tissue microarrays of tumours derived from 287 patients with grade II-IV diffuse astrocytomas.
  • Amplification was found in 32% of the tumours with a highly significant association with histological grade (4% in grade II, 21% in grade III and 39% in grade IV; P < 0.001).
  • Overexpression of EGFR mRNA and protein (wild-type and vIII variant) was found to correlate with EGFR gene amplification (P = 0.028, P = 0.035 and P = 0.014 respectively), but wild-type EGFR protein was also frequently overexpressed in tumours without EGFR gene amplification.
  • Patients with older age (P < 0.001) and tumours with lack of p53 overexpression (P = 0.03) and higher apoptosis rate (P < 0.001) had significantly more EGFR gene amplifications than their counterparts.
  • The survival of patients with EGFR gene-amplified grade III tumours was significantly shorter than in those with grade III non-amplified tumours (P = 0.03).
  • No such difference was noted in glioblastomas (grade IV tumours).
  • Our data verify the central role of EGFR in the pathobiology of astrocytic tumours, and highlight the advantages of CISH as a simple and practical assay to screen for EGFR gene amplification in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Apoptosis / physiology. Child. Child, Preschool. Chromogenic Compounds. Female. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Protein Array Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Survival Rate. Tumor Suppressor Protein p53

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  • [ErratumIn] Neuropathol Appl Neurobiol. 2006 Oct;32(5):568. Järvellä, S [corrected to Järvelä, Sally]; Järvellä, T [corrected to Järvelä, Timo]
  • (PMID = 16866989.001).
  • [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 / Chromogenic Compounds; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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28. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • Novel animal models will provide us with the opportunity to comprehensively study this multilayered disease and explore novel therapeutic approaches in vivo.
  • [MeSH-major] Brain Neoplasms / genetics
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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29. Juhász C, Chugani DC, Muzik O, Wu D, Sloan AE, Barger G, Watson C, Shah AK, Sood S, Ergun EL, Mangner TJ, Chakraborty PK, Kupsky WJ, Chugani HT: In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors. J Cereb Blood Flow Metab; 2006 Mar;26(3):345-57
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  • [Title] In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors.
  • Abnormal metabolism of tryptophan has been implicated in modulation of tumor cell proliferation and immunoresistance. alpha-[(11)C]Methyl-L-tryptophan (AMT) is a PET tracer to measure cerebral tryptophan metabolism in vivo.
  • In the present study, we have measured tumor tryptophan uptake in 40 patients with primary brain tumors using AMT PET and standard uptake values (SUV).
  • All grade II to IV gliomas and glioneuronal tumors showed increased AMT SUV, including all recurrent/residual tumors.
  • Low-grade astrocytic gliomas showed increased tryptophan metabolism, as measured by k(3)'.
  • In astrocytic tumors, low grade was associated with high k(3)' and lower VD', while high-grade tumors showed the reverse pattern.
  • The findings show high AMT uptake in primary and residual/recurrent gliomas and glioneuronal tumors.
  • Increased AMT uptake can be due to increased metabolism of tryptophan and/or high volume of distribution, depending on tumor type and grade.
  • High tryptophan metabolic rates in low-grade tumors may indicate activation of the kynurenine pathway, a mechanism regulating tumor cell growth.
  • AMT PET might be a useful molecular imaging method to guide therapeutic approaches aimed at controlling tumor cell proliferation by acting on tryptophan metabolism.
  • [MeSH-major] Brain Neoplasms / metabolism. Cerebral Cortex / metabolism. Tryptophan / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Aged. Carbon Radioisotopes. Child. Child, Preschool. Electroencephalography / methods. Electroencephalography / standards. Female. Gadolinium. Glucose / metabolism. Humans. Infant. Magnetic Resonance Imaging / methods. Magnetic Resonance Imaging / standards. Male. Middle Aged. Neoplasm Staging. Positron-Emission Tomography / methods. Positron-Emission Tomography / standards. Seizures / metabolism. Sensitivity and Specificity

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  • (PMID = 16079785.001).
  • [ISSN] 0271-678X
  • [Journal-full-title] Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • [ISO-abbreviation] J. Cereb. Blood Flow Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan; AU0V1LM3JT / Gadolinium; IY9XDZ35W2 / Glucose
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30. Wrensch M, Fisher JL, Schwartzbaum JA, Bondy M, Berger M, Aldape KD: The molecular epidemiology of gliomas in adults. Neurosurg Focus; 2005 Nov;19(5):E5
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  • [Title] The molecular epidemiology of gliomas in adults.
  • Several biomarkers do predict prognosis, but only evaluation of loss of 1p and 19q in oligodendroglial tumors are incorporated in clinical practice.
  • Ongoing research focuses on classifying homogeneous groups of tumors on the basis of molecular markers and identifying inherited polymorphisms that may influence survival or risk.
  • Improving survival rates for patients harboring astrocytic tumors will probably require many randomized clinical trials of novel treatment strategies.
  • [MeSH-minor] Adult. Brain Neoplasms / epidemiology. Brain Neoplasms / genetics. Genetic Markers / genetics. Humans. Molecular Epidemiology. Polymorphism, Genetic / genetics. Risk Factors

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  • (PMID = 16398469.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01CA52689; United States / NCI NIH HHS / CA / R03CA103379
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 191
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31. Yorgancılar E, Yıldırım M, Gün R, Büyükbayram H, Meriç F: Ganglioglioma in the nasal cavity: a case report. Kulak Burun Bogaz Ihtis Derg; 2010 Sep-Oct;20(5):267-70
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  • Ganglioglioma is a tumor containing both astrocytic and neuronal components.
  • Nasal glial heterotopia (also known as ''nasal glioma''), is a rare developmental abnormality seen in a wide age group.
  • Gangliogliomas may also manifest as a nasal glial heterotopia, and neurogenic tumors should be considered in the presence of a nasal mass.
  • [MeSH-major] Ganglioglioma / surgery. Nose Neoplasms / surgery
  • [MeSH-minor] Endoscopy. Female. Humans. Nasal Cavity / enzymology. Nasal Cavity / surgery. Nasolacrimal Duct / surgery. Phosphopyruvate Hydratase / analysis. S100 Proteins / analysis. Young Adult

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  • (PMID = 20815807.001).
  • [ISSN] 1300-7475
  • [Journal-full-title] Kulak burun boğaz ihtisas dergisi : KBB = Journal of ear, nose, and throat
  • [ISO-abbreviation] Kulak Burun Bogaz Ihtis Derg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / S100 Proteins; EC 4.2.1.11 / Phosphopyruvate Hydratase
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32. Klink B, Schlingelhof B, Klink M, Stout-Weider K, Patt S, Schrock E: Glioblastomas with oligodendroglial component - common origin of the different histological parts and genetic subclassification. Anal Cell Pathol (Amst); 2010;33(1):37-54
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  • BACKGROUND: Glioblastomas are the most common and most malignant brain tumors in adults.
  • Our objective was to genetically characterize the oligodendroglial and the astrocytic parts of GBMOs and correlate morphologic and genetic features with clinical data.
  • METHODS: The oligodendroglial and the "classic" glioblastoma parts of 13 GBMO were analyzed separately by interphase fluorescence in situ hybridization (FISH) on paraffin sections using a custom probe set (regions 1p, 1q, 7q, 10q, 17p, 19q, cen18, 21q) and by comparative genomic hybridization (CGH) of microdissected paraffin embedded tumor tissue.
  • RESULTS: We identified four distinct genetic subtypes in 13 GBMOs: an "astrocytic" subtype (9/13) characterized by +7/-10; an "oligodendroglial" subtype with -1p/-19q (1/13); an "intermediate" subtype showing +7/-1p (1/13), and an "other" subtype having none of the former aberrations typical for gliomas (2/13).
  • The different histological tumor parts of GBMO revealed common genetic changes in all tumors and showed additional aberrations specific for each part.
  • CONCLUSION: Our findings demonstrate the monoclonal origin of GBMO followed by the development of the astrocytic and oligodendroglial components.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Glioblastoma / genetics. Glioblastoma / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology
  • [MeSH-minor] Adult. Aged. Female. Humans. Image Processing, Computer-Assisted. Imaging, Three-Dimensional. In Situ Hybridization, Fluorescence. Male. Middle Aged

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  • (PMID = 20966543.001).
  • [ISSN] 2210-7185
  • [Journal-full-title] Analytical cellular pathology (Amsterdam)
  • [ISO-abbreviation] Anal Cell Pathol (Amst)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC4605661
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33. Haapasalo J, Mennander A, Helen P, Haapasalo H, Isola J: Ultrarapid Ki-67 immunostaining in frozen section interpretation of gliomas. J Clin Pathol; 2005 Mar;58(3):263-8
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  • BACKGROUND: Astrocytic tumours, the most common gliomas, are often classified intraoperatively using standard morphological staining.
  • AIMS: To investigate a new rapid Ki-67 immunohistochemical test for its use in an intraoperative setting.
  • METHODS: The new Ki-67 immunostaining (Ultrarapid-Ki67) method on frozen sections can be carried out in 10 minutes.
  • A comparison of Ultrarapid-Ki67 and MIB-1 immunostaining of paraffin wax sections showed almost identical quantitative correlation in astrocytic gliomas (r = 0.916; p<0.001).
  • The Ultrarapid-Ki67 indices (percentage of positive cells) of low grade (I/II) astrocytomas ranged from 0% to 6.1%, whereas those of representative high grade (III/IV) tumours were significantly higher (range, 5.6-45%; p<0.001).
  • CONCLUSION: Ultrarapid-Ki67 immunostaining is a useful adjunct to morphological diagnosis and grading of astrocytic tumours, and as a fast test (approximately 10 minutes for staining plus three to four minutes for scoring), it could be used in routine intraoperative diagnosis of gliomas and other neoplastic diseases.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Ki-67 Antigen / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Antinuclear / immunology. Antibodies, Monoclonal / immunology. Child. Child, Preschool. Diagnosis, Differential. Female. Frozen Sections. Humans. Immunoenzyme Techniques. Intraoperative Care / methods. Male. Middle Aged. Neoplasm Proteins / analysis. Prognosis. Time Factors

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  • [Cites] J Clin Pathol. 1999 Jun;52(6):461-3 [10562816.001]
  • [Cites] Neuropathol Appl Neurobiol. 2000 Aug;26(4):319-31 [10931365.001]
  • [Cites] J Histochem Cytochem. 2001 May;49(5):623-30 [11304800.001]
  • [Cites] Am J Surg Pathol. 1986 Sep;10(9):611-7 [2428262.001]
  • [Cites] Am J Clin Pathol. 1989 Jan;91(1):63-6 [2462785.001]
  • [Cites] J Surg Oncol. 1989 Nov;42(3):209-14 [2478837.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Jan;58(1):46-53 [10068313.001]
  • [Cites] Cancer. 1994 Oct 1;74(7):1921-6 [7521787.001]
  • [Cites] J Pathol. 1994 Dec;174(4):275-82 [7884589.001]
  • [Cites] Pathol Int. 1995 Feb;45(2):108-15 [7742923.001]
  • [Cites] J Neurosurg. 1997 Jan;86(1):121-30 [8988090.001]
  • [Cites] Histopathology. 1998 Jan;32(1):43-50 [9522215.001]
  • [Cites] Acta Cytol. 1998 Sep-Oct;42(5):1149-54 [9755673.001]
  • [Cites] J Pathol. 1992 Dec;168(4):357-63 [1484317.001]
  • (PMID = 15735157.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Ki-67 Antigen; 0 / MIB-1 antibody; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC1770597
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34. Ng WH, Lim T, Yeo TT: Pleomorphic xanthoastrocytoma in elderly patients may portend a poor prognosis. J Clin Neurosci; 2008 Apr;15(4):476-8
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  • Pleomorphic xanthoastrocytoma (PXA) is a rare primary astrocytic tumour of the nervous system usually involving the superficial temporal cortex of children and young adults.
  • Although the tumour may exhibit histological features of pleomorphism or cellular atypia, the overall prognosis is good compared with other glial tumours, with only 30% of PXA recurring and 20% undergoing anaplastic transformation.
  • Increased mitotic activity, high MIB-1 and proliferating cell nuclear antigen labelling indices and necrosis are poor prognostic factors, whereas abundant lymphocytic infiltration is associated with more benign biological behaviour.
  • We report the case of a 76-year-old woman who presented with dysphasia and right hemiparesis.
  • Although a rare and benign tumour type, PXA in the elderly tend to be more malignant, may have the radiological appearance of a malignant tumour and have poor prognosis.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis

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  • (PMID = 18255294.001).
  • [ISSN] 0967-5868
  • [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
  • [Chemical-registry-number] 0 / Ki-67 Antigen
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35. Wakabayashi T, Natsume A, Hatano H, Fujii M, Shimato S, Ito M, Ohno M, Ito S, Ogura M, Yoshida J: p16 promoter methylation in the serum as a basis for the molecular diagnosis of gliomas. Neurosurgery; 2009 Mar;64(3):455-61; discussion 461-2
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  • OBJECTIVE: Deoxyribonucleic acid (DNA) methylation of tumor origin can be detected in the serum/plasma of cancer patients.
  • METHODS: The methylation-specific polymerase chain reaction was used to detect p16 methylation in the DNA extracted from 20 astrocytic tumors and 20 oligodendroglial tumors and the corresponding serum samples.
  • In addition, the serum DNA in 7 patients with a brainstem tumor (4 gliomas, 1 schwannoma, 1 cavernous angioma, and 1 ependymoma) was analyzed.
  • Similar methylations were detected in the serum of 9 (75%) of the 12 patients with aberrant methylation in the tumor tissues.
  • No methylated p16 sequences were detected in the peripheral serum of the patients having tumors without these methylation changes or in the 10 healthy controls.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. Genes, p16. Glioma / diagnosis. Glioma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. DNA Methylation / genetics. Female. Genetic Predisposition to Disease / genetics. Humans. Male. Middle Aged. Reproducibility of Results. Sensitivity and Specificity. Young Adult

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  • (PMID = 19240607.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm
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36. Laywell ED, Steindler DA, Silver DJ: Astrocytic stem cells in the adult brain. Neurosurg Clin N Am; 2007 Jan;18(1):21-30, viii
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  • [Title] Astrocytic stem cells in the adult brain.
  • The adult mammalian brain harbors a population of neural stem cells (NSCs) that are responsible for persistent neurogenesis in the olfactory system and hippocampus and may also play a role in tumorigenesis.
  • Here, the authors review the evidence that NSCs within the adult brain are a special type of astrocyte.
  • Finally, the authors compare and contrast the functional characteristics of NSCs and hematopoietic stem cells and review the potential oncogenic transformation of astrocyte NSCs that may underlie brain tumorigenesis as seen in glioblastoma and other primary brain tumors.
  • [MeSH-major] Adult Stem Cells / cytology. Astrocytes / cytology. Dentate Gyrus / cytology. Ependyma / cytology
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic. Humans

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  • (PMID = 17244551.001).
  • [ISSN] 1042-3680
  • [Journal-full-title] Neurosurgery clinics of North America
  • [ISO-abbreviation] Neurosurg. Clin. N. Am.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL070143; United States / NINDS NIH HHS / NS / NS37556
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 59
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37. Min HS, Kim B, Park SH: Array-based comparative genomic hybridization and immunohistochemical studies in gliomatosis cerebri. J Neurooncol; 2008 Dec;90(3):259-66
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  • Gliomatosis cerebri (GC) are extensively infiltrative glial tumors classified as astrocytic tumors in the current World Health Organization (WHO) classification scheme.
  • In histological and immunohistochemical review, 18 cases (64%) were of astrocytic lineage, three (11%) were of oligodendroglial lineage, and seven (25%) were of uncommitted lineage.
  • These altered genetic foci are not known to be involved in the development of conventional glial tumors, including astrocytic tumors.
  • In conclusion, despite the dominant astrocytic differentiation of GC histologically, novel genomic aberrations found in our GC cases were different from those of astrocytic tumors.
  • [MeSH-major] Comparative Genomic Hybridization / methods. Immunohistochemistry / methods. Neoplasms, Neuroepithelial / genetics. Neoplasms, Neuroepithelial / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD34 / metabolism. Child. Child, Preschool. Cluster Analysis. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Infant. Infant, Newborn. Intermediate Filament Proteins / metabolism. Male. Middle Aged. Nerve Tissue Proteins / metabolism. Nestin. Receptor, Epidermal Growth Factor / metabolism. Retrospective Studies. Survival Analysis. Tumor Suppressor Proteins / metabolism. Young Adult

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  • [Cites] J Neurooncol. 2005 Apr;72 (2):115-22 [15925990.001]
  • [Cites] Nat Genet. 1998 Oct;20(2):207-11 [9771718.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Sep;61(9):806-14 [12230327.001]
  • [Cites] Hum Pathol. 1997 Oct;28(10):1166-79 [9343324.001]
  • [Cites] Acta Neurochir (Wien). 1998;140(8):755-62 [9810441.001]
  • [Cites] Nat Genet. 2005 Jun;37 Suppl:S11-7 [15920524.001]
  • [Cites] Acta Neurochir (Wien). 2000;142(4):469-72 [10883346.001]
  • [Cites] J Neurooncol. 2006 Jan;76(2):201-5 [16200347.001]
  • [Cites] Bioinformatics. 2005 Mar;21(6):821-2 [15531610.001]
  • [Cites] Neurosurgery. 2003 Aug;53(2):261-71; discussion 271 [12925240.001]
  • [Cites] J Neurooncol. 2007 Mar;82(1):23-7 [16955219.001]
  • [Cites] Genes Chromosomes Cancer. 1995 Oct;14(2):149-53 [8527397.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 May;83(9):2934-8 [3458254.001]
  • [Cites] Nucleic Acids Res. 2002 Feb 15;30(4):e15 [11842121.001]
  • [Cites] Ann Neurol. 2002 Oct;52(4):390-9 [12325066.001]
  • [Cites] Acta Neuropathol. 2003 Jun;105(6):529-36 [12734658.001]
  • [Cites] Clin Genet. 2004 Dec;66(6):488-95 [15521975.001]
  • [Cites] Acta Neuropathol. 2005 Dec;110(6):527-36 [16222524.001]
  • [Cites] Hum Pathol. 2003 Jan;34(1):102-6 [12605375.001]
  • [Cites] J Neurooncol. 2003 Jan;61(1):1-5 [12587789.001]
  • [Cites] Lab Invest. 2006 Sep;86(9):968-78 [16751780.001]
  • (PMID = 18704270.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 6.5.1.- / DNA Repair Enzymes
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38. Wiencke JK, Aldape K, McMillan A, Wiemels J, Moghadassi M, Miike R, Kelsey KT, Patoka J, Long J, Wrensch M: Molecular features of adult glioma associated with patient race/ethnicity, age, and a polymorphism in O6-methylguanine-DNA-methyltransferase. Cancer Epidemiol Biomarkers Prev; 2005 Jul;14(7):1774-83
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  • [Title] Molecular features of adult glioma associated with patient race/ethnicity, age, and a polymorphism in O6-methylguanine-DNA-methyltransferase.
  • BACKGROUND: Risk factors for adult glioma in the San Francisco Bay Area include well-known demographic features such as age and race/ethnicity, and our previous studies indicated that these characteristics are associated with the TP53 mutation status of patients' tumors.
  • We enlarged our study to assess the relationships of risk factors with TP53 as well as epidermal growth factor receptor (EGFR) and murine double minute-2 (MDM2) gene amplification and expression and the germ line Leu84Phe polymorphism in the DNA repair protein O6-methylguanine-DNA-methyltransferase (MGMT).
  • METHODS: Molecular analyses were carried out on 556 incident astrocytic tumors.
  • RESULTS: The tumor data confirm the inverse relationships between TP53 mutation and MDM2 (P = 0.04) or EGFR (P = 0.004) amplification and that patients whose tumors contain TP53 mutations are younger than those without (P < 0.001).
  • Although there was little difference in age of patient by EGFR amplification or expression among glioblastoma multiforme cases, EGFR gene amplification was associated with much older age of onset of anaplastic astrocytoma; for example, EGFR-amplified anaplastic astrocytoma cases were on average 63 years old compared with 48 years for nonamplified cases (P = 0.005).
  • An increased prevalence of TP53 mutation positive glioblastoma multiforme was noted among nonwhites (African American and Asian) compared with whites (Latino and non-Latino; P = 0.004).
  • Carriers of the MGMT variant 84Phe allele were significantly less likely to have tumors with TP53 overexpression (odds ratio, 0.30; 95% confidence interval, 0.13-0.71) and somewhat less likely to have tumors with any TP53 mutation (odds ratio, 0.47; 95% confidence interval, 0.13-1.69) after adjusting for age, gender, and ethnicity.
  • The data on MGMT show that an inherited factor involving the repair of methylation and other alkylation damage, specifically to the O6 position of guanine, may be associated with the development of tumors that proceed in their development without TP53 mutations or accumulation of TP53 protein and possibly also those that do not involve amplification of the EGFR locus.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Molecular Biology. Nuclear Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Polymorphism, Genetic. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Biomarkers, Tumor / genetics. Ethnic Groups. Female. Gene Amplification. Genes, p53. Humans. Male. Middle Aged. Prevalence. Proto-Oncogene Proteins c-mdm2. San Francisco / epidemiology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16030116.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES04705; United States / NIEHS NIH HHS / ES / ES06717; United States / NCI NIH HHS / CA / P50CA097257; United States / NCI NIH HHS / CA / R01CA52689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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39. Isolan GR, Ribas Filho JM, Isolan PM, Giovanini A, Malafaia O, Dini LI, Kummer A Jr, Negrão AW: [Astrocytic neoplasms and correlation with mutate p53 and Ki-67 proteins]. Arq Neuropsiquiatr; 2005 Dec;63(4):997-1004
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  • [Title] [Astrocytic neoplasms and correlation with mutate p53 and Ki-67 proteins].
  • [Transliterated title] Neoplasias astrocitárias e correlação com as proteínas p53 mutada e Ki-67.
  • The astrocytic neoplasms respond by 60% of the central nervous system tumors, being the study of the molecular biology an important step for the understanding of the genesis and biological behavior of these diseases.
  • The Ki-67 proteins, which are markers of the cellular proliferation, and p53, which is the product of the tumor suppressor gene TP53, are both important tumoral markers.
  • This study intends to identify and quantify the Ki-67 and p53 proteins in astrocytic tumors of different grades of malignancy, as well as to analyze their relations with age and gender.
  • Ki-67 and p53 proteins in 47 patients with surgically resected astrocytic neoplasms were studied through immunohistochemistry.
  • For the Ki-67 they were absent, <5% and >5% and for p53 they were absent (0), <25% (1+), between 25 and 50% (2+), between 50 and 75% (3+), and higher than 75% (4+).
  • The hypotheses of a greater presence of Ki-67 and p53 in astrocytic neoplasms with a higher degree of malignancy, except for the correlation between grade III and p53, is corroborated by the results of this study.
  • [MeSH-major] Astrocytoma / chemistry. Central Nervous System Neoplasms / chemistry. Ki-67 Antigen / analysis. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cross-Sectional Studies. Female. Humans. Immunohistochemistry. Male. Middle Aged. Retrospective Studies

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  • (PMID = 16400419.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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40. Gologorsky Y, DeLaMora P, Souweidane MM, Greenfield JP: Cerebellar cryptococcoma in an immunocompetent child. Case report. J Neurosurg; 2007 Oct;107(4 Suppl):314-7
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  • Isolated cryptococcomas of the central nervous system (CNS) have been previously described in immunocompetent adults; however, this is the first report of a cryptococcoma in a child.
  • The patient underwent excision of the mass, and analysis of frozen sections suggested the presence of an astrocytic tumor with pilocytic features; therefore gross-total resection was performed.

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  • (PMID = 17941497.001).
  • [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
  • [Chemical-registry-number] 0 / Antifungal Agents
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41. Fountzilas G, Karkavelas G, Kalogera-Fountzila A, Karina M, Ignatiadis M, Koukoulis G, Plataniotis G, Misailidou D, Bobos M, Pectasides D, Razis E, Karavelis A, Selviaridis P: Post-operative combined radiation and chemotherapy with temozolomide and irinotecan in patients with high-grade astrocytic tumors. A phase II study with biomarker evaluation. Anticancer Res; 2006 Nov-Dec;26(6C):4675-86
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  • [Title] Post-operative combined radiation and chemotherapy with temozolomide and irinotecan in patients with high-grade astrocytic tumors. A phase II study with biomarker evaluation.
  • BACKGROUND: Clinical studies have shown that temozolomide (TMZ) and irinotecan demonstrate activity in high grade astrocytic tumors (HGAT).
  • PATIENTS AND METHODS: In the present study, a total of 45 HGAT patients, 38 with glioblastoma multiforme (GBM) and 7 with anaplastic astrocytoma (AA), were treated with TMZ, 150 mg/m(2) on days 1-5, followed by irinotecan, 150 mg/m(2) on days 6 and 17, every 4 weeks for 6 cycles or until the occurrence of unacceptable toxicity or disease progression.
  • Most frequently recorded side-effects included neutropenia (37%), nausea/vomiting (66%), diarrhea (31%) and infection (44%).
  • Five episodes of vaso-occlusive disease, all of them fatal, were observed.
  • Two out of the five biomarkers studied, epidermal growth factor receptor (EGFR) and vascular endothelial growth factor-C (VEGF-C), were found to be overexpressed in 74% of the tumors, however they had no predictive value for progression-free or overall survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / metabolism. Astrocytoma / therapy. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Glioblastoma / metabolism. Glioblastoma / therapy
  • [MeSH-minor] Adult. Aged. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Combined Modality Therapy. Cyclooxygenase 2 / biosynthesis. Dacarbazine / administration & dosage. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Feasibility Studies. Female. Humans. Ki-67 Antigen / biosynthesis. Male. Middle Aged. PTEN Phosphohydrolase / biosynthesis. Patient Compliance. Postoperative Care. Vascular Endothelial Growth Factor C / biosynthesis

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  • (PMID = 17214326.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Vascular Endothelial Growth Factor C; 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; XT3Z54Z28A / Camptothecin
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42. Stojic J, Hagemann C, Haas S, Herbold C, Kühnel S, Gerngras S, Roggendorf W, Roosen K, Vince GH: Expression of matrix metalloproteinases MMP-1, MMP-11 and MMP-19 is correlated with the WHO-grading of human malignant gliomas. Neurosci Res; 2008 Jan;60(1):40-9
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  • [Title] Expression of matrix metalloproteinases MMP-1, MMP-11 and MMP-19 is correlated with the WHO-grading of human malignant gliomas.
  • Glioblastomas (GBM) are the most prevalent type of malignant primary brain tumor in adults.
  • They may manifest de novo or develop from low-grade astrocytomas (LGA) or anaplastic astrocytomas.
  • They are characterized by an aggressive local growth pattern and a marked degree of invasiveness, resulting in poor prognosis.
  • Tumor progression is facilitated by an increased activity of proteolytic enzymes such as matrix metalloproteinases (MMPs).
  • However, data for some MMPs, like MMP-1, are controversially discussed and other MMPs like MMP-11 and MMP-19 have as yet not been analysed in detail.
  • We examined the expression of MMP-1, MMP-9, MMP-11 and MMP-19 in NB, LGA and GBM by semiquantitative RT-PCR, Western blotting and immunohistochemistry and found an enhanced expression of these MMPs in GBM compared to LGA or NB in signal strength and in the percentage of tumors displaying MMP expression.
  • Therefore, MMP-1, MMP-11 and MMP-19 might be of importance for the development of high-grade astrocytic tumors and may be promising targets for therapy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / enzymology. Glioma / diagnosis. Glioma / enzymology. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 11 / metabolism. Matrix Metalloproteinases, Secreted / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Disease Progression. Female. Gene Expression Regulation, Enzymologic / genetics. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Matrix Metalloproteinase 9 / genetics. Middle Aged. Neoplasm Invasiveness / genetics. Predictive Value of Tests. Prognosis. RNA, Messenger / analysis. RNA, Messenger / metabolism. World Health Organization

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  • (PMID = 17980449.001).
  • [ISSN] 0168-0102
  • [Journal-full-title] Neuroscience research
  • [ISO-abbreviation] Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 3.4.24.- / Matrix Metalloproteinase 11; EC 3.4.24.- / Matrix Metalloproteinases, Secreted; EC 3.4.24.- / matrix metalloproteinase 19; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
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43. Huang X, Bai HM, Chen L, Li B, Lu YC: Reduced expression of LC3B-II and Beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors. J Clin Neurosci; 2010 Dec;17(12):1515-9
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  • [Title] Reduced expression of LC3B-II and Beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors.
  • The aim of this study was to investigate the expression of microtubule-associated protein 1 light chain 3B (LC3B) and the autophagy-related gene Beclin 1 in astrocytic tumors and to analyze their expression profiles with respect to the development of astrocytic tumors.
  • The expression patterns of LC3B and Beclin 1 were analyzed by immunohistochemistry and/or western blotting in tumor samples from 62 patients with different grades of astrocytic tumor.
  • Western blot analysis indicated that the average optical densitometry (OD) ratio of Beclin 1 in high-grade astrocytic tumors (World Health Organization [WHO] grade III/IV) was lower than in low-grade astrocytic tumors (WHO grade I/II, p = 0.036).
  • The expression of LC3B-I exhibited no significant difference among the various grades of astrocytic tumor.
  • However, the average OD ratio of LC3B-II was lower in glioblastoma multiforme (GBM) than in other grades of astrocytic tumor (p = 0.030).
  • The progression of astrocytic tumors was related to a decrease in autophagic capacity represented by the loss of LC3B-II and Beclin 1 expression.
  • [MeSH-major] Apoptosis Regulatory Proteins / biosynthesis. Brain Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Glioblastoma / pathology. Membrane Proteins / biosynthesis. Microtubule-Associated Proteins / biosynthesis
  • [MeSH-minor] Adult. Astrocytoma / metabolism. Astrocytoma / pathology. Autophagy. Blotting, Western. Disease Progression. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20863706.001).
  • [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 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / light chain 3, human
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44. 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.
  • S100 proteins are Ca(2+)-binding polypeptides involved in the tumourigenesis of several human neoplasms.
  • 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.
  • Moreover, both S100A13 and VEGF-A expression significantly correlated with microvessel density and tumour grading.
  • 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
  • [MeSH-minor] Adult. Aged. Female. Fibroblast Growth Factors / metabolism. Humans. Male. Middle Aged. Severity of Illness Index. Statistics, Nonparametric. Up-Regulation

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  • [Cites] Anticancer Res. 2004 Jul-Aug;24(4):2511-4 [15330206.001]
  • [Cites] J Cell Biol. 2002 Jul 22;158(2):201-8 [12135982.001]
  • [Cites] Adv Exp Med Biol. 2003;530:593-601 [14562756.001]
  • [Cites] Neuropathol Appl Neurobiol. 2000 Feb;26(1):76-90 [10736069.001]
  • [Cites] Acta Neurochir Suppl. 2003;88:169-77 [14531575.001]
  • [Cites] J Biol Chem. 1995 Jan 6;270(1):33-6 [7529229.001]
  • [Cites] Anticancer Res. 2001 Jan-Feb;21(1A):77-88 [11299793.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23 ):2335-42 [15175435.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22217-23 [9712835.001]
  • [Cites] Reprod Biol. 2005 Mar;5(1):51-67 [15821778.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22224-31 [9712836.001]
  • [Cites] Oncology. 2003;64(4):374-9 [12759535.001]
  • [Cites] J Neurosurg. 1998 Mar;88(3):513-20 [9488306.001]
  • [Cites] Anal Quant Cytol Histol. 2000 Jun;22(3):267-74 [10872046.001]
  • [Cites] Q J Nucl Med. 2003 Sep;47(3):149-61 [12897707.001]
  • [Cites] Integr Cancer Ther. 2002 Dec;1(4):327-37 [14664727.001]
  • [Cites] Br J Cancer. 1998 Sep;78(6):765-70 [9743297.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22209-16 [9712834.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6613-25 [14583454.001]
  • [Cites] J Neurooncol. 2000 Oct-Nov;50(1-2):165-72 [11245275.001]
  • [Cites] J Biol Chem. 1985 Sep 25;260(21):11389-92 [3900060.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6549-56 [14528279.001]
  • [Cites] Neurochem Int. 2006 Aug;49(3):294-303 [16519964.001]
  • [Cites] Pancreas. 1998 Aug;17(2):169-75 [9700949.001]
  • [Cites] Oncogene. 2001 Aug 2;20(34):4685-95 [11498791.001]
  • [Cites] Exp Toxicol Pathol. 1995 May;47(2-3):89-94 [7580112.001]
  • [Cites] J Neurooncol. 2004 May;67(3):345-9 [15164991.001]
  • [Cites] Biochim Biophys Acta. 2002 Nov 4;1600(1-2):74-83 [12445462.001]
  • [Cites] J Neurooncol. 2000 Oct-Nov;50(1-2):189-200 [11245279.001]
  • [Cites] J Cell Physiol. 1995 Mar;162(3):388-99 [7860646.001]
  • [Cites] Anticancer Res. 2002 Jul-Aug;22(4):2179-84 [12174901.001]
  • [Cites] J Biol Chem. 2001 Jul 6;276(27):25549-57 [11432880.001]
  • [Cites] Thromb Haemost. 1999 Aug;82(2):748-54 [10605778.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2806-13 [12767094.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 16):15-8 [12516034.001]
  • [Cites] Int J Cancer. 1999 Oct 29;83(3):415-23 [10495436.001]
  • [Cites] Int J Biochem Cell Biol. 2001 Jul;33(7):637-68 [11390274.001]
  • [Cites] Structure. 2000 Feb 15;8(2):175-84 [10673436.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):22544-52 [11410600.001]
  • [Cites] J Cell Biol. 1990 Apr;110(4):1417-26 [1691192.001]
  • [Cites] Am J Hematol. 2002 Apr;69(4):247-54 [11921018.001]
  • [Cites] Front Biosci. 2003 Jan 01;8:d100-16 [12456339.001]
  • [Cites] Int J Cancer. 1996 Nov 4;68(3):325-32 [8903474.001]
  • [Cites] Brain Pathol. 2003 Apr;13(2):133-43 [12744467.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6700-5 [12754378.001]
  • [Cites] J Clin Oncol. 2002 Nov 1;20(21):4368-80 [12409337.001]
  • (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] United States
  • [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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45. Shapiro WR, Carpenter SP, Roberts K, Shan JS: (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma. Expert Opin Biol Ther; 2006 May;6(5):539-45
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  • [Title] (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma.
  • Treatment of malignant glioma is therapeutically challenging.
  • Despite improvements in neurosurgery, radiotherapy and chemotherapy, few patients diagnosed with anaplastic astrocytoma (AA) or glioblastoma multiforme (GBM) (WHO grades 3 and 4, respectively) will live beyond 2 years.
  • Poor survival is due to the highly invasive nature and protected location of these tumours.
  • Most malignant gliomas cannot be completely resected or irradiated due to their ability to infiltrate diffusely into normal brain tissue.
  • Brain tissue is protected from the systemic circulation via the blood-brain barrier (BBB), which impedes entry of water-soluble chemotherapeutic agents into the tumour at therapeutic concentrations. (131)I-chTNT-1/B mAb (Cotara) employs an innovative strategy to treat the invasive portion of the tumour and the core lesion. (131)I-chTNT-1/B mAb is a genetically engineered, radiolabelled, chimeric monoclonal antibody specific for a universal intracellular antigen (i.e., DNA/histone H1 complex) exposed in the necrotic core of malignant gliomas.
  • This antigen provides an abundant, insoluble, non-diffusible anchor for the mAb.
  • Once localised to necrotic regions of the tumour, (131)I-chTNT-1/B mAb delivers a cytotoxic dose of (131)I radiation to the core lesion. (131)I-chTNT-1/B mAb is delivered via convection-enhanced delivery in order to maximise coverage to the tumour and the invasive front of the glial tumour.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Astrocytoma / radiotherapy. Iodine Radioisotopes / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Clinical Trials as Topic. DNA / immunology. DNA / metabolism. Female. Histones / immunology. Histones / metabolism. Humans. Male. Middle Aged. Radioimmunotherapy / methods

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  • (PMID = 16610983.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Histones; 0 / Iodine Radioisotopes; 9007-49-2 / DNA
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46. Erdamar S, Bagci P, Oz B, Dirican A: Correlation of endothelial nitric oxide synthase and vascular endothelial growth factor expression with malignancy in patients with astrocytic tumors. J BUON; 2006 Apr-Jun;11(2):213-6
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  • [Title] Correlation of endothelial nitric oxide synthase and vascular endothelial growth factor expression with malignancy in patients with astrocytic tumors.
  • PURPOSE: Many characteristics of malignant brain tumors (increased vascular permeability, vasodilatation, neovascularisation and free radical injury to the tumor and adjacent normal tissues) are believed to be mediated by nitric oxide (NO) synthetized by endothelial NO synthase (eNOS).
  • Overexpression of vascular endothelial growth factor (VEGF) is associated with several central nervous system (CNS) diseases and tumors.
  • Our aim was to study immunohistochemically the coexpression of eNOS and VEGF in astrocytic tumors and to analyse their possible correlation with tumor grade, angiogenesis and proliferation index.
  • MATERIALS AND METHODS: Sections from 120 randomly selected patients with supratentorial astrocytic tumors [38 glioblastomas (GB), 22 anaplastic astrocytomas (AA) and 20 low-grade astrocytomas (LA)], also including oligodendrogliomas (n=20) and mixed oligoastrocytomas (n=20), were immunostained with monoclonal antibodies for eNOS and VEGF using the avidin-biotin method.
  • The proliferative potential was assessed as the MIB-1 staining index for tumor cells.
  • CONCLUSION: Overexpressions of eNOS and VEGF in astrocytic tumors were significantly correlated with histological grade, proliferative potential and malignant transformation.
  • The expression of VEGF in a necrotic and ischemic tumor such as GB is more intense and diffuse than low-grade astrocytomas.
  • These findings suggest that eNOS overexpression in tumor vasculature would be precipitated by transformation into an angiogenic phenotype in the process of neovascularisation in astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Nitric Oxide Synthase Type III / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Adult. Aged. Humans. Immunohistochemistry. Middle Aged. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology

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  • (PMID = 17318973.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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47. Yoo H, Sohn S, Nam BH, Min HS, Jung E, Shin SH, Gwak HS, Lee SH: The expressions of carbonic anhydrase 9 and vascular endothelial growth factor in astrocytic tumors predict a poor prognosis. Int J Mol Med; 2010 Jul;26(1):3-9
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  • [Title] The expressions of carbonic anhydrase 9 and vascular endothelial growth factor in astrocytic tumors predict a poor prognosis.
  • Hypoxia in the tumor microenvironment triggers a variety of genetic and adoptive responses that regulate tumor growth.
  • Tumor hypoxia is often associated with a malignant phenotype, resistance to therapy, and poor survival.
  • The objectives of this study were to evaluate the expressions of carbonic anhydrase 9 (CA9) and vascular endothelial growth factor (VEGF) in astrocytic gliomas and to relate patterns of expression with prognosis, that is with histological grade and survival.
  • We investigated 78 World Health Organization (WHO) grade II, III, and IV astrocytic gliomas.
  • Fourteen tumors were grade II, 30 were grade III, and 34 were grade IV.
  • There were 3 CA9 positive tumors in grade II (21.4%), 10 in grade III (33.3%), and 27 in grade IV (79.4%).
  • For all tumors and WHO grade II, overall survival was found to be significantly dependent on CA9 expression (p=0.004, p=0.01).
  • Furthermore, VEGF expression was found to be significantly related to tumor grade (p=0.02) and tended to be related to overall survival (p=0.1).
  • Nevertheless, the expressions of CA9 and VEGF were found to be associated with tumor grade and possibly with survival.
  • Further studies on a larger patient population are needed to determine the correlation between the expressions of CA9, and VEGF in astrocytic gliomas and clinical outcome.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Astrocytoma / metabolism. Carbonic Anhydrases / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry / statistics & numerical data. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models

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  • (PMID = 20514415.001).
  • [ISSN] 1791-244X
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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48. Gelpi E, Popovic M, Preusser M, Budka H, Hainfellner J: Pleomorphic xanthoastrocytoma with anaplastic features presenting without GFAP immunoreactivity: implications for differential diagnosis. Neuropathology; 2005 Sep;25(3):241-6
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  • Pleomorphic xanthoastrocytoma (PXA) is an uncommon, usually low-grade, astrocytic tumor.
  • Characteristic histological features include tumor cell pleomorphism and lipidization of tumor cells.
  • In these cases, the differential diagnosis needs to exclude other malignancies, for example, glioblastoma or malignant fibrous histiocytoma.
  • Immunocytochemical detection of GFAP may support exclusion of non-glial neoplasms resembling PXA.
  • A 43-year-old woman was operated on for a left occipital parasagital tumor attached to the dura.
  • Histopathology showed a pleomorphic tumor with moderate mitotic activity and necrosis, lack of GFAP immunoreactivity and ultrastructural detection of premelanosome-like structures.
  • Three years later she had local tumor recurrence and underwent another operation.
  • The recurrent tumor showed similar plain histology as the first specimen.
  • In contrast, anti-GFAP immunoreactivity was now detectable in pleomorphic tumor cells.
  • Focal GFAP staining of tumor cells was now achieved.
  • We conclude that non-standard GFAP staining protocols may enhance sensitivity and thus lead to detection of a low level of GFAP expression in tumor specimens, in which PXA is considered in the differential diagnosis.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Glial Fibrillary Acidic Protein / metabolism
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods. Melanoma / pathology. Microscopy, Confocal. Microscopy, Electron, Transmission. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology

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  • (PMID = 16193842.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein
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49. Pan JW, Zhan RY, Tong Y, Zhou YQ, Zhang M: Expression of endothelial nitric oxide synthase and vascular endothelial growth factor in association with neovascularization in human primary astrocytoma. J Zhejiang Univ Sci B; 2005 Jul;6(7):693-8
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  • [Title] Expression of endothelial nitric oxide synthase and vascular endothelial growth factor in association with neovascularization in human primary astrocytoma.
  • OBJECTIVE: To investigate the relationship between the expression of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and angiogenesis in primary astrocytoma.
  • METHODS: Thirty-seven primary astrocytomas and 4 astrocytic hyperplasia samples were collected and divided into three groups according to histological grade.
  • The intensity of immunoreactivity was graded according to the percentage of positive tumor cells.
  • RESULTS: No eNOS and VEGF were expressed in the astrocytes and vascular endothelium in astrocytic hyperplasia.
  • Lower microvascular density was found in low grade astrocytoma than that in higher grade malignant ones.
  • The expressions of eNOS and VEGF were correlated with microvascular density and tumor malignancy.
  • CONCLUSION: This finding suggests that eNOS and VEGF may have cooperative effect in tumor angiogenesis and play an important role in the pathogenesis of primary astrocytoma.
  • [MeSH-major] Astrocytoma / blood supply. Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged

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  • [Cites] Blood. 2000 Jan 1;95(1):189-97 [10607702.001]
  • [Cites] Cardiovasc Res. 1999 Mar;41(3):773-80 [10435050.001]
  • [Cites] Circ Res. 2000 Apr 28;86(8):892-6 [10785512.001]
  • [Cites] Anal Quant Cytol Histol. 2000 Jun;22(3):267-74 [10872046.001]
  • [Cites] Br J Neurosurg. 2000 Dec;14(6):543-8 [11272032.001]
  • [Cites] Cardiovasc Res. 2001 Feb 16;49(3):568-81 [11166270.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2604-9 [11226286.001]
  • [Cites] J Neurooncol. 2000 Oct-Nov;50(1-2):139-48 [11245273.001]
  • [Cites] Int J Cancer. 2001 Mar 1;91(5):607-11 [11267968.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2001 Jul;281(1):L278-90 [11404271.001]
  • [Cites] Leukemia. 2001 Sep;15(9):1433-41 [11516104.001]
  • [Cites] Ann Anat. 2003 Dec;185(6):549-54 [14704000.001]
  • [Cites] J Clin Invest. 1998 Jun 1;101(11):2567-78 [9616228.001]
  • [Cites] Acta Neuropathol. 1998 Nov;96(5):453-62 [9829808.001]
  • [Cites] Nature. 1999 Jun 10;399(6736):597-601 [10376602.001]
  • [Cites] Neurosurgery. 1999 Jul;45(1):24-8; discussion 29 [10414562.001]
  • [Cites] Anticancer Res. 2000 Jan-Feb;20(1A):299-304 [10769671.001]
  • (PMID = 15973775.001).
  • [ISSN] 1673-1581
  • [Journal-full-title] Journal of Zhejiang University. Science. B
  • [ISO-abbreviation] J Zhejiang Univ Sci B
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC1389807
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50. Choi KC, Kwak SE, Kim JE, Sheen SH, Kang TC: Enhanced glial fibrillary acidic protein-delta expression in human astrocytic tumor. Neurosci Lett; 2009 Oct 9;463(3):182-7
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  • [Title] Enhanced glial fibrillary acidic protein-delta expression in human astrocytic tumor.
  • Astrocytic tumor is one of the most common primary tumors of the adult brain.
  • Although there are several biochemical markers for the categorization of astrocytic tumor, few markers are used for histopathological diagnosis.
  • In tissue samples from patients with low-grade astrocytic tumor (grades I and II), GFAP-delta(+) cells appeared stellate, polygonal or round shape.
  • In tissue samples from patients with high-grade astrocytic tumor (grades III and IV), GFAP-delta(+) cells showed round or spindle shape.
  • GFAP-delta immunoreactivities in grades III and IV astrocytic tumor cells were increased by 1.4- and 1.7-fold in comparison to grade I astrocytic tumor cells.
  • GFAP-delta immunoreactivity was also observed in cell bodies along the margins of astrocytic tumor showing normal histological findings, even though astroglia had normal morphology (showing strong GFAP and glutamine synthase immunoreactivities and a stellate shape with well-developed processes).
  • Furthermore, the malignancy of astrocytic tumor was directly correlated with the degree of GFAP-delta immunoreactivity.
  • These findings suggest that GFAP-delta may be a useful diagnostic marker for the evaluation of functional cataplasia or proliferation of astrocytic tumor.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Glial Fibrillary Acidic Protein / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Alternative Splicing. Child. Female. Glutamate-Ammonia Ligase / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Young Adult

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  • (PMID = 19647039.001).
  • [ISSN] 1872-7972
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; EC 6.3.1.2 / Glutamate-Ammonia Ligase
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51. Kaloshi G, Mokhtari K, Carpentier C, Taillibert S, Lejeune J, Marie Y, Delattre JY, Godbout R, Sanson M: FABP7 expression in glioblastomas: relation to prognosis, invasion and EGFR status. J Neurooncol; 2007 Sep;84(3):245-8
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  • FABP7 expression was associated with pure GBM histology and shorter survival (15.7 months versus 21.5 months).
  • Nuclear expression of FABP7 was more specifically related to EGFR amplification and more invasive tumors.
  • These data, although they need to be confirmed by further studies, support the relation between FABP7, astrocytic features, invasion and poor prognosis and suggests that EGFR amplification is associated with nuclear translocation of FABP7.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Carrier Proteins / biosynthesis. Glioblastoma / pathology. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Nucleus / metabolism. Cytoplasm / metabolism. Fatty Acid-Binding Protein 7. Female. Gene Amplification. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Invasiveness / pathology. Prognosis. Protein Transport / physiology

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  • [Cites] J Neuropathol Exp Neurol. 2001 Sep;60(9):863-71 [11556543.001]
  • [Cites] BMC Clin Pathol. 2005 Jul 15;5:6 [16018821.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]
  • [Cites] BMC Cancer. 2006 Apr 19;6:97 [16623952.001]
  • [Cites] Oncogene. 2007 Apr 26;26(19):2695-706 [17057735.001]
  • [Cites] Cancer. 2006 May 15;106(10 ):2218-23 [16568472.001]
  • [Cites] Oncogene. 1998 Apr 16;16(15):1955-62 [9591779.001]
  • [Cites] Prog Lipid Res. 2004 Jul;43(4):328-49 [15234551.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 19;102(16):5814-9 [15827123.001]
  • [Cites] Genes Dev. 2005 May 1;19(9):1028-33 [15879553.001]
  • [Cites] Neuron. 1994 Apr;12 (4):895-908 [8161459.001]
  • (PMID = 17415524.001).
  • [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] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / FABP7 protein, human; 0 / Fatty Acid-Binding Protein 7; 0 / Tumor Suppressor Proteins; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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52. Comincini S, Paolillo M, Barbieri G, Palumbo S, Sbalchiero E, Azzalin A, Russo MA, Schinelli S: Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens. J Biomed Biotechnol; 2009;2009:924565
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  • [Title] Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens.
  • To verify if this correlation was conserved in gliomas, PTEN and MMP9 expression was further investigated in an additional panel of 16 anaplastic astrocytoma specimens and, in parallel, in different human normal and astrocytic tumor cell lines.
  • In conclusion, this gene expression survey highlighted that the combined measurement of PTEN and MMP9 transcripts might represent a novel reliable tool for the differential diagnosis of high-grade gliomas, and it also suggested a functional link involving these genes in glial tumors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Glioma / diagnosis. Glioma / enzymology. Matrix Metalloproteinase 9 / metabolism. PTEN Phosphohydrolase / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

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  • [Cites] Genome Biol. 2001;2(1):RESEARCH0003 [11178280.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3286-94 [18451155.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6885-91 [11559565.001]
  • [Cites] Brain Pathol. 2002 Jan;12(1):108-16 [11771519.001]
  • [Cites] Neuro Oncol. 2002 Jul;4(3):196-211 [12084351.001]
  • [Cites] Anal Biochem. 2002 Oct 15;309(2):293-300 [12413463.001]
  • [Cites] Biotechniques. 2004 Jan;36(1):84-6, 88, 90-1 [14740490.001]
  • [Cites] Science. 2004 Feb 20;303(5661):1179-81 [14976311.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):1943-50 [15026328.001]
  • [Cites] Curr Opin Oncol. 1999 May;11(3):162-7 [10328589.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):137-60 [15674475.001]
  • [Cites] Brain Tumor Pathol. 2004;21(3):105-12 [15696970.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):686-91 [15705860.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Apr 19;102(16):5814-9 [15827123.001]
  • [Cites] Biochim Biophys Acta. 2005 Aug 1;1751(1):110-7 [16054021.001]
  • [Cites] N Engl J Med. 2005 Nov 10;353(19):2012-24 [16282176.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):867-74 [16424019.001]
  • [Cites] Cancer Sci. 2006 May;97(5):341-7 [16630129.001]
  • [Cites] Int J Oncol. 2006 Jul;29(1):73-81 [16773187.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 May;65(5):516-27 [16772875.001]
  • [Cites] J Neurooncol. 2006 Aug;79(1):1-7 [16557350.001]
  • [Cites] Curr Med Chem. 2006;13(29):3483-92 [17168718.001]
  • [Cites] Oncogene. 2007 Mar 29;26(14):2006-16 [17001310.001]
  • [Cites] Am J Pathol. 2007 May;170(5):1445-53 [17456751.001]
  • [Cites] Cancer. 2007 Jul 1;110(1):13-24 [17520692.001]
  • [Cites] BMC Genomics. 2007;8:243 [17640361.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):7960-5 [17804702.001]
  • [Cites] Annu Rev Pathol. 2006;1:97-117 [18039109.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):779-86 [11549567.001]
  • (PMID = 19657395.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2718324
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53. Comincini S, Chiarelli LR, Zelini P, Del Vecchio I, Azzalin A, Arias A, Ferrara V, Rognoni P, Dipoto A, Nano R, Valentini G, Ferretti L: Nuclear mRNA retention and aberrant doppel protein expression in human astrocytic tumor cells. Oncol Rep; 2006 Dec;16(6):1325-32
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  • [Title] Nuclear mRNA retention and aberrant doppel protein expression in human astrocytic tumor cells.
  • It is abundant in testis and, unlike PrP, it is expressed at low levels in the adult central nervous system (CNS).
  • Besides, Dpl overexpression correlates with some prion-disease pathological features, such as ataxia and death of cerebellar neurons.
  • Recently, ectopic expression of doppel was found in two different tumor types, specifically in glial and haematological cancers.
  • Immunohistochemistry experiments demonstrated that Dpl was mainly localised in the cytoplasm of the astrocytic tumor cells, and that it failed to be GPI-anchored to the cell membrane.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cell Nucleus / metabolism. Prions / biosynthesis. RNA, Messenger / metabolism
  • [MeSH-minor] Blotting, Northern. Blotting, Western. Cell Line, Tumor. Cytoplasm / metabolism. GPI-Linked Proteins. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Protein Biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transfection

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  • (PMID = 17089057.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions; 0 / RNA, Messenger
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54. Ono A, Kanno H, Hayashi A, Nishimura S, Kyuma Y, Sato H, Ito S, Shimizu N, Chang CC, Gondo G, Yamamoto I, Sasaki T, Tanaka M: Collagen gel matrix assay as an in vitro chemosensitivity test for malignant astrocytic tumors. Int J Clin Oncol; 2007 Apr;12(2):125-30
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  • [Title] Collagen gel matrix assay as an in vitro chemosensitivity test for malignant astrocytic tumors.
  • METHODS: We examined the chemosensitivites for four anticancer agents - 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3 (2-chloroethyl)-3-nitrosourea hydrochloride (ACNU), carboplatin, cisplatin, and etoposide - of 43 malignant astrocytic tumors (21 anaplastic astrocytomas and 22 glioblastomas) by using a collagen gel matrix assay, and we also determined the survival periods of the tumor-bearing patients.
  • The chemosensitivity was evaluated in terms of the growth inhibition rate, using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) method.
  • RESULTS: For the anaplastic astrocytomas, the mean growth inhibitory rate was 33.2% with cisplatin, 37.2% with carboplatin, 28.0% with ACNU, and 24.8% with etoposide.
  • The median overall and progression-free survivals of anaplastic astrocytoma-bearing patients who had undergone chemotherapy with two anticancer drugs, both of which showed significant anticancer activity (growth inhibitory rate >30%) were significantly longer than those of the patients who had been treated with two drugs, one or both of which did not show significant anticancer activity.
  • Individual chemotherapy for malignant astrocytic tumors, based on chemosensitivity data, could contribute to longer survival, particularly in anaplastic astrocytoma-bearing patients.
  • [MeSH-minor] Adult. Aged. Central Nervous System Neoplasms / drug therapy. Disease Progression. Disease-Free Survival. Drug Screening Assays, Antitumor. Female. Fibrin Foam. Follow-Up Studies. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Japan. Karnofsky Performance Status. Male. Middle Aged. Sensitivity and Specificity. Survival Analysis. Tissue Adhesives. Treatment Outcome. Tumor Burden / drug effects. Tumor Cells, Cultured / drug effects

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  • [Cites] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2694-8 [3458228.001]
  • [Cites] Prog Clin Biol Res. 1980;48:259-76 [7208520.001]
  • [Cites] J Neurooncol. 1983;1(2):149-66 [6088712.001]
  • [Cites] Int J Urol. 2005 Jan;12(1):67-72 [15661056.001]
  • [Cites] Lancet. 1982 Apr 17;1(8277):885-7 [6122104.001]
  • [Cites] Jpn J Cancer Res. 1991 May;82(5):607-12 [1648053.001]
  • [Cites] Eur J Cancer. 1996 Feb;32A(2):226-30 [8664032.001]
  • [Cites] Br J Cancer. 1983 Feb;47(2):205-14 [6297528.001]
  • [Cites] Urol Res. 1993 Mar;21(2):83-8 [8503152.001]
  • [Cites] Cancer Treat Rep. 1986 Dec;70(12):1379-82 [3791251.001]
  • [Cites] J Cancer Res Clin Oncol. 1999 Aug-Sep;125(8-9):481-6 [10480340.001]
  • [Cites] J Neurooncol. 1994;21(3):225-32 [7699417.001]
  • [Cites] Cancer Res. 1985 Sep;45(9):4200-5 [4028010.001]
  • [Cites] Cancer Res. 1982 Mar;42(3):992-8 [7199383.001]
  • (PMID = 17443280.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fibrin Foam; 0 / Tissue Adhesives; 0S726V972K / Nimustine; 6PLQ3CP4P3 / Etoposide; 9007-34-5 / Collagen; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
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55. Daumas-Duport C, Koziak M, Miquel C, Nataf F, Jouvet A, Varlet P: [Reappraisal of the Sainte-Anne Hospital classification of oligodendrogliomas in view of retrospective studies]. Neurochirurgie; 2005 Sep;51(3-4 Pt 2):247-53
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  • [Transliterated title] Classification des oligodendrogliomes de l'hôpital Sainte-Anne. Mise au point à l'usage des études rétrospectives.
  • PURPOSE: Definition of homogeneous tumor groups of oligodendrogliomas or oligo-astrocytomas is a basic condition for an adequate evaluation and comparison of the results of treatments in patients from various institutions.
  • However, increasing discordances are observed in the histological diagnosis of these tumors.
  • PATIENTS AND METHODS: This study included 251 adult patients in whom a SA grade A or B oligodendroglioma or oligo-astrocytoma was newly diagnosed at our institution from 1984 to 2003.
  • Routine histological preparations and post-contrast preoperative MRI/CT-scan were simultaneously reviewed in order to assess the impact on survival of the following features: presence or absence of a polymorphous or gemistocytic astrocytic component, of necrosis and of contrast enhancement (CH); endothelial hyperplasia (EH) assessed as absent, present minor (HE+) or (HE++) when conform to the threshold of HE defined in the SA grading system of oligodendrogliomas.
  • The tumors were graded A: no CH and no EH; in B: CH and /or HE++, and A/B: EH + but no CE.
  • RESULTS: 70.1% of the tumors were classified as "pure" oligodendroglioma, 19.5% as "polymorphous oligo-astroastrocytoma" and 10.3% as "gemistocytic oligo-astrocytoma".
  • In grade A, or B tumors, the presence of a polymorphous or a gemistocytic component had no significant influence on survival; however respectively 53% and 65% of these tumours versus 32% of "pure" oligodendrogliomas were grade B at the time of diagnosis.
  • After regrouping of the histological subtypes and of the tumors with HE+ or absent, the series included 153 oligodendrogliomas grade A and 98 grade B.
  • Survival in patients with grade A versus grade B tumors was respectively 142 versus 52 months (p<0.0001).
  • In grade B tumors, necrosis had no significant influence on survival.
  • In tumors with or without CE, patient survival was respectively 148 versus 40 months (p<0.0001).
  • On post contrast MRI done in 235 patients, only 7 tumors (3%) were grade A/B (EH++ but no CH).
  • 1) tumors diagnosed according to the Ste-Anne classification as oligodendroglioma or oligo-astrocytoma be regrouped in a unique category, 2) independent of their histological type and grade according to the WHO, gliomas that do not show CE be regrouped with SA oligodendrogliomas grade A, 3) concerning gliomas that show CE on MRI: oligodendrogliomas or oligo-astrocytomas WHO grade II or III, as well as WHO secondary glioblastomas or glioblastomas with an oligodendroglial component, be regrouped with SA oligodendrogliomas grade B; however tumors that show ring-like CE surrounding large foci of necrosis and finger-like "peritumoral" edema should be excluded or analysed separately.
  • [MeSH-major] Brain / pathology. Brain / radiography. Brain Neoplasms / classification. Glioma / classification. Oligodendroglioma / classification
  • [MeSH-minor] Adult. France. Hospitals. Humans. Magnetic Resonance Imaging. Neoplasm Staging. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed

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  • (PMID = 16292168.001).
  • [ISSN] 0028-3770
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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56. Novillo López ME, Gómez-Ibáñez A, Rosenfeld M, Dalmau J: [Gliomatosis cerebri: review of 22 patients]. Neurologia; 2010 Apr;25(3):168-73
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  • [Transliterated title] Gliomatosis cerebral: estudio de 22 pacientes.
  • INTRODUCTION: gliomatosis cerebri is a diffuse astrocytic neoplasm that involves more than two lobes of the brain.
  • RESULTS: we identified 17 men and 5 women (median age 54 years) seen in a Division of Neuro-oncology over a 6 year period.
  • All patients had bilateral involvement; the regions involved included, temporal (19), basal ganglia (18), frontal (17), parietal (17), corpus callosum (10), and occipital (9).
  • Nine patients were diagnosed within the first month of symptom development, 11 between the first month and 1 year, and 2 after one year.
  • In this study de median survival of patients who received treatment was similar to that reported in series of glioblastoma multiforme.
  • [MeSH-major] Brain Neoplasms. Neoplasms, Neuroepithelial
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Retrospective Studies. Young Adult

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  • [Copyright] Published by Elservier España, S.L. All rights reserved.
  • (PMID = 20492863.001).
  • [ISSN] 0213-4853
  • [Journal-full-title] Neurología (Barcelona, Spain)
  • [ISO-abbreviation] Neurologia
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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57. Murakami R, Hirai T, Sugahara T, Fukuoka H, Toya R, Nishimura S, Kitajima M, Okuda T, Nakamura H, Oya N, Kuratsu J, Yamashita Y: Grading astrocytic tumors by using apparent diffusion coefficient parameters: superiority of a one- versus two-parameter pilot method. Radiology; 2009 Jun;251(3):838-45
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  • [Title] Grading astrocytic tumors by using apparent diffusion coefficient parameters: superiority of a one- versus two-parameter pilot method.
  • PURPOSE: To assess the utility of both minimum apparent diffusion coefficients (ADCs) and ADC difference values for grading astrocytic tumors at magnetic resonance imaging.
  • Fifty patients (23 male patients, 27 female patients; median age, 53 years) with newly diagnosed astrocytic tumors were evaluated.
  • Two observers blinded to clinical information independently measured the ADCs by manually placing three to five regions of interest (40-60 mm(2)) within the solid tumor either with or without contrast material-enhanced components and calculated the average ADC.
  • Minimum and maximum ADCs were selected, and the difference between them was recorded as the ADC difference value.
  • These ADC values were used as the parameters for tumor grading and were compared by using the Kruskal-Wallis test and receiver operating characteristic (ROC) curve analysis.
  • RESULTS: According to ROC analyses for distinguishing tumor grade, minimum ADCs showed the largest areas under the ROC curve.
  • Minimum ADCs optimally helped distinguish grade 1 from higher-grade tumors at a cutoff value of 1.47 x 10(-3) mm(2)/sec and grade 4 from lower-grade tumors at a cutoff value of 1.01 x 10(-3) mm(2)/sec (P < .001 for both).
  • ADC difference values helped distinguish grade 2 from grade 3 tumors at a cutoff value of 0.31 x 10(-3) mm(2)/sec (P < .001).
  • When tumors were graded by using the combined minimum ADC and ADC difference cutoff values mentioned above (the two-parameter method), the following positive predictive values were obtained: grade 1 tumors, 73% (eight of 11); grade 2 tumors, 100% (five of five); grade 3 tumors, 67% (eight of 12); and grade 4 tumors, 91% (20 of 22).
  • CONCLUSION: Using a combination of minimum ADCs and ADC difference values (the two-parameter method) facilitates the accurate grading of astrocytic tumors.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Contrast Media. Female. Gadolinium DTPA. Humans. Image Interpretation, Computer-Assisted. Male. Middle Aged. Neoplasm Staging. Pilot Projects. ROC Curve. Retrospective Studies

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  • (PMID = 19318585.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; K2I13DR72L / Gadolinium DTPA
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58. Mennel HD, Lell B: Ganglioside (GD2) expression and intermediary filaments in astrocytic tumors. Clin Neuropathol; 2005 Jan-Feb;24(1):13-8
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  • [Title] Ganglioside (GD2) expression and intermediary filaments in astrocytic tumors.
  • The search of proliferation markers in astrocytic tumors that may serve as targets for therapeutic interventions, is in full progress.
  • Membrane-bound signal transducers for growth factors are amongst the substances of interest.
  • Gangliosides are lipid-sugar compounds localized on the cell membrane that are thought to modify pertinent signals and, therefore, may influence a variety of functions in normal and pathologic conditions including those that act upon tumor growth.
  • Intracranial supratentorial astrocytic gliomas of the adult represent a tumor group, that may be divided into three grades of malignancy, the most anaplastic member being the glioblastoma.
  • In earlier investigations, it had been shown that there is a tendency towards formation of more simple members of the ganglioside family with ongoing malignancy of those tumors.
  • Yet, the results were only partly congruent and the correlation to tumor grades rather loose.
  • We, therefore, investigated the occurrence of triaose gangliosides within these tumors in situ by immunohistochemistry.
  • Thus, the conclusion must be drawn that the correlation of ganglioside patterns to the proliferation of astrocytic tumors is as poor as that of GFAP or vimentin expression, respectively.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gangliosides / metabolism. Intermediate Filaments / metabolism

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  • (PMID = 15696779.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Gangliosides; 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin; 65988-71-8 / ganglioside, GD2
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59. Pittock SJ, Lennon VA: Aquaporin-4 autoantibodies in a paraneoplastic context. Arch Neurol; 2008 May;65(5):629-32
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  • Its antigen is the astrocytic water channel aquaporin-4; NMO-IgG has not been described in a cancer context.
  • (1) 31 patients (88% female) identified incidentally among 180 000 patients evaluated for paraneoplastic autoantibodies and (2) 141 patients identified through physician-requested serological evaluation for a suspected NMO-spectrum disorder.
  • An NMO-spectrum disorder was diagnosed in 26 patients (93%), of whom 6 had a neoplasm (5 carcinomas [2 breast, 1 lung, 1 thymic, and 1 uterine cervical] and 1 B-cell lymphoma) and 1 had monoclonal gammopathy.
  • In 4 patients, NMO-related symptoms followed neoplasia detection (median, 14 [range 3-18] months), and in 2 patients, symptoms preceded neoplasia detection (by 5 and 3 months).
  • Two patients had carcinoma (1 breast and 1 lung) without neurological evidence of an NMO-spectrum disorder.
  • In the second group, neoplasms were recorded in 7 seropositive patients (5.0%) with a clinically diagnosed NMO-spectrum disorder: 3 carcinomas (all breast), 1 thyroid Hürthle cell, 1 carcinoid, 1 pituitary somatotropinoma, and 1 B-cell lymphoma.
  • [MeSH-major] Aquaporin 4 / immunology. Autoantibodies / immunology. Autoimmune Diseases of the Nervous System / immunology. Neoplasms / immunology. Paraneoplastic Syndromes, Nervous System / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers / analysis. Comorbidity. Female. Humans. Immunoglobulin G / blood. Immunoglobulin G / immunology. Male. Middle Aged. Neuromyelitis Optica / immunology. Paraproteinemias / epidemiology. Paraproteinemias / immunology. Paraproteinemias / physiopathology. Predictive Value of Tests. Retrospective Studies

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  • [ErratumIn] Arch Neurol. 2008 Oct;65(10):1394
  • (PMID = 18474738.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aquaporin 4; 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G
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60. Woodworth G, McGirt MJ, Samdani A, Garonzik I, Olivi A, Weingart JD: Accuracy of frameless and frame-based image-guided stereotactic brain biopsy in the diagnosis of glioma: comparison of biopsy and open resection specimen. Neurol Res; 2005 Jun;27(4):358-62
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  • OBJECTIVES: Tissue heterogeneity and rapid tumor progression may decrease the accuracy a prognostic value of stereotactic brain biopsy in the diagnosis of gliomas.
  • Correct tumor grading is therefore dependent on the accuracy of biopsy needle placement.
  • METHODS: The diagnoses of 21 astrocytic brain tumors were derived using image-guided stereotactic biopsy (12 frame-based, nine frameless) and followed by open resection of the lesion 1.5 (0.5-4) months later.
  • The histologic diagnoses yielded by the biopsy were compared with subsequent histologic diagnosis from open tumor resection.
  • RESULTS: Histology of 21 stereotactic biopsies accurately represented the greater lesion at open resection a median of 45 days later in 16 (76%) cases and correctly guided therapy in 19 (91%) cases.
  • Biopsy accuracy of frameless versus frame-based stereotaxis was similar (89 versus 66%, p=0.21).
  • In three (14%) cases, biopsy specimens were adequate to diagnose glioma; however, histology was insufficient for definitive tumor grading.
  • Biopsy of new onset glioblastoma multiforme (GBM) yielded necrosis/gliosis and was termed non-diagnostic in one patient.
  • Tumors <50 cm(3) were 8-fold less likely to accurately represent the grade of the entire lesion at resection compared with lesions <50 cm(3) (OR, 8.8; 95% CI, 0.9-100, p=0.05).
  • Large tumor volume had a higher incidence of non-concordance.
  • Increasing the number of specimens taken through the long dimension of large tumors may improve diagnostic accuracy.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Magnetic Resonance Imaging. Stereotaxic Techniques
  • [MeSH-minor] Adult. Biopsy. Female. Humans. Image Processing, Computer-Assisted / methods. Male. Middle Aged. Neurosurgical Procedures / methods. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity. Surgery, Computer-Assisted / methods

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  • (PMID = 15949232.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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61. Angileri FF, Aguennouz M, Conti A, La Torre D, Cardali S, Crupi R, Tomasello C, Germanò A, Vita G, Tomasello F: Nuclear factor-kappaB activation and differential expression of survivin and Bcl-2 in human grade 2-4 astrocytomas. Cancer; 2008 May 15;112(10):2258-66
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  • [Title] Nuclear factor-kappaB activation and differential expression of survivin and Bcl-2 in human grade 2-4 astrocytomas.
  • It is triggered by the interaction of the tumor necrosis factor (TNF) with its receptors and recruitment of the intermediate factor TNF-receptor associated factor (TRAF) 2.
  • The authors investigated the activity of NF-kappaB, and the mRNA expression of TNFalpha, TNFalpha receptor, TRAF1, TRAF2, and TRAF-associated NF-kappaB activator (TANK), and the antiapoptotic genes Bcl-2, c-IAP 1 and 2, and Survivin in human astrocytic tumors.
  • RESULTS: NF-kappaB hyperactivity was detected in tumor samples. mRNA of antiapoptotic genes, particularly BCL-2 and Survivin, was hyperexpressed in gliomas.
  • NF-kappaB-activated antiapoptotic genes were hyperexpressed in tumor samples, but showed a differential expression with higher levels of Bcl-2 in LGAs and higher levels of Survivin in GBMs.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Microtubule-Associated Proteins / metabolism. NF-kappa B / metabolism. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Adult. Aged. Case-Control Studies. Cell Differentiation. Electrophoretic Mobility Shift Assay. Female. Humans. Inhibitor of Apoptosis Proteins / genetics. Inhibitor of Apoptosis Proteins / metabolism. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. TNF Receptor-Associated Factor 1 / genetics. TNF Receptor-Associated Factor 1 / metabolism. TNF Receptor-Associated Factor 2 / genetics. TNF Receptor-Associated Factor 2 / metabolism. Tankyrases / genetics. Tankyrases / metabolism

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  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18327814.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / TANK protein, human; 0 / TNF Receptor-Associated Factor 1; 0 / TNF Receptor-Associated Factor 2; EC 2.4.2.30 / Tankyrases; EC 2.4.4.30 / TNKS protein, human
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62. Nawashiro H, Otani N, Shinomiya N, Fukui S, Ooigawa H, Shima K, Matsuo H, Kanai Y, Endou H: L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors. Int J Cancer; 2006 Aug 1;119(3):484-92
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  • [Title] L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors.
  • We have investigated for the first time, the expression of the transporter in the human primary astrocytic tumor tissue from 60 patients.
  • BCH inhibited the growth of C6 glioma cells in vitro and in vivo in a dose-dependent manner.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Large Neutral Amino Acid-Transporter 1 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acids, Cyclic / pharmacology. Animals. Antigens, CD98 Heavy Chain / analysis. Cell Line, Tumor. Cell Survival / drug effects. Child. Female. Glioma / drug therapy. Glioma / mortality. Glioma / pathology. Humans. Immunohistochemistry. Infant, Newborn. Male. Middle Aged. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / mortality. Neoplasms, Experimental / pathology. Rats. Rats, Wistar. Survival Analysis. Survival Rate

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16496379.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Cyclic; 0 / Antigens, CD98 Heavy Chain; 0 / Large Neutral Amino Acid-Transporter 1; 20448-79-7 / 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid
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63. Parafiniuk D, Jezewski D, Nowacki P: [Malignant astrocytoma as a recurrance of astrocytoma II WHO after 13 years. Case report and literature review]. Ann Acad Med Stetin; 2010;56(2):45-50
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  • [Title] [Malignant astrocytoma as a recurrance of astrocytoma II WHO after 13 years. Case report and literature review].
  • Astrocytomas--neroepithelial originated tumors that belong to the big, differential group of tumors, which derive from astrocytic glial.
  • They include slow growing tumors such as fibillary astrocytoma or very malignant glioblastoma multiforme.
  • The case which is being presented is of a forty nine year old woman operated in July 1997 because of a protoplasmic astrocytoma II WHO in the left frontal lobe.
  • 13 years later epilepsy seizures with syncope showed up again.
  • Due to this adverse event MRI was ordered and suspicion of tumor recurrence was put forward.
  • According to literature, the factors regarding remission time, tumor malignancy and therapeutic aim were analyzed.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Adult. Astrocytoma. Female. Frontal Lobe. Humans. Reoperation. Seizures / etiology

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  • (PMID = 21473001.001).
  • [ISSN] 1427-440X
  • [Journal-full-title] Annales Academiae Medicae Stetinensis
  • [ISO-abbreviation] Ann Acad Med Stetin
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Poland
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64. Kirsch M, Mörz M, Pinzer T, Schackert HK, Schackert G: Frequent loss of the CDKN2C (p18INK4c) gene product in pituitary adenomas. Genes Chromosomes Cancer; 2009 Feb;48(2):143-54
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  • Genomic alterations of cyclin-dependent kinase inhibitors have been demonstrated in a variety of tumor types including brain tumors.
  • Among them, the cyclin-dependent kinase inhibitor 2A (CDKN2A or p16(INK4a)) gene has been shown to be frequently deleted or inactivated in astrocytic tumors.
  • LOH at the CDKN2C gene locus was detected in 25% of pituitary adenomas, whereas the RB1 and CDKN2A loci were altered in only 10%.
  • This is the first report to describe that the tumor suppressor gene CDKN2C is frequently targeted by genomic alterations in pituitary adenoma.
  • [MeSH-major] Adenoma / genetics. Cyclin-Dependent Kinase Inhibitor p18 / genetics. Gene Expression Regulation, Neoplastic. Pituitary Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. DNA Methylation / genetics. Female. Humans. Immunohistochemistry. Infant. Loss of Heterozygosity. Male. Middle Aged. Pituitary Gland / metabolism. Promoter Regions, Genetic. Retinoblastoma Protein / genetics. Retinoblastoma Protein / metabolism. Sequence Analysis, DNA. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Protein p14ARF / metabolism


65. Balss J, Meyer J, Mueller W, Korshunov A, Hartmann C, von Deimling A: Analysis of the IDH1 codon 132 mutation in brain tumors. Acta Neuropathol; 2008 Dec;116(6):597-602
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  • [Title] Analysis of the IDH1 codon 132 mutation in brain tumors.
  • We analyzed the genomic region spanning wild type R132 of IDH1 by direct sequencing in 685 brain tumors including 41 pilocytic astrocytomas, 12 subependymal giant cell astrocytomas, 7 pleomorphic xanthoastrocytomas, 93 diffuse astrocytomas, 120 adult glioblastomas, 14 pediatric glioblastomas, 105 oligodendrogliomas, 83 oligoastrocytomas, 31 ependymomas, 58 medulloblastomas, 9 supratentorial primitive neuroectodermal tumors, 17 schwannomas, 72 meningiomas and 23 pituitary adenomas.
  • The very high frequency of IDH1 mutations in WHO grade II astrocytic and oligodendroglial gliomas suggests a role in early tumor development.
  • [MeSH-major] Brain Neoplasms / genetics. Isocitrate Dehydrogenase / genetics. Mutation
  • [MeSH-minor] Astrocytoma / genetics. Astrocytoma / pathology. Base Sequence. DNA Mutational Analysis. Disease Progression. Gene Frequency. Glioblastoma / genetics. Glioblastoma / pathology. Glioma / etiology. Glioma / pathology. Humans. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Polymerase Chain Reaction

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  • (PMID = 18985363.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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66. Jha P, Agarwal S, Pathak P, Srivastava A, Suri V, Sharma MC, Chosdol K, Srivastava T, Gupta D, Gupta A, Suri A, Sarkar C: Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India. Cancer Genet Cytogenet; 2010 Apr 15;198(2):126-34
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  • [Title] Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India.
  • There are few reports of loss of heterozygosity (LOH) of 1p and 19q in astrocytic tumors, especially glioblastoma multiforme (GBM).
  • We evaluated 1p and 19q (either or both) heterozygosity status in 71 astrocytomas, including 6 pediatric cases: 20 diffuse astrocytomas (DA), 9 anaplastic astrocytomas (AA), and 42 GBM.
  • In the GBMs, p53 protein expression was assessed by immunohistochemistry and epidermal growth factor receptor (EGFR) gene amplification by fluorescence in situ hybridization; TP53 sequencing was done in 15 of the GBMs.
  • In adults, LOH of 1p or 19q was detected in 16% of DAs and 50% of GBMs; none of the AAs showed this alteration.
  • Thus, 1p and 19q LOH can occur in astrocytic tumors, most commonly in secondary GBMs without morphological correlation with an oligodendroglial histology.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Gene Amplification. Genes, erbB-1. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Child. Female. Heterozygote. Humans. India. Loss of Heterozygosity. Male. Middle Aged. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20362227.001).
  • [ISSN] 1873-4456
  • [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
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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67. Choi YL, Kim CJ, Matsuo T, Gaetano C, Falconi R, Suh YL, Kim SH, Shin YK, Park SH, Chi JG, Thiele CJ: HUlip, a human homologue of unc-33-like phosphoprotein of Caenorhabditis elegans; Immunohistochemical localization in the developing human brain and patterns of expression in nervous system tumors. J Neurooncol; 2005 May;73(1):19-27
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  • [Title] HUlip, a human homologue of unc-33-like phosphoprotein of Caenorhabditis elegans; Immunohistochemical localization in the developing human brain and patterns of expression in nervous system tumors.
  • HUlip is a human homologue of a C. elegans gene, unc-33, that is developmentally regulated during maturation of the nervous system.
  • HUlip is highly expressed only in the fetal brain and spinal cord, and is undetected in the adult brain.
  • The purpose of this study was to investigate the pattern of hUlip expression in the developing human brain and nervous system tumors.
  • Ten human brains at different developmental stages and 118 cases of nervous system tumor tissues were examined by immunohistochemistry.
  • Twelve related tumor cell lines were also analyzed by northern blotting and immunoblotting.
  • Among tumors, hUlip expression was easily detected in tumor cells undergoing neuronal differentiation such as ganglioneuroblastomas and ganglioneuromas.
  • Furthermore, hUlip immunoreactivity was also found in various brain tumors showing neuronal differentiation: central neurocytomas (6 of 6 cases were positive), medulloblastomas (5/11), atypical teratoid rhabdoid tumor (1/1) and gangliogliomas (4/7).
  • Some astrocytic tumors also showed weak positivity: astrocytomas (1 of 5 cases), anaplastic astrocytomas (2/5), and glioblastomas (3/11).
  • The results of this study indicate that the expression of hUlip protein is distinctly restricted to the late fetal and early postnatal periods of human nervous system development and to certain subsets of nervous system tumors.
  • The exact function of hUlip needs to be further clarified; yet the results of our study strongly imply that hUlip function is important in human nervous system development and its aberrant expression in various types of nervous system tumors suggests a role of hUlip as an oncofetal neural antigen.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Developmental / physiology. Gene Expression Regulation, Neoplastic / physiology. Muscle Proteins / metabolism
  • [MeSH-minor] Astrocytes / cytology. Astrocytes / metabolism. Cell Differentiation / genetics. Cell Differentiation / physiology. Cell Line, Tumor. Female. Gestational Age. Humans. Immunohistochemistry. Male. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neurons / cytology. Neurons / metabolism

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  • [Cites] Eur J Neurosci. 1999 Dec;11(12):4226-32 [10594648.001]
  • [Cites] Lab Invest. 1990 Apr;62(4):498-509 [2159086.001]
  • [Cites] Brain Dev. 1998 Mar;20(2):88-94 [9545178.001]
  • [Cites] Brain Res Dev Brain Res. 1997 Sep 20;102(2):305-8 [9352115.001]
  • [Cites] Genetics. 1992 Nov;132(3):675-89 [1468626.001]
  • [Cites] J Neuroophthalmol. 2001 Sep;21(3):164-7 [11725180.001]
  • [Cites] Brain Dev. 1999 Jan;21(1):41-50 [10082252.001]
  • [Cites] Dev Biol. 1985 Sep;111(1):158-70 [3928418.001]
  • [Cites] Annu Rev Neurosci. 1995;18:385-408 [7605067.001]
  • [Cites] Brain Res. 2002 Oct 18;952(2):153-8 [12376175.001]
  • [Cites] J Neurosci. 2003 Apr 1;23(7):2815-23 [12684468.001]
  • [Cites] Neuron. 1994 Oct;13(4):805-11 [7524558.001]
  • [Cites] Lab Invest. 1989 Dec;61(6):635-43 [2557487.001]
  • [Cites] Biol Neonate. 1996;69(4):257-67 [8724654.001]
  • [Cites] Cereb Cortex. 1996 Nov-Dec;6(6):794-806 [8922336.001]
  • [Cites] J Natl Cancer Inst. 1984 Aug;73(2):405-16 [6589432.001]
  • [Cites] Gene. 1996 Nov 21;180(1-2):157-63 [8973361.001]
  • [Cites] Gene. 2000 Jan 25;242(1-2):175-82 [10721710.001]
  • [Cites] Hum Genet. 1996 Feb;97(2):240-3 [8566961.001]
  • [Cites] J Biol Chem. 1997 May 2;272(18):12195-201 [9115293.001]
  • [Cites] J Neurosci. 1995 Oct;15(10):6757-66 [7472434.001]
  • [Cites] Int J Cancer. 1990 Jun 15;45(6):1079-87 [2161798.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Oct;60(10):984-93 [11589429.001]
  • [Cites] J Neurosci. 1996 Oct 1;16(19):6197-207 [8815901.001]
  • [Cites] Acta Neuropathol. 1986;70(3-4):320-6 [3020862.001]
  • [Cites] Cancer. 1992 Apr 15;69(8):2197-211 [1544125.001]
  • [Cites] J Comp Neurol. 1995 May 8;355(3):369-79 [7636019.001]
  • [Cites] Neuropathol Appl Neurobiol. 1984 Jan-Feb;10(1):63-75 [6738805.001]
  • [Cites] Nature. 1995 Aug 10;376(6540):509-14 [7637782.001]
  • [Cites] Nat Biotechnol. 1997 Jun;15(6):574-80 [9181582.001]
  • [Cites] Neuron. 1993 Aug;11(2):321-31 [8394722.001]
  • [Cites] J Biol Chem. 1995 Oct 20;270(42):24725-31 [7559588.001]
  • (PMID = 15933812.001).
  • [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] United States
  • [Chemical-registry-number] 0 / DPYSL3 protein, human; 0 / Muscle Proteins
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68. Hiremath GK, Bingaman WE, Prayson RA, Nair D: Oligoastrocytoma presenting with intractable epilepsy. Epileptic Disord; 2007 Sep;9(3):315-22
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  • OBJECTIVE: Oligoastrocytomas (OA) are mixed gliomas with distinct oligodendroglial and astrocytic neoplastic components.
  • Median age at diagnosis was 25 years (range 19-44 years).
  • Tumors arose from the left side in all patients and from the temporal lobe in five patients.
  • Median length of refractory epilepsy prior to surgery was 10.5 years (range 1-28 years), and the median number of antiepileptic drugs used was 2 (range 1-10).
  • There were no surgical complications, clinical or radiographic tumor recurrence at a mean follow up period of 3.2 years (range 2-8).
  • CONCLUSION: As a result of our small sample size, general conclusions may be imprecise, but this review suggests that OA behave similar to other tumors related to intractable epilepsy: they usually have a preoperative seizure course of many years, an excellent rate of seizure-freedom following surgery, and are in general, low-grade tumors with an indolent course for which serial imaging is sufficient follow-up.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Epilepsy / drug therapy. Epilepsy / etiology
  • [MeSH-minor] Adolescent. Adult. Anticonvulsants / therapeutic use. Craniotomy. Drug Resistance. Epilepsy, Complex Partial / etiology. Epilepsy, Complex Partial / surgery. Female. Humans. Magnetic Resonance Imaging. Male. Memory / physiology. Neoplasm Recurrence, Local. Neurosurgical Procedures. Temporal Lobe / pathology. Temporal Lobe / surgery

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  • (PMID = 17884756.001).
  • [ISSN] 1294-9361
  • [Journal-full-title] Epileptic disorders : international epilepsy journal with videotape
  • [ISO-abbreviation] Epileptic Disord
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anticonvulsants
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69. Torii K, Tsuyuguchi N, Kawabe J, Sunada I, Hara M, Shiomi S: Correlation of amino-acid uptake using methionine PET and histological classifications in various gliomas. Ann Nucl Med; 2005 Dec;19(8):677-83
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  • OBJECTIVE: The uptake of L-methyl-11C-methionine (MET) by gliomas is greater than that by intact tissue, making methionine very useful for evaluation of tumor extent.
  • If the degree of malignancy of brain tumors can be evaluated by MET-PET, the usefulness of MET-PET as a means of diagnosing brain tumors will increase.
  • METHODS: We performed this study on 67 glioma patients between 3 and 69 years of age (36 males and 31 females).
  • Tumors included diffuse astrocytoma, anaplastic astrocytoma, glioblastoma, ependymoma, oligodendroglioma, medulloblastoma, dysembryoplastic neuroepithelial tumor, choroid plexus papilloma, central neurocytoma, optic glioma, gliomatosis cerebri, pleomorphic xanthoastrocytoma, and ganglioglioma.
  • Tumor activity and degree of malignancy were evaluated using Ki-67LI (LI: labeling index) and Kaplan-Meier survival curves.
  • The correlations between methionine uptake and tumor proliferation (tumor versus contralateral gray matter ratio (T/N) and Ki-67LI) were determined for the group of all subjects.
  • The existence of significant correlations between T/N and Ki-67LI and between SUV and Ki-67LI was determined for astrocytic tumors.
  • Receiver operating characteristics (ROC) analysis of T/N and standardized uptake value (SUV) was performed for the group of astrocytic tumors.
  • Ki-67LI differed significantly between the high-grade group and low-grade group at T/N levels between 1.5 and 1.8 on analysis using tumor proliferative potential (p = 0.019-0.031).
  • CONCLUSIONS: When analysis was confined to cases of astrocytic tumor, a correlation was noted between methionine accumulation and Ki-67LI.
  • For the astrocytic tumors, T/N ratio seemed to be more useful as a diagnostic indicator than SUV.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / radionuclide imaging. Glioma / pathology. Glioma / radionuclide imaging. Methionine / pharmacokinetics. Positron-Emission Tomography / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Image Interpretation, Computer-Assisted / methods. Male. Middle Aged. ROC Curve. Radiopharmaceuticals / pharmacokinetics. Reproducibility of Results. Sensitivity and Specificity. Statistics as Topic. Tissue Distribution


70. Shrestha P, Saito T, Hama S, Arifin MT, Kajiwara Y, Yamasaki F, Hidaka T, Sugiyama K, Kurisu K: Geminin: a good prognostic factor in high-grade astrocytic brain tumors. Cancer; 2007 Mar 1;109(5):949-56
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  • [Title] Geminin: a good prognostic factor in high-grade astrocytic brain tumors.
  • For this study, the authors investigated geminin expression in high-grade astrocytic tumors, including anaplastic astrocytoma (AA) and glioblastoma multiforme (GBM), with a view to predicting clinical outcomes on this basis in patients with these malignant brain tumors.
  • METHODS: Immunohistochemistry was used to detect geminin expression in 51 patients with high-grade astrocytic tumors (19 AA and 32 GBM).
  • Samples were categorized by taking the median value as the cut-off point for constructing Kaplan-Meier curves.
  • The relation of geminin expression to clinical outcome in these malignant brain tumors was analyzed by using the Kaplan-Meier method and a Cox proportional hazards regression model.
  • RESULTS: Geminin was expressed in all high-grade astrocytomas (mean geminin labeling index [LI], 24.90%).
  • Kaplan-Meier curves showed that the group with higher geminin LI (>or=22.50%) had a better prognosis than the group with lower LI (<22.50%; P = .0296).
  • CONCLUSIONS: Although it is an inhibitor of DNA proliferation and, thus, is a cell cycle inhibitor, geminin expression was found in all malignant astrocytic tumors.
  • The geminin LI was a significant predictive factor of outcomes in patients with high-grade astrocytoma, with higher expression indicating a good prognosis.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cell Cycle Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Child. Female. Geminin. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Survival Analysis

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  • (PMID = 17262828.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / GMNN protein, human; 0 / Geminin
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71. Abel TJ, Hebb AO, Keene CD, Born DE, Silbergeld DL: Parahippocampal corpora amylacea: case report. Neurosurgery; 2010 Jun;66(6):E1206-7
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  • OBJECTIVE: Corpora amylacea (CA) normally accumulate within perivascular, subpial, and subependymal astrocytic processes.
  • CA are associated with a number of conditions including normal aging, hippocampal sclerosis associated with temporal lobe epilepsy, multiple sclerosis, Lafora-type progressive myoclonic epilepsy, and adult polyglucosan body disease.
  • CLINICAL PRESENTATION: A 49-year-old woman, with a long-standing history of migraine headaches, presented to her primary care provider for increased headache duration.
  • Specimens obtained during the operation revealed focal high-density accumulation of CA with no evidence of neoplasm, ischemia, or hypoxic injury.

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  • (PMID = 20495392.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucans; 9012-72-0 / polyglucosan
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72. Mabrouk GM, Ali EM, El-Rehany MA, El-Samoly HM: TGF-beta1, TNF-alpha and cytochrome c in human astrocytic tumors: a short-term follow up and correlation with survival. Clin Biochem; 2007 Feb;40(3-4):255-60
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  • [Title] TGF-beta1, TNF-alpha and cytochrome c in human astrocytic tumors: a short-term follow up and correlation with survival.
  • DESIGN AND METHODS: We measured TGF-beta1, TNF-alpha and cytoplasmic cytochrome c in 30 astrocytic tumors Grade II, III and IV.
  • Patients with astrocytic tumors having elevated cytochrome c showed a better survival rate compared to those with less release.
  • [MeSH-major] Astrocytoma / diagnosis. Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Cytochromes c / analysis. Transforming Growth Factor beta1 / analysis. Tumor Necrosis Factor-alpha / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 17070791.001).
  • [ISSN] 0009-9120
  • [Journal-full-title] Clinical biochemistry
  • [ISO-abbreviation] Clin. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 9007-43-6 / Cytochromes c
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73. Marton E, Feletti A, Orvieto E, Longatti P: Malignant progression in pleomorphic xanthoastrocytoma: personal experience and review of the literature. J Neurol Sci; 2007 Jan 31;252(2):144-53
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  • [Title] Malignant progression in pleomorphic xanthoastrocytoma: personal experience and review of the literature.
  • Pleomorphic xanthoastrocytoma (PXA) is a rare primary low-grade astrocytic tumor, recently classified as a neuroglial tumor.
  • It generally occurs in children and young adults and shows benign behaviour (WHO II), although an anaplastic variant and malignant potential have been described.
  • Pleomorphic xanthoastrocytomas with malignant transformation have been reported in three out of eight patients operated on for this type of tumor in our department in the last 15 years.
  • The three patients were two adult women and a child, the primary tumors were located in the cortex of the right temporal lobe, and treatment consisted of complete surgical resection.
  • Histological examination revealed simple PXA in two patients and a PXA with anaplastic foci in the other.
  • Mean recurrence time was 5.7 years, with the original xanthoastrocytoma evolving to glioblastoma in two cases and anaplastic astrocytoma in the third.
  • Two died from tumor progression and one from brain edema after intracerebral haemorrhage.
  • A review of the available PXA literature dating back to 1979 revealed 16 cases of primary anaplastic astrocytoma and 21 cases of PXA with malignant transformation.
  • Our experience adds three more cases of malignant transformations, outlining once again the potential malignancy of pleomorphic xanthoastrocytomas and the fact that prognosis in these cases is the same as for primary anaplastic astrocytoma and glioblastoma.
  • Accordingly, these tumors demand close long-term clinical and radiological follow-up.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic. Child. Disease Progression. Fatal Outcome. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Neoplasm Recurrence, Local / pathology. Tomography, X-Ray Computed


74. Park S, Suh YL, Nam DH, Kim ST: Gliomatosis cerebri: clinicopathologic study of 33 cases and comparison of mass forming and diffuse types. Clin Neuropathol; 2009 Mar-Apr;28(2):73-82
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  • OBJECTIVE: Gliomatosis cerebri (GC) is defined as a diffuse neoplastic glial cell infiltration of the brain with the preservation of anatomical architecture and the sparing of neurons and can be classified into Type 1 (diffuse) and Type 2 (mass forming) GCs macroscopically.
  • METHODS: Clinical information included patients' age, sex, tumor extent, treatment modality and survival.
  • Pathologic features included the amount of rod cells and cytologic anaplasia such as multinucleated tumor giant cells, endothelial cell proliferation, or mitosis.
  • RESULTS: Median age at diagnosis was older (56 years) in Type 1 than in Type 2 (44 years).
  • Mean survival time was shorter (21 months) in Type 2 than in Type 1 GCs (24 months) (p = 0.0447).
  • Immunohistochemical results demonstrated that the infiltrating tumor cells were undifferentiated cells with astrocytic or oligodendroglial differentiation.
  • [MeSH-major] Brain / pathology. Neoplasms, Neuroepithelial / pathology. Neoplasms, Neuroepithelial / physiopathology
  • [MeSH-minor] Adult. Anaplasia. Astrocytes / pathology. Astrocytes / physiology. Cell Proliferation. Endothelial Cells / pathology. Female. Giant Cells / pathology. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Oligodendroglia / pathology. Oligodendroglia / physiology. Survival Analysis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19353837.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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75. Murakami H, Sawa H, Kamada H: [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors]. No To Shinkei; 2006 Jan;58(1):43-9
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  • [Title] [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors].
  • Cyclooxygenase (COX)-2 of astrocytic tumors was studied by immunohistochemistry.
  • COX-2 was detected by an immnoblotting in 2 of 9 human glioblastoma cell lines (KNS42 and U138).
  • The result showed that COX-2 expression may be related with histological grades and COX-2 inhibitors will be one of promising therapeutic tools in human astrocytic tumors.
  • [MeSH-minor] Adult. Aged. Etodolac / pharmacology. Female. Glioblastoma / drug therapy. Glioblastoma / enzymology. Humans. Immunoblotting. Immunohistochemistry. Male. Middle Aged. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured

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  • (PMID = 16482921.001).
  • [ISSN] 0006-8969
  • [Journal-full-title] Nō to shinkei = Brain and nerve
  • [ISO-abbreviation] No To Shinkei
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitrobenzenes; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 2M36281008 / Etodolac; EC 1.14.99.1 / Cyclooxygenase 2
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76. Sadetzki S, Zach L, Chetrit A, Nass D, Hoffmann C, Ram Z, Zaaroor M, Umansky F, Rappaport ZH, Cohen A, Wald U, Rothman S, Hadani M: Epidemiology of gliomas in Israel: a nationwide study. Neuroepidemiology; 2008;31(4):264-9
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  • BACKGROUND: Glial brain tumors span a wide range of neoplasms with distinct clinical and histopathological features.
  • This report presents the descriptive epidemiology of glial tumors by histological subtype and tumor behavior.
  • METHODS: The study population included all incident cases of glial tumors diagnosed in Israel during March 2001 to July 2003.
  • RESULTS: A total of 548 tumors were diagnosed, of which 520 had histological confirmation.
  • The ASR of all adult (>20 years) glial tumors was 5.82/100,000 (7.11 for males; 4.75 for females, p < 0.001).
  • The majority of tumors (78%) were classified as high grade; astrocytic tumors were the most frequent (85%), with glioblastoma multiforme accounting for 70% of them.
  • CONCLUSIONS: In general, these results describing data of incident cases of pathologically validated glial tumors are consistent with previous reports.
  • To enhance our understanding of these diseases, epidemiological studies should rely on well-defined histological tumor types, incorporating comprehensive information which will allow comparability between different groups of patients.
  • [MeSH-major] Brain Neoplasms / epidemiology. Glioma / epidemiology. Jews / statistics & numerical data
  • [MeSH-minor] Adult. Africa / epidemiology. Aged. Aged, 80 and over. Americas / epidemiology. Asia / epidemiology. Ethnic Groups / statistics & numerical data. Europe / epidemiology. Female. Global Health. Humans. Incidence. Israel / epidemiology. Magnetic Resonance Imaging. Male. Middle Aged. Prevalence. Sex Characteristics

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • [CommentIn] Neuroepidemiology. 2008;31(4):270 [18931524.001]
  • (PMID = 18931523.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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77. Samaras V, Piperi C, Korkolopoulou P, Zisakis A, Levidou G, Themistocleous MS, Boviatsis EI, Sakas DE, Lea RW, Kalofoutis A, Patsouris E: Application of the ELISPOT method for comparative analysis of interleukin (IL)-6 and IL-10 secretion in peripheral blood of patients with astroglial tumors. Mol Cell Biochem; 2007 Oct;304(1-2):343-51
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  • [Title] Application of the ELISPOT method for comparative analysis of interleukin (IL)-6 and IL-10 secretion in peripheral blood of patients with astroglial tumors.
  • Glioblastoma, (grade IV astrocytoma), is characterized by rapid growth and resistance to treatment.
  • Identification of markers of aggressiveness in this tumor could represent new therapeutic targets.
  • Interleukins (IL)-6 and IL-10 may be considered as possible candidates, regulating cell growth, resistance to chemotherapy and angiogenesis.
  • IL-6 and IL-10 secretion levels were determined using ELISPOT methodology in peripheral blood mononuclear cells of 18 patients with astrocytic neoplasms (3 grade II and 15 grade IV), in parallel with 18 healthy controls.
  • Additionally, immunohistochemical expression of these two cytokines was performed in paraffin-embedded neoplastic tissue in 12 of these patients.
  • In addition, IL-10 secretion from peripheral mononuclear and tumor cells of glioma patients was also higher as compared to healthy controls (P = 0.0002).
  • Based on immunohistochemical staining, IL-6 expression was localized in tumor cells and macrophages as well as in areas of large ischemic necrosis, while the major source of IL-10 expression in glioblastomas was the microglia/macrophage cells.
  • It is suggested that IL-10 contributes to the progression of astrocytomas by suppressing the patient's immune response, whereas IL-6 provides an additional growth advantage.
  • This study demonstrates for the first time the usefulness of ELISPOT in estimating the secretion of IL-6 and IL-10 from peripheral blood and the correlation of their expression in neoplastic cells.
  • [MeSH-major] Astrocytoma / blood. Brain Neoplasms / blood. Enzyme-Linked Immunosorbent Assay / methods. Interleukin-10 / blood. Interleukin-10 / secretion. Interleukin-6 / blood. Interleukin-6 / secretion
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Glioblastoma / blood. Humans. Leukocytes / secretion. Male. Middle Aged

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  • [Cites] Cancer Res. 1992 Nov 1;52(21):6020-4 [1394227.001]
  • [Cites] J Neurochem. 1998 Nov;71(5):1837-45 [9798907.001]
  • [Cites] Neuroimmunomodulation. 1998 May-Aug;5(3-4):214-9 [9730688.001]
  • [Cites] Am J Pathol. 1995 Feb;146(2):317-22 [7856743.001]
  • [Cites] J Immunol Methods. 1988 Nov 25;115(1):31-7 [3057075.001]
  • [Cites] Int J Cancer. 1999 Jul 2;82(1):12-6 [10360813.001]
  • [Cites] J Clin Immunol. 1992 Jul;12(4):239-47 [1512298.001]
  • [Cites] Br J Cancer. 2001 Aug 17;85(4):518-22 [11506489.001]
  • [Cites] J Neurochem. 1994 Sep;63(3):980-7 [7519668.001]
  • [Cites] J Immunol. 1999 Apr 15;162(8):4882-92 [10202033.001]
  • [Cites] Neurosurgery. 1995 Dec;37(6):1160-6; discussion 1166-7 [8584157.001]
  • [Cites] J Clin Neurosci. 2005 Nov;12(8):930-3 [16326273.001]
  • [Cites] J Neurosurg. 2001 Jan;94(1):97-101 [11147905.001]
  • [Cites] J Exp Med. 1991 Oct 1;174(4):915-24 [1655948.001]
  • [Cites] J Immunol. 2001 Jan 1;166(1):121-9 [11123284.001]
  • [Cites] Ann N Y Acad Sci. 1993 Jun 23;685:713-39 [8363277.001]
  • [Cites] Neurosurgery. 1994 Apr;34(4):669-72; discussion 672-3 [8008165.001]
  • [Cites] Oncogene. 2004 Apr 22;23(19):3308-16 [15064729.001]
  • [Cites] J Neurooncol. 2002 Jan;56(1):29-34 [11949824.001]
  • [Cites] Cancer Res. 1990 Oct 15;50(20):6683-8 [2208133.001]
  • [Cites] Acta Neuropathol. 2002 Feb;103(2):171-8 [11810184.001]
  • [Cites] J Immunol. 1992 Feb 15;148(4):1143-8 [1737931.001]
  • [Cites] Anticancer Res. 1997 Sep-Oct;17(5A):3217-24 [9413151.001]
  • [Cites] J Immunol Methods. 1997 Dec 29;210(2):149-66 [9520298.001]
  • [Cites] Int J Cancer. 2005 Jun 10;115(2):202-13 [15688401.001]
  • [Cites] Pathol Oncol Res. 1999;5(1):56-60 [10079380.001]
  • [Cites] Semin Oncol. 2000 Jun;27(3 Suppl 6):1-10 [10866344.001]
  • [Cites] J Neurosurg. 1992 Aug;77(2):265-73 [1625016.001]
  • [Cites] J Exp Med. 1993 Feb 1;177(2):523-7 [8426121.001]
  • [Cites] J Cell Physiol. 1997 Dec;173(3):335-42 [9369946.001]
  • [Cites] Brain Res. 1994 Jun 27;649(1-2):122-8 [7953624.001]
  • [Cites] J Immunol. 1992 Oct 1;149(7):2358-66 [1382099.001]
  • [Cites] J Immunol. 1994 Mar 15;152(6):2720-8 [8144879.001]
  • [Cites] J Neurooncol. 1998 Nov;40(2):113-22 [9892093.001]
  • [Cites] J Immunol. 1992 May 15;148(10):3133-9 [1578140.001]
  • [Cites] J Neuroimmunol. 1998 Dec 1;92(1-2):50-9 [9916879.001]
  • [Cites] Clin Chem Lab Med. 2002 Sep;40(9):903-10 [12435107.001]
  • [Cites] Surg Neurol. 1980 Mar;13(3):161-3 [7368063.001]
  • [Cites] J Biol Chem. 1995 May 12;270(19):11463-71 [7744784.001]
  • (PMID = 17551671.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / IL10 protein, human; 0 / IL6 protein, human; 0 / Interleukin-6; 130068-27-8 / Interleukin-10
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78. Kuroki K, Sugiyama K, Taguchi H, Yukawa O, Kurokawa M, Kajiwara Y, Usui S, Kurisu K: [Gliomatosis cerebri. Report of two cases]. No Shinkei Geka; 2006 May;34(5):513-8
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  • Gliomatosis cerebri is a rare tumor of the central nervous system, and here we report two cases of this tumor.
  • Case 1: A 41-year-old female was admitted to our department for evaluation of activity loss and mental changes.
  • The patient had no neurological deficits and no abnormal findings in clinical laboratory data, including data for the cerebral spinal fluid.
  • A specimen obtained by open biopsy revealed widespread infiltration of neuronal structures by small astrocytic cells, although without destruction of the neuronal structures.
  • Case 2: A 56-year-old male was admitted for numbness of the face and extremities.
  • MR imaging revealed a high intensity lesion in the bilateral thalamus and a ringed enhanced lesion in the right thalamus.
  • Radiation at 54Gy, chemotherapy (ACNU, vincristine) and gamma-knife surgery were performed, and two months later MR imaging showed that the tumor (including the ringed enhanced lesion) had shrunk markedly.
  • [MeSH-major] Brain Neoplasms / diagnosis. Neoplasms, Neuroepithelial / diagnosis. Oligodendroglioma / diagnosis
  • [MeSH-minor] Adult. Combined Modality Therapy. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged

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  • (PMID = 16689395.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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79. Felsberg J, Yan PS, Huang TH, Milde U, Schramm J, Wiestler OD, Reifenberger G, Pietsch T, Waha A: DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours. Neuropathol Appl Neurobiol; 2006 Oct;32(5):517-24
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  • [Title] DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours.
  • Cytogenetic and molecular genetic studies have shown frequent losses on the long arm of chromosome 14 in different types of human gliomas.
  • Using differential methylation hybridization as a genome-wide screening approach to determine DNA methylation patterns in gliomas, we recently identified two DNA fragments in 14q23.1 (CGI-clone musical sharp396) and 14q32.12 (CGI-clone musical sharp519) that were differentially methylated between astrocytic gliomas and mixed oligoastrocytomas.
  • To validate this observation, we examined these 14q32.12 locus for methylation in an extended series of 43 astrocytic and oligodendroglial gliomas.
  • All tumours were additionally investigated for loss of heterozygosity (LOH).
  • Microsatellite analysis showed LOH in seven of 28 (25%) oligodendroglial tumours and three of 15 (20%) astrocytic tumours.
  • Seven tumours demonstrated LOH at all informative 14q loci whereas three tumours carried partial deletions defining a commonly deleted region at 14q22.3-q32.1 between the microsatellite markers D14S282 and D14S995.
  • Hypermethylation was restricted to tumours with oligodendroglial differentiation (12 of 28 tumours, 43%).
  • However, none of the hypermethylated tumours demonstrated LOH on 14q and vice versa.
  • In total, 19 of 28 oligodendroglial tumours (68%) showed either hypermethylation at the 14q32.12 locus or LOH at 14q22.3-q32.2.
  • Taken together, our data lend further support for the location of one or more yet to be identified glioma-associated tumour suppressor gene(s) on 14q.
  • In addition, the restriction of 14q32.12 methylation to oligodendroglial tumours suggests a role for epigenetic DNA modifications in these particular gliomas.
  • [MeSH-major] Brain Neoplasms / pathology. Chromosomes, Human, Pair 14 / genetics. DNA Methylation. Oligodendroglia / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Alleles. Child. Child, Preschool. DNA, Neoplasm / drug effects. Female. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Sulfites / pharmacology

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  • (PMID = 16972885.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Sulfites; TZX5469Z6I / sodium bisulfite
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80. 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
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  • 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.
  • A positive correlation occurred between COX-2 and angiogenic factors such as vascular endothelial growth factor (VEGF) (p<0.0001) and hypoxia inducible factor (HIF)-1alpha (p=0.005), as well as the tumours' proliferative activity (expressed as the percentage of Ki-67 positive cells) (p=0.032), and total vascular area (TVA) (p=0.040).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Ki-67 Antigen / metabolism. Male. Middle Aged. Proportional Hazards Models. Survival Analysis. Vascular Endothelial Growth Factor A / metabolism

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  • [Cites] Biol Chem. 1997 Jul;378(7):609-16 [9278140.001]
  • [Cites] Fundam Clin Pharmacol. 1996;10(1):1-17 [8900495.001]
  • [Cites] Ann Clin Lab Sci. 2001 Oct;31(4):325-48 [11688844.001]
  • [Cites] Acta Neuropathol. 1999 Sep;98(3):240-4 [10483780.001]
  • [Cites] J Biol Chem. 1991 Jul 15;266(20):12866-72 [1712772.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4356-62 [10485483.001]
  • [Cites] Am J Pathol. 2000 Jul;157(1):29-35 [10880372.001]
  • [Cites] Ann Neurol. 1998 Jun;43(6):738-47 [9629843.001]
  • [Cites] Clin Cancer Res. 1997 Oct;3(10):1679-83 [9815550.001]
  • [Cites] Cancer Res. 1989 Mar 15;49(6):1505-8 [2493982.001]
  • [Cites] Int Urol Nephrol. 2005;37(1):47-53 [16132759.001]
  • [Cites] J Clin Invest. 2000 Jun;105(11):1589-94 [10841517.001]
  • [Cites] FASEB J. 1998 Sep;12(12):1063-73 [9737710.001]
  • [Cites] Neuropathology. 2004 Sep;24(3):201-7 [15484698.001]
  • [Cites] Clin Cancer Res. 2000 Oct;6(10):4064-8 [11051257.001]
  • [Cites] Cancer Res. 1997 Jun 15;57(12):2452-9 [9192825.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 1996 Sep;55(3):179-83 [8931116.001]
  • [Cites] Neuropathol Appl Neurobiol. 2002 Feb;28(1):57-66 [11849564.001]
  • [Cites] Cancer Res. 1995 Apr 1;55(7):1464-72 [7882354.001]
  • [Cites] N Engl J Med. 1993 May 6;328(18):1313-6 [8385741.001]
  • [Cites] Acta Neuropathol. 2001 Aug;102(2):181-7 [11563634.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13926-31 [12242329.001]
  • [Cites] J Clin Pathol. 2006 Apr;59(4):382-6 [16467169.001]
  • [Cites] J Clin Invest. 1994 Feb;93(2):493-8 [8113389.001]
  • [Cites] J Biol Chem. 1999 Apr 16;274(16):10911-5 [10196169.001]
  • [Cites] Adv Prostaglandin Thromboxane Leukot Res. 1995;23:109-11 [7732812.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4375-81 [11389063.001]
  • [Cites] N Engl J Med. 1995 Dec 28;333(26):1757-63 [7491141.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4926-31 [10987308.001]
  • [Cites] Cell. 1996 Nov 29;87(5):803-9 [8945508.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 21;90(20):1529-36 [9790545.001]
  • [Cites] Cancer. 1996 Jan 15;77(2):362-72 [8625246.001]
  • [Cites] Cancer. 2003 Oct 1;98(7):1465-72 [14508834.001]
  • [Cites] Int J Cancer. 1994 Nov 15;59(4):520-9 [7525492.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5040-4 [11016626.001]
  • [Cites] J Neurosurg. 1999 Jan;90(1):72-7 [10413158.001]
  • [Cites] Annu Rev Cell Dev Biol. 1999;15:551-78 [10611972.001]
  • [Cites] Neuropathol Appl Neurobiol. 2004 Jun;30(3):267-78 [15175080.001]
  • [Cites] J Neurosurg Sci. 1989 Jan-Mar;33(1):65-9 [2674360.001]
  • [Cites] Eur Urol. 2006 Nov;50(5):1021-31; discussion 1031 [16522350.001]
  • [Cites] Nature. 1992 Feb 27;355(6363):846-7 [1311419.001]
  • [Cites] N Engl J Med. 1991 Dec 5;325(23):1593-6 [1669840.001]
  • [Cites] Cancer Res. 1996 Oct 15;56(20):4566-9 [8840961.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2513-20 [10873107.001]
  • [Cites] Pathobiology. 2005;72(5):241-9 [16374068.001]
  • (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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81. Li NY, Zhou XJ, Jin XZ, Meng K, Ma HH, Zheng XG, Jiang SJ, Sun GQ: [A clinicopathologic study of dysembryoplstic neuroepithelial tumor]. Zhonghua Bing Li Xue Za Zhi; 2005 Sep;34(9):561-5
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  • [Title] [A clinicopathologic study of dysembryoplstic neuroepithelial tumor].
  • OBJECTIVE To study the clinicopathologic features, radiologic findings, treatment modalities and prognosis of dysembryoplastic neuroepithelial tumor (DNT).
  • The age of these patients ranged from 3 to 46 (mean age = 22. 8 years).
  • The history of epilepsy could be as long as 17 years.
  • On magnetic resonance imaging (MRI) study, the tumor was hypodense on T1 and hyperdense on T2.
  • Ten cases were treated by complete surgical excision and the remaining 8 tumors were partially excised.
  • In the 14 patients with follow-up data available, 13 survived for 1.4 to 11 years after the operation (with more than 10 years survival observed in 2 patients).
  • The average survival period was 5.5 years.
  • None of the cases showed tumor recurrence after operation.
  • Histologically, all tumors demonstrated a multinodular architecture and were intracortical in location, sometimes with extension into the white matter.
  • The tumor was formed by an admixture of oligodendrocyte-like cells, mature neurons and astrocytes, with obvious microcystic changes.
  • Immunohistochemical study demonstrated positivity for synaptophysin, neurofilament and S-100 protein in the neurons and some oligodendrocyte-like cells.
  • Electron microscopy showed early neuronal, astrocytic and oligodendroglial differentiation of the oligodendrocyte-like cells.
  • CONCLUSIONS: DNT is a benign tumor (corresponding to WHO grade I) that can be cured by surgical excision, despite sometimes incomplete tumor removal.
  • [MeSH-major] Brain Neoplasms / pathology. Cerebral Cortex / pathology. Neoplasms, Neuroepithelial / pathology. Oligodendroglia / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neurofilament Proteins / metabolism. S100 Proteins / metabolism. Survival Rate. Synaptophysin / metabolism

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  • (PMID = 16468305.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neurofilament Proteins; 0 / S100 Proteins; 0 / Synaptophysin
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82. Benito R, Gil-Benso R, Quilis V, Perez M, Gregori-Romero M, Roldan P, Gonzalez-Darder J, Cerdá-Nicolas M, Lopez-Gines C: Primary glioblastomas with and without EGFR amplification: relationship to genetic alterations and clinicopathological features. Neuropathology; 2010 Aug;30(4):392-400
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  • Glioblastomas express a notable heterogeneity in both the histological and cell patterns with glial astrocytic differentiation.
  • Primary glioblastoma, which is the most frequent presentation (90-95%), occurs mainly in older patients and arises de novo, without any clinical or histological evidence of a less malignant precursor lesion.
  • EGFR amplification was observed in 24 cases (53%), while in the remaining 21 cases (47%) this alteration was not displayed.
  • The amplification of EGFR was associated with amplifications in MDM2 and CDK4 and a higher percentage of cases with promoter methylation of INK4a.
  • The genetic studies suggest the existence of molecular subtypes within primary glioblastoma that may, when fully defined, contribute toward the development of drugs that specifically target tumors with divergent genetic profiles.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Genes, erbB-1 / genetics. Glioblastoma / genetics. Glioblastoma / pathology
  • [MeSH-minor] Adult. Aged. Cyclin-Dependent Kinase 4 / genetics. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Middle Aged. Polymerase Chain Reaction. Proto-Oncogene Proteins c-mdm2 / genetics. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 20051017.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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83. Dim DC, Lingamfelter DC, Taboada EM, Fiorella RM: Papillary glioneuronal tumor: a case report and review of the literature. Hum Pathol; 2006 Jul;37(7):914-8
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  • [Title] Papillary glioneuronal tumor: a case report and review of the literature.
  • Papillary glioneuronal tumor is a recently described central nervous system neoplasm that almost always occurs adjacent to the lateral ventricle.
  • We present a case of this rare entity, representing the 21st case of this lesion, which exhibits a mixed astrocytic and neuronal differentiation.
  • This case was an incidental finding in a young woman who presented secondary to a traumatic injury to the left eye.
  • Histologic evaluation after surgical removal showed a cystic tumor consisting of 2 distinct components: a unique pseudopapillary architecture admixed with foci of solid areas.
  • The combination of cytologic benignity, lack of necrosis, and low proliferative index as evidenced by immunohistochemistry using antibody to Ki-67 confirmed the low malignant potential of this tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Carcinoma, Papillary / pathology. Ganglioglioma / pathology
  • [MeSH-minor] Adult. Chromogranin A. Chromogranins / metabolism. Eye Injuries / complications. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Neurofilament Proteins / metabolism. S100 Proteins / metabolism. Synaptophysin / metabolism

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  • (PMID = 16784993.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Neurofilament Proteins; 0 / S100 Proteins; 0 / Synaptophysin
  • [Number-of-references] 12
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84. Jacobs JF, Grauer OM, Brasseur F, Hoogerbrugge PM, Wesseling P, Gidding CE, van de Rakt MW, Figdor CG, Coulie PG, de Vries IJ, Adema GJ: Selective cancer-germline gene expression in pediatric brain tumors. J Neurooncol; 2008 Jul;88(3):273-80
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  • [Title] Selective cancer-germline gene expression in pediatric brain tumors.
  • Cancer-germline genes (CGGs) code for immunogenic antigens that are present in various human tumors and can be targeted by immunotherapy.
  • Their expression has been studied in a wide range of human tumors in adults.
  • We measured the expression of 12 CGGs in pediatric brain tumors, to identify targets for therapeutic cancer vaccines.
  • Real Time PCR was used to quantify the expression of genes MAGE-A1, MAGE-A2, MAGE-A3, MAGE-A4, MAGE-A6, MAGE-A10, MAGE-A12, MAGE-C2, NY-ESO-1 and GAGE-1,2,8 in 50 pediatric brain tumors of different histological subtypes.
  • Fifty-five percent of the medulloblastomas (n = 11), 86% of the ependymomas (n = 7), 40% of the choroid plexus tumors (n = 5) and 67% of astrocytic tumors (n = 27) expressed one or more CGGs.
  • With exception of a minority of tumors, the overall level of CGG expression in pediatric brain tumors was low.
  • CGG-encoded antigens are therefore suitable targets in a very selected group of pediatric patients with a brain tumor.
  • Interestingly, glioblastomas from adult patients expressed CGGs more often and at significantly higher levels compared to pediatric glioblastomas.
  • This observation is in line with the notion that pediatric and adult glioblastomas develop along different genetic pathways.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression. Genes, Neoplasm
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Humans. Immunohistochemistry. Infant. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] In Vivo. 2002 Nov-Dec;16(6):583-8 [12494904.001]
  • [Cites] Immunol Rev. 2002 Oct;188:51-64 [12445281.001]
  • [Cites] Nat Rev Immunol. 2003 Jul;3(7):569-81 [12876559.001]
  • [Cites] Clin Neuropathol. 2003 Jul-Aug;22(4):180-6 [12908754.001]
  • [Cites] J Neurooncol. 2003 Aug-Sep;64(1-2):3-11 [12952281.001]
  • [Cites] Int J Cancer. 2008 Feb 15;122(4):777-84 [17957795.001]
  • [Cites] Int Rev Immunol. 2003 Mar-Apr;22(2):113-40 [12962272.001]
  • [Cites] Science. 1991 Dec 13;254(5038):1643-7 [1840703.001]
  • [Cites] Int J Cancer. 1993 May 28;54(3):527-8 [8509230.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 1;91(3):1004-8 [8302824.001]
  • [Cites] Annu Rev Immunol. 1994;12:337-65 [8011285.001]
  • [Cites] Neurosurgery. 1994 Jun;34(6):967-72; discussion 972-3 [8084407.001]
  • [Cites] N Engl J Med. 1995 Jan 19;332(3):143-9 [7800006.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2236-9 [7757970.001]
  • [Cites] Mod Pathol. 1995 Apr;8(3):333-8 [7617661.001]
  • [Cites] Ther Immunol. 1995 Jun;2(3):173-81 [8885135.001]
  • [Cites] Am J Pathol. 1997 Jun;150(6):2143-52 [9176405.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Jul;56(7):782-9 [9210874.001]
  • [Cites] Biotechniques. 1997 Sep;23(3):456-60 [9298216.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 16;91(12):1051-8 [10379968.001]
  • [Cites] Nat Rev Cancer. 2005 Aug;5(8):615-25 [16034368.001]
  • [Cites] Neurol Res. 2005 Oct;27(7):692-702 [16197806.001]
  • [Cites] Int J Cancer. 2007 Jan 1;120(1):67-74 [17019710.001]
  • [Cites] Cancer Immunol Immunother. 2007 Feb;56(2):259-69 [16758204.001]
  • [Cites] Neurosurgery. 2006 Nov;59(5):988-99; discussioin 999-1000 [17143233.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] J Exp Med. 2007 Sep 3;204(9):2023-30 [17682068.001]
  • [Cites] Int J Oncol. 2000 Jan;16(1):81-96 [10601552.001]
  • [Cites] Int J Cancer. 2000 Jun 15;86(6):835-41 [10842198.001]
  • [Cites] Transplantation. 2000 Jun 15;69(11):2366-73 [10868642.001]
  • [Cites] Clin Cancer Res. 2000 Oct;6(10):3916-22 [11051238.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1525-32 [11290570.001]
  • [Cites] Int J Cancer. 2001 Jun 15;92(6):856-60 [11351307.001]
  • [Cites] Nature. 2001 May 17;411(6835):380-4 [11357146.001]
  • [Cites] Clin Chem. 2002 Jan;48(1):25-34 [11751535.001]
  • [Cites] Vaccine. 2003 Jan 30;21(7-8):781-6 [12531359.001]
  • (PMID = 18398575.001).
  • [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
  • [Other-IDs] NLM/ PMC2440921
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85. Strojnik T, Kavalar R, Trinkaus M, Lah TT: Cathepsin L in glioma progression: comparison with cathepsin B. Cancer Detect Prev; 2005;29(5):448-55
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  • OBJECTIVE: Lysosomal cysteine cathepsins have been implicated in tumor progression.
  • This study is aimed to reveal differential expression and compare the prognostic significance of cathepsins B and L in glioma patients.
  • METHODS: The histological slides of 82 patients with primary astrocytic tumors were reviewed.
  • We evaluated the immunostaining of the cathepsins in tumor and endothelial cells.
  • RESULTS: Cathepsins B and L stained positive in 98 and 88% of cases, respectively.
  • The total score was significantly higher in malignant than in benign tumors, both for cathepsin B (p<0.001) and for cathepsin L (p<0.01).
  • The IHC score in endothelial cells in the malignant group was significantly higher only for cathepsin B (p<0.0001).
  • Survival analysis indicated that in contrast to the prognostic significance of total cathepsin B and endothelial cells associated cathepsin B for shorter patients' survival, the prognostic role of cathepsin L was not confirmed.
  • CONCLUSION: Cathepsin L is preferentially expressed in tumor cells, increasing with glioma progression, but is not significantly associated with new vasculature of glioblastoma.
  • [MeSH-major] Brain Neoplasms / chemistry. Brain Neoplasms / pathology. Cathepsin B / biosynthesis. Cathepsin B / physiology. Cathepsins / biosynthesis. Cathepsins / physiology. Cysteine Endopeptidases / biosynthesis. Cysteine Endopeptidases / physiology. Glioma / chemistry. Glioma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Cathepsin L. Child. Child, Preschool. Disease Progression. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neovascularization, Pathologic. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16183211.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.- / Cathepsins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / CTSL1 protein, human; EC 3.4.22.15 / Cathepsin L
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86. Alaraj A, Chan M, Oh S, Michals E, Valyi-Nagy T, Hersonsky T: Astroblastoma presenting with intracerebral hemorrhage misdiagnosed as dural arteriovenous fistula: review of a rare entity. Surg Neurol; 2007 Mar;67(3):308-13
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  • BACKGROUND: Astroblastoma is one of the most unusual types of tumors whose histogenesis has been recently clarified.
  • It occurs mainly among children and young adults.
  • Immunohistochemically, the tumor cells show diffuse strong positivity for GFAP, S-100 protein, vimentin, as well as neuron-specific enolase and focal positivity for EMA.
  • CASE DESCRIPTION: Our patient is a 33-year-old gentleman who presented with intraparenchymal hemorrhage in the left temporal lobe.
  • Because of its high degree of proliferation, the presence of astroblastic pseudorosettes, prominent perivascular hyalinization, regional hyaline changes, and pushing borders with regard to the adjacent brain, the tumor was considered anaplastic.
  • CONCLUSIONS: Astroblastoma is a rare pure pathologic entity--a distinct form of astrocytic gliomas.
  • The diagnosis of astroblastoma is often difficult because of the astroblastic aspects that can be found in astrocytic tumors, in ependymomas, and in nonneuroepithelial tumors.
  • [MeSH-major] Central Nervous System Vascular Malformations / diagnosis. Cerebral Hemorrhage. Diagnostic Errors. Neoplasms, Neuroepithelial
  • [MeSH-minor] Adult. Cerebral Angiography. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging

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  • (PMID = 17320647.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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87. Ichimura K, Vogazianou AP, Liu L, Pearson DM, Bäcklund LM, Plant K, Baird K, Langford CF, Gregory SG, Collins VP: 1p36 is a preferential target of chromosome 1 deletions in astrocytic tumours and homozygously deleted in a subset of glioblastomas. Oncogene; 2008 Mar 27;27(14):2097-108
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  • [Title] 1p36 is a preferential target of chromosome 1 deletions in astrocytic tumours and homozygously deleted in a subset of glioblastomas.
  • Astrocytic, oligodendroglial and mixed gliomas are the commonest gliomas in adults.
  • Co-deletions of total 1p and 19q are found in the majority of oligodendrogliomas and considered as a diagnostic marker and a prognostic indicator.
  • Using a chromosome 1 tile path array, we investigated 108 adult astrocytic tumours for copy number alterations.
  • However, the CpG island of TNFRSF9 was hypermethylated in 19% of astrocytic tumours and 87% of glioma cell lines.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Deletion. Chromosomes, Human, Pair 1 / genetics. Glioblastoma / genetics

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  • [Cites] J Neuropathol Exp Neurol. 1999 Nov;58(11):1170-83 [10560660.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):417-24 [10667596.001]
  • [Cites] Hum Mol Genet. 2000 May 22;9(9):1433-42 [10814707.001]
  • [Cites] J Neurosurg. 2000 Jun;92(6):983-90 [10839259.001]
  • [Cites] J Neuropathol Exp Neurol. 2000 Jun;59(6):544-58 [10850867.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):509-18 [11208845.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1253-62 [11290543.001]
  • [Cites] Cell Growth Differ. 2001 Apr;12(4):201-10 [11331249.001]
  • [Cites] Int J Oncol. 2001 Sep;19(3):609-12 [11494043.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Sep;60(9):863-71 [11556543.001]
  • [Cites] Clin Cancer Res. 2002 Jan;8(1):196-201 [11801559.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Apr;61(4):321-8 [11939587.001]
  • [Cites] Am J Pathol. 2002 Jul;161(1):313-9 [12107116.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jun;135(2):147-59 [12127399.001]
  • [Cites] Acta Neuropathol. 2002 Oct;104(4):357-62 [12200621.001]
  • [Cites] Nat Med. 1997 Jun;3(6):682-5 [9176498.001]
  • [Cites] Genes Chromosomes Cancer. 1998 May;22(1):9-15 [9591629.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4144-52 [10435596.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):137-60 [15674475.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1119-28 [15709179.001]
  • [Cites] Annu Rev Immunol. 2005;23:23-68 [15771565.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2653-61 [15805262.001]
  • [Cites] Adv Cancer Res. 2005;94:29-86 [16095999.001]
  • [Cites] Ann Neurol. 2005 Sep;58(3):483-7 [16130103.001]
  • [Cites] J Mol Med (Berl). 2005 Nov;83(11):917-26 [16133418.001]
  • [Cites] Oncogene. 2006 Feb 23;25(8):1261-71 [16205629.001]
  • [Cites] Nature. 2006 May 18;441(7091):315-21 [16710414.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2707-14 [16782910.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2715-22 [16782911.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Sep;65(9):846-54 [16957578.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Oct;65(10):988-94 [17021403.001]
  • [Cites] Cancer Res. 2006 Oct 15;66(20):9852-61 [17047046.001]
  • [Cites] Cell. 2007 Feb 9;128(3):459-75 [17289567.001]
  • [Cites] J Neuropathol Exp Neurol. 2007 Jun;66(6):545-51 [17549014.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Oct;35(2):170-5 [12203781.001]
  • [Cites] J Urol. 2003 Mar;169(3):1138-42 [12576869.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Feb;62(2):111-26 [12578221.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):361-74 [12619160.001]
  • [Cites] Cancer. 2003 May 1;97(9):2254-61 [12712480.001]
  • [Cites] Brain Pathol. 2003 Oct;13(4):507-18 [14655756.001]
  • [Cites] Mod Pathol. 2004 Jun;17(6):617-22 [15133472.001]
  • [Cites] Brain Pathol. 2004 Apr;14(2):121-30 [15193024.001]
  • [Cites] Br J Cancer. 2004 Sep 13;91(6):1105-11 [15475940.001]
  • [Cites] Cancer Res. 1988 Jan 15;48(2):405-11 [3335011.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(3):636-45 [10653879.001]
  • (PMID = 17934521.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2650419; NLM/ UKMS4022
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88. Crespo-Rodríguez AM, Smirniotopoulos JG, Rushing EJ: MR and CT imaging of 24 pleomorphic xanthoastrocytomas (PXA) and a review of the literature. Neuroradiology; 2007 Apr;49(4):307-15
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  • [Title] MR and CT imaging of 24 pleomorphic xanthoastrocytomas (PXA) and a review of the literature.
  • INTRODUCTION: The aim of our study was to review the imaging appearance of PXA, a rare and usually low-grade, astrocytic tumor that typically occurs in young adults.
  • Two morphologic patterns were defined according to imaging features.
  • RESULTS: All the neoplasms were supratentorial and superficial in location with obvious leptomeningeal contact in 22 patients, although leptomeningeal enhancement was demonstrated in only 3.
  • Common locations were temporal (42%), frontal (33%) and parietal (21%), and more than one lobe was involved in 21% of patients.
  • On CT without contrast enhancement, PXA was an iso- or hypoattenuating mass, and calcification was seen in six tumors and inner table remodeling was seen in three patients younger than 12 years.
  • [MeSH-major] Astrocytoma / diagnosis. Magnetic Resonance Imaging / methods. Supratentorial Neoplasms / diagnosis. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Retrospective Studies. Statistics, Nonparametric

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  • [Cites] Childs Nerv Syst. 1993 Feb;9(1):39-42 [8481944.001]
  • [Cites] Cancer. 1999 May 1;85(9):2033-45 [10223246.001]
  • [Cites] Neuroradiology. 1999 Jan;41(1):30-4 [9987765.001]
  • [Cites] AJR Am J Roentgenol. 1993 Jun;160(6):1272 [8498232.001]
  • [Cites] Neurosurgery. 2003 Jun;52(6):1465-8; discussion 1468-9 [12762893.001]
  • [Cites] Am J Surg Pathol. 1997 Jul;21(7):763-71 [9236832.001]
  • [Cites] Neuroradiology. 2004 Oct;46(10):825-9 [15289955.001]
  • [Cites] J Comput Assist Tomogr. 1995 Nov-Dec;19(6):860-5 [8537516.001]
  • [Cites] Neuropathol Appl Neurobiol. 1987 Nov-Dec;13(6):481-7 [3447073.001]
  • [Cites] Surg Neurol. 1983 Sep;20(3):235-8 [6879424.001]
  • [Cites] Br J Neurosurg. 1999 Aug;13(4):420-2 [10616574.001]
  • [Cites] Radiographics. 2001 Nov-Dec;21(6):1533-56 [11706224.001]
  • [Cites] Childs Nerv Syst. 2004 Feb;20(2):119-22 [14669022.001]
  • [Cites] Acta Neurochir (Wien). 2006 Jan;148(1):67-71; discussion 71 [15912255.001]
  • [Cites] Neurosurgery. 1992 Aug;31(2):353-5 [1513442.001]
  • [Cites] J Comput Assist Tomogr. 1988 Mar-Apr;12 (2):351-2 [3280627.001]
  • [Cites] Acta Neuropathol. 1973 Feb 19;23(3):187-99 [4348056.001]
  • [Cites] J Neurosurg. 2005 Feb;102(2):376-81 [15739569.001]
  • [Cites] Cancer. 1979 Nov;44(5):1839-52 [498051.001]
  • [Cites] AJNR Am J Neuroradiol. 1993 Nov-Dec;14 (6):1397-404 [8279337.001]
  • [Cites] Noshuyo Byori. 1996 Apr;13(1):79-83 [8916131.001]
  • [Cites] J Neurosurg. 1992 Jul;77(1):143-7 [1607956.001]
  • [Cites] J Comput Assist Tomogr. 1992 Nov-Dec;16(6):856-9 [1385498.001]
  • [Cites] Neuro Oncol. 2001 Jul;3(3):184-92 [11465399.001]
  • [Cites] Pediatr Neurosurg. 2002 Nov;37(5):254-7 [12411717.001]
  • [Cites] AJNR Am J Neuroradiol. 1996 Jan;17 (1):154-6 [8770268.001]
  • [Cites] Neurosurgery. 2005 Jul;57(1):E191; discussion E191 [15987556.001]
  • [Cites] Neurosurgery. 2001 Dec;49(6):1458-60; discussion 1460-1 [11846948.001]
  • [Cites] AJR Am J Roentgenol. 1992 Dec;159(6):1287-90 [1442403.001]
  • [Cites] J Neurosurg. 1994 Mar;80(3):564-9 [8113873.001]
  • [Cites] Neurosurgery. 2001 Jun;48(6):1358-61 [11383742.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):822-8; discussion 828-9 [8692406.001]
  • [Cites] Arch Pathol Lab Med. 2000 Nov;124(11):1707-9 [11079032.001]
  • [Cites] Clin Neurol Neurosurg. 1997 Feb;99(1):40-5 [9107467.001]
  • [Cites] Neurosurgery. 1994 Nov;35(5):947-50; discussion 950-1 [7838347.001]
  • [Cites] Neurosurgery. 2002 Oct;51(4):1079-82; discussion 1082 [12234421.001]
  • [Cites] J Neurosurg. 1993 Nov;79(5):761-8 [8410257.001]
  • [Cites] Am J Surg Pathol. 1999 Jan;23(1):79-81 [9888706.001]
  • [Cites] AJNR Am J Neuroradiol. 1992 Sep-Oct;13(5):1330-2 [1414823.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):269-74 [8293186.001]
  • [Cites] J Neurooncol. 2005 Jan;71(2):169-71 [15690134.001]
  • [Cites] Acta Neurochir (Wien). 1996;138(5):590-1 [8800336.001]
  • [Cites] Neuroradiology. 1994 Aug;36(6):446-7 [7991088.001]
  • (PMID = 17205313.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 44
  •  go-up   go-down


89. Dimitriadi M, Poulogiannis G, Liu L, Bäcklund LM, Pearson DM, Ichimura K, Collins VP: p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumours. Br J Cancer; 2008 Oct 07;99(7):1144-52
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  • [Title] p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumours.
  • The MDM2 gene is amplified and/or overexpressed in about 10% of glioblastomas and constitutes one of a number of ways the p53 pathway is disrupted in these tumours.
  • Transcription from P2 is believed to be controlled by p53 and a single-nucleotide polymorphism (SNP309, T>G) in P2 is reported to be associated with increased risk for, and early development of, malignancies.
  • We used RT-PCR to study P1- and P2-MDM2 transcript expression in astrocytic tumours, xenografts and cell lines with known MDM2, TP53 and p14(ARF) gene status.
  • Both promoters were used in all genetic backgrounds including the use of the P2 promoter in TP53 null cells, indicating a p53-independent induction of transcription.
  • Transcripts from the P1 promoter formed a greater proportion of the total MDM2 transcripts in tumours with MDM2 amplification, despite these tumours having two wild-type TP53 alleles.
  • Examination of SNP309 in glioblastoma patients showed a borderline association with survival but no apparent correlation with age at diagnosis nor with TP53 and p14(ARF) status of their tumours.
  • Our findings also indicate that elevated MDM2 mRNA levels in tumours with MDM2 amplification are preferentially driven by the P1 promoter and that the P2 promoter is not only regulated by p53 but also by other transcription factor(s).
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins c-mdm2 / genetics. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Adult. Genotype. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] Eur J Cancer. 1999 Jul;35(7):1083-8 [10533452.001]
  • [Cites] Neurol Med Chir (Tokyo). 2007 May;47(5):203-8; discussion 208-9 [17527046.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14517-22 [10588737.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):417-24 [10667596.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(6):2023-30 [10688649.001]
  • [Cites] Oncogene. 2000 Feb 10;19(6):831-5 [10698502.001]
  • [Cites] Int J Cancer. 2000 May 20;89(3):265-70 [10861503.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):587-96 [10934161.001]
  • [Cites] Cell. 2000 Oct 13;103(2):321-30 [11057904.001]
  • [Cites] Cancer Lett. 2001 Mar 26;164(2):177-88 [11179833.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1598-603 [11245471.001]
  • [Cites] Oncogene. 2001 May 31;20(25):3193-205 [11423969.001]
  • [Cites] Oral Oncol. 2001 Dec;37(8):620-31 [11590071.001]
  • [Cites] Oncol Rep. 2002 May-Jun;9(3):557-63 [11956627.001]
  • [Cites] Oncogene. 2002 Mar 27;21(13):1955-62 [11960368.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2616-23 [12750288.001]
  • [Cites] J Biol Chem. 2003 Jul 11;278(28):25716-21 [12730202.001]
  • [Cites] Clin Cancer Res. 2003 Sep 15;9(11):4151-8 [14519639.001]
  • [Cites] Mol Cancer Res. 2003 Dec;1(14):1017-26 [14707285.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(8):3536-51 [15060172.001]
  • [Cites] J Biol Chem. 2004 Jul 9;279(28):29841-8 [15090541.001]
  • [Cites] Int Rev Exp Pathol. 1983;24:135-202 [6601641.001]
  • [Cites] Cell. 1992 Jun 26;69(7):1237-45 [1535557.001]
  • [Cites] Cancer Res. 1993 Jun 15;53(12):2736-9 [8504413.001]
  • [Cites] Genes Dev. 1994 Aug 1;8(15):1739-49 [7958853.001]
  • [Cites] Leuk Lymphoma. 1995 Mar;17(1-2):13-8 [7773150.001]
  • [Cites] Nucleic Acids Res. 1995 Jul 25;23(14):2584-92 [7651818.001]
  • [Cites] Oncogene. 1996 Sep 5;13(5):1065-72 [8806696.001]
  • [Cites] Nature. 1997 May 15;387(6630):296-9 [9153395.001]
  • [Cites] Nature. 1997 May 15;387(6630):299-303 [9153396.001]
  • [Cites] Cancer Res. 1997 Aug 15;57(16):3562-8 [9270029.001]
  • [Cites] Oncogene. 1998 Apr 30;16(17):2249-57 [9619834.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8292-7 [9653180.001]
  • [Cites] Nucleic Acids Res. 1998 Aug 1;26(15):3453-9 [9671804.001]
  • [Cites] Cancer Res. 1998 Nov 15;58(22):5061-5 [9823311.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):864-72 [9858609.001]
  • [Cites] Cell. 2004 Nov 24;119(5):591-602 [15550242.001]
  • [Cites] Clin Cancer Res. 2007 Jun 1;13(11):3215-20 [17545525.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Cancer Cell. 2007 Oct;12(4):303-12 [17936556.001]
  • [Cites] J Neurooncol. 2007 Dec;85(3):241-4 [17568997.001]
  • [Cites] Brain Res. 2008 Mar 10;1198:16-20 [18262501.001]
  • [Cites] Oncogene. 2008 Mar 27;27(14):2097-108 [17934521.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1119-28 [15709179.001]
  • [Cites] Curr Cancer Drug Targets. 2005 Feb;5(1):9-20 [15720185.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Jun;43(2):181-93 [15770670.001]
  • [Cites] J Biol Chem. 2005 Apr 29;280(17):16651-8 [15723837.001]
  • [Cites] Genes Dev. 2005 Sep 15;19(18):2122-37 [16131611.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9582-7 [16230424.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1996-8 [16167062.001]
  • [Cites] J Mol Med (Berl). 2005 Nov;83(11):917-26 [16133418.001]
  • [Cites] Oncogene. 2006 Jul 13;25(30):4183-93 [16501602.001]
  • [Cites] Cancer Lett. 2006 Aug 28;240(2):195-7 [16239061.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1559-61 [16896050.001]
  • [Cites] Int J Cancer. 2007 Feb 1;120(3):563-5 [17096342.001]
  • [Cites] Anticancer Res. 2006 Nov-Dec;26(6C):4975-7 [17214373.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1317-23 [17322917.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Nov;58(11):1170-83 [10560660.001]
  • (PMID = 18781178.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2567066
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90. Nakamura M, Shimada K, Ishida E, Higuchi T, Nakase H, Sakaki T, Konishi N: Molecular pathogenesis of pediatric astrocytic tumors. Neuro Oncol; 2007 Apr;9(2):113-23
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  • [Title] Molecular pathogenesis of pediatric astrocytic tumors.
  • Astrocytomas are the most common pediatric brain tumors, accounting for 7%-8% of all childhood cancers.
  • Relatively few studies have been performed on their molecular properties; therefore, classification of pediatric astrocytic tumors into genetic subtypes similar to that of adult tumors remains to be defined.
  • Here, we report an extensive characterization of 44 pediatric astrocytomas--16 diffuse astrocytomas (WHO grade II), 10 anaplastic astrocytomas (WHO grade III), and 18 glioblastomas (WHO grade IV)--in terms of genetic alterations frequently observed in adult astrocytomas.
  • Loss of heterozygosity (LOH) on 1p/19q and 10p/10q was less common in pediatric astrocytic tumors than in those seen in adults, but the frequency of LOH on 22q was comparable, occurring in 44% of diffuse astrocytomas, 40% of anaplastic astrocytomas, and 61% of glioblastomas.
  • Interestingly, a higher frequency of p53 mutations and LOH on 19q and 22q in tumors from children six or more years of age at diagnosis was found, compared with those from younger children.
  • Our results suggest some differences in children compared to adults in the genetic pathways leading to the formation of de novo astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 22. DNA Mutational Analysis. Female. Gene Amplification. Genes, p53. Glioblastoma / genetics. Humans. Loss of Heterozygosity. Male. Mutation. PTEN Phosphohydrolase / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics

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  • [Cites] Hum Pathol. 1999 Nov;30(11):1284-90 [10571506.001]
  • [Cites] Acta Neuropathol. 2005 Oct;110(4):402-10 [16155764.001]
  • [Cites] Lab Invest. 2000 Jan;80(1):65-72 [10653004.001]
  • [Cites] Brain Pathol. 2000 Apr;10(2):249-59 [10764044.001]
  • [Cites] J Neuropathol Exp Neurol. 2000 Jun;59(6):539-43 [10850866.001]
  • [Cites] Lab Invest. 2001 Jan;81(1):77-82 [11204276.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2124-8 [11280776.001]
  • [Cites] Am J Pathol. 2001 Apr;158(4):1253-62 [11290543.001]
  • [Cites] Brain Pathol. 2001 Apr;11(2):159-68 [11303791.001]
  • [Cites] Carcinogenesis. 2001 Oct;22(10):1715-9 [11577014.001]
  • [Cites] Childs Nerv Syst. 2001 Sep;17(9):503-11 [11585322.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Nov;60(11):1099-104 [11706939.001]
  • [Cites] Cancer. 2001 Dec 15;92(12):3155-64 [11753995.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Acta Neuropathol. 2002 Mar;103(3):267-75 [11907807.001]
  • [Cites] Curr Treat Options Oncol. 2001 Dec;2(6):529-36 [12057098.001]
  • [Cites] J Neurooncol. 2002 Sep;59(2):117-22 [12241104.001]
  • [Cites] Cancer Res. 2003 Feb 15;63(4):737-41 [12591717.001]
  • [Cites] Brain Pathol. 2004 Apr;14(2):131-6 [15193025.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178.001]
  • [Cites] Cancer Res. 1990 May 15;50(10):2987-90 [2334901.001]
  • [Cites] Cancer. 1993 May 15;71(10 Suppl):3229-36 [8490859.001]
  • [Cites] Brain Pathol. 1993 Jan;3(1):19-26 [8269081.001]
  • [Cites] Oncogene. 1994 Mar;9(3):949-54 [8108140.001]
  • [Cites] Neurosurgery. 1994 Feb;34(2):213-9; discussion 219-20 [8177380.001]
  • [Cites] J Neurosurg. 1994 Sep;81(3):427-36 [8057151.001]
  • [Cites] Neurosurgery. 1994 Jun;34(6):967-72; discussion 972-3 [8084407.001]
  • [Cites] Brain Pathol. 1996 Jul;6(3):217-23; discussion 23-4 [8864278.001]
  • [Cites] Neurosurgery. 1996 Feb;38(2):258-64 [8869052.001]
  • [Cites] Cytogenet Cell Genet. 1996;72(2-3):100-12 [8978759.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):304-9 [9000573.001]
  • [Cites] Brain Pathol. 1997 Apr;7(2):755-64 [9161727.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Jul;56(7):782-9 [9210874.001]
  • [Cites] Nat Genet. 1997 Sep;17(1):32-9 [9288095.001]
  • [Cites] Genes Chromosomes Cancer. 1998 May;22(1):9-15 [9591629.001]
  • [Cites] Acta Neuropathol. 1998 Jun;95(6):559-64 [9650746.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Jul;57(7):684-9 [9690672.001]
  • [Cites] Clin Cancer Res. 1999 Jul;5(7):1786-92 [10430083.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4144-52 [10435596.001]
  • [Cites] Lab Invest. 2005 Feb;85(2):165-75 [15592495.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):4085-90 [10632344.001]
  • (PMID = 17327574.001).
  • [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] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC1871665
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91. Rao AA, Laack NN, Giannini C, Wetmore C: Pleomorphic xanthoastrocytoma in children and adolescents. Pediatr Blood Cancer; 2010 Aug;55(2):290-4
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  • BACKGROUND: Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic tumor occurring primarily in children and young adults.
  • The superficial location of the tumor facilitates gross total resection (GTR) thus conferring a relatively favorable outcome with a reported 10-year overall survival (OS) of 70%.
  • PROCEDURE: A retrospective case analysis of children and adolescents diagnosed and treated with PXA in our institution between January 1980 and March 2009 and a literature review.
  • Only one of seven patients with less than a GTR did not recur and median time to recurrence was under 1 year in patients who did not have a GTR.
  • Two of three patients with anaplastic features or malignant transformation at initial presentation progressed.
  • Five-year OS and recurrence free survival (RFS) was 85.7% and 49%, respectively.
  • [MeSH-minor] Adolescent. Brain Neoplasms. Child. Combined Modality Therapy. Diagnostic Imaging. Humans. Neurosurgical Procedures / statistics & numerical data. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20582976.001).
  • [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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92. Kashimura H, Inoue T, Beppu T, Ogasawara K, Ogawa A: Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy--three case reports. Clin Neurol Neurosurg; 2007 Jan;109(1):106-10
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  • [Title] Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy--three case reports.
  • Fractional anisotropy (FA) is influenced by histological data such as cellularity, vascularity and/or fiber structure in astrocytic tumors.
  • We describe two patients with tumor recurrence and one patient with radiation necrosis who were diagnosed using assessment of FA value.
  • The assessment of FA value in enhanced lesions after radiotherapy may be able to differentiate radiation necrosis from tumor recurrence.
  • [MeSH-major] Brain / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging. Glioblastoma / pathology. Neoplasm Recurrence, Local / pathology. Radiation Injuries / pathology
  • [MeSH-minor] Adult. Aged. Anisotropy. Female. Humans. Middle Aged. Necrosis. Radiotherapy / adverse effects

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  • (PMID = 16793199.001).
  • [ISSN] 0303-8467
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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93. Ren XH, Cui XL, Lin S, Wang ZC: [The correlation between combining 1p/19q LOH and pathology in gliomas]. Zhonghua Yi Xue Za Zhi; 2010 Jul 6;90(25):1781-4
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  • METHODS: Tumor samples from 127 glioma patients were collected.
  • RESULTS: The frequencies of combining 1p/19q LOH in astrocytic, oligoastrocytic and oligodendroglial tumors were 19.30%, 50.00% and 80.77% respectively.
  • The frequencies of combining 1p/19q LOH in oligoastrocytic and oligodendroglial tumors were higher than those in astrocytic tumors (P < 0.01) and the frequencies of combining 1p/19q LOH in oligodendroglial tumors was higher than those in oligoastrocytic tumors (P < 0.05).
  • The frequencies of 1p/19q LOH in astrocytic, oligoastrocytic and oligodendroglial tumors were 12.28%, 11.36 and 0 respectively.
  • [MeSH-minor] Adolescent. Adult. Aged. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Female. Humans. Male. Middle Aged. Oligodendroglia / pathology. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Young Adult

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  • (PMID = 20979900.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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94. Weckesser M, Langen KJ, Rickert CH, Kloska S, Straeter R, Hamacher K, Kurlemann G, Wassmann H, Coenen HH, Schober O: O-(2-[18F]fluorethyl)-L-tyrosine PET in the clinical evaluation of primary brain tumours. Eur J Nucl Med Mol Imaging; 2005 Apr;32(4):422-9
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  • [Title] O-(2-[18F]fluorethyl)-L-tyrosine PET in the clinical evaluation of primary brain tumours.
  • PURPOSE: The aim of this study was to evaluate the differential uptake of O-(2-[18F]fluorethyl)-L-tyrosine (FET) in suspected primary brain tumours.
  • METHODS: Positron emission tomography (PET) was performed in 44 patients referred for the evaluation of a suspected brain tumour.
  • Tumour uptake was calculated as the ratio of maximal tumour intensity to mean activity within a reference region (FETmax).
  • RESULTS: FET uptake above the cortical level was observed in 35/44 lesions.
  • No uptake was observed in nine lesions (one inflammatory lesion, one dysembryoplastic neuroepithelial tumour, one mature teratoma, six lesions without histological confirmation).
  • An analysis of uptake dynamics was done in the patients with increased FET uptake (22 gliomas, three lymphomas, three non-neoplastic lesions, three lesions with unknown histology and four other primaries).
  • Upon classification of tumours into low (i.e.
  • ), with FETmax=2.0 in low-grade and 3.2 in high-grade tumours (p<0.05); no significant differences were found in frame 4 (30-40 min p.i.
  • Similar results were obtained when the analysis was applied only to astrocytic tumours (2.0 vs 3.1 in the first frame; 2.4 vs 2.6 in the fourth frame).
  • CONCLUSION: These initial results indicate that FET PET is a useful method to identify malignant brain lesions.
  • It appears that high- and low-grade brain tumours exhibit a different uptake kinetics of FET.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Brain Neoplasms / metabolism. Fluorine Radioisotopes / pharmacokinetics. Positron-Emission Tomography / methods. Tyrosine / analogs & derivatives. Tyrosine / pharmacokinetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Reproducibility of Results. Sensitivity and Specificity

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  • [Cites] Eur J Nucl Med Mol Imaging. 2003 Apr;30(4):519-24 [12589478.001]
  • [Cites] J Nucl Med. 2004 Aug;45(8):1293-8 [15299051.001]
  • [Cites] Radiology. 2002 Nov;225(2):567-74 [12409596.001]
  • [Cites] Eur J Nucl Med. 1999 Feb;26(2):144-51 [9933348.001]
  • [Cites] J Nucl Med. 2001 Aug;42(8):1144-50 [11483672.001]
  • [Cites] J Nucl Med. 1999 Aug;40(8):1367-73 [10450690.001]
  • [Cites] J Nucl Med. 2001 Mar;42(3):432-45 [11337520.001]
  • [Cites] Eur J Nucl Med. 2000 May;27(5):542-9 [10853810.001]
  • [Cites] Eur J Nucl Med. 2000 May;27(5):550-8 [10853811.001]
  • [Cites] J Nucl Med. 1998 Jan;39(1):23-7 [9443732.001]
  • [Cites] Nucl Med Biol. 2003 Jul;30(5):501-8 [12831987.001]
  • [Cites] Neurology. 1998 May;50(5):1316-22 [9595980.001]
  • [Cites] J Nucl Med. 1997 Apr;38(4):517-22 [9098193.001]
  • [Cites] Appl Radiat Isot. 2002 Dec;57(6):853-6 [12406628.001]
  • [Cites] Childs Nerv Syst. 2002 Aug;18(8):445-9 [12192504.001]
  • [Cites] Acta Radiol. 1989 May-Jun;30(3):225-32 [2660886.001]
  • [Cites] Neurosurgery. 2002 May;50(5):958-64; discussion 964-5 [11950398.001]
  • [Cites] Eur J Nucl Med. 1997 Apr;24(4):428-34 [9096095.001]
  • [Cites] J Comput Assist Tomogr. 1983 Dec;7(6):1062-6 [6415134.001]
  • [Cites] Radiology. 1993 Jan;186(1):45-53 [8380108.001]
  • [Cites] Eur J Nucl Med. 2001 Jul;28(7):855-61 [11504082.001]
  • [Cites] J Nucl Med. 1998 May;39(5):778-85 [9591574.001]
  • [Cites] J Nucl Med. 1999 Jan;40(1):205-12 [9935078.001]
  • [Cites] Eur J Nucl Med. 1996 May;23 (5):583-6 [8698067.001]
  • (PMID = 15650870.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / O-(2-fluoroethyl)tyrosine; 0 / Radiopharmaceuticals; 42HK56048U / Tyrosine
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95. Suzuki T, Izumoto S, Fujimoto Y, Maruno M, Ito Y, Yoshimine T: Clinicopathological study of cellular proliferation and invasion in gliomatosis cerebri: important role of neural cell adhesion molecule L1 in tumour invasion. J Clin Pathol; 2005 Feb;58(2):166-71
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  • [Title] Clinicopathological study of cellular proliferation and invasion in gliomatosis cerebri: important role of neural cell adhesion molecule L1 in tumour invasion.
  • Because the nosological definition and histogenesis of GC remain controversial, the morphology and immunohistochemical staining patterns of neoplastic GC cells were compared with those of other gliomas.
  • METHODS: An immunohistochemical analysis of neoplastic cells from four patients with GC and 20 with astrocytic tumours using antibodies against Ki-67, GFAP, and L1, the last of which is a neural cell adhesion molecule putatively related to glioma invasion.
  • RESULTS: GC tumour cells can be divided into two types, those mainly composed of strongly GFAP and L1 positive gemistocytic cells, the other composed of small, GFAP and L1 negative spindle shaped cells.
  • CONCLUSION: The strong expression of L1 in patients with GC and its poor expression in the 20 patients with other types of glioma, including those with GFAP positive gemistocytic astrocytomas, suggest that L1 expression may play a role in the histogenesis of GC.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasms, Neuroepithelial / pathology. Neural Cell Adhesion Molecule L1 / analysis
  • [MeSH-minor] Adult. Aged. Antibodies, Neoplasm / analysis. Astrocytoma / chemistry. Astrocytoma / pathology. Brain Chemistry. Cell Division / physiology. Female. Glial Fibrillary Acidic Protein / analysis. Glioblastoma / chemistry. Glioblastoma / pathology. Humans. Immunohistochemistry / methods. Ki-67 Antigen / immunology. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness

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  • [Cites] Mol Biol Cell. 2001 Sep;12(9):2699-710 [11553709.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):2935-40 [9679949.001]
  • [Cites] Lancet. 2003 Sep 13;362(9387):869-75 [13678974.001]
  • [Cites] J Biol Chem. 2004 Jul 9;279(28):28880-8 [15128735.001]
  • [Cites] Nature. 1983 Sep 29-Oct 5;305(5933):427-30 [6621692.001]
  • [Cites] Nature. 1985 Aug 22-28;316(6030):725-8 [2412126.001]
  • [Cites] Clin Neuropathol. 1985 Jul-Aug;4(4):135-48 [4053456.001]
  • [Cites] J Cell Biol. 1987 Oct;105(4):1893-9 [2444603.001]
  • [Cites] Development. 1988 Apr;102(4):639-55 [3048970.001]
  • [Cites] Surg Neurol. 1991 Dec;36(6):431-40 [1759182.001]
  • [Cites] J Biol Chem. 1992 May 25;267(15):10752-8 [1587850.001]
  • [Cites] Neuroreport. 1992 Jun;3(6):481-4 [1391752.001]
  • [Cites] Neurosci Lett. 1992 Sep 14;144(1-2):221-4 [1436706.001]
  • [Cites] J Neurosci. 1993 Nov;13(11):4764-75 [8229197.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • [Cites] Mol Cell Biol. 1995 Apr;15(4):1942-52 [7891688.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1440-4 [8640837.001]
  • [Cites] J Clin Pathol. 1998 Jan;51(1):13-7 [9577364.001]
  • [Cites] J Cell Biol. 2001 Nov 12;155(4):661-73 [11706054.001]
  • (PMID = 15677537.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Neural Cell Adhesion Molecule L1
  • [Other-IDs] NLM/ PMC1770574
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96. Mahzouni P, Mohammadizadeh F, Mougouei K, Moghaddam NA, Chehrei A, Mesbah A: Determining the relationship between "microvessel density" and different grades of astrocytoma based on immunohistochemistry for "factor VIII-related antigen" (von Willebrand factor) expression in tumor microvessels. Indian J Pathol Microbiol; 2010 Oct-Dec;53(4):605-10
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  • [Title] Determining the relationship between "microvessel density" and different grades of astrocytoma based on immunohistochemistry for "factor VIII-related antigen" (von Willebrand factor) expression in tumor microvessels.
  • BACKGROUND: Astrocytic brain tumors are the most common primary central nervous system tumors, which are classified into four grades.
  • Because tumor angiogenesis is a necessary factor for growth and invasiveness of malignancies, microvessel density (MVD) and intensity of angiogenesis may be used to determine the grade of astrocytomas and plan therapy accordingly.
  • RESULTS: Thirty-six (56%) patients were male and 28 (44%) were female.
  • "Vwf vessel index" (MVD staining intensity of microvessels) was 23.84, 25.62, 31.62, and 62.43 in grades I, II, III, and IV astrocytomas, respectively.
  • The intensity of microvessel stain increases in parallel with increasing tumor grade.
  • [MeSH-minor] Adult. Child. Female. Formaldehyde. Humans. Immunohistochemistry / methods. Male. Microscopy. Middle Aged. Paraffin Embedding. Pathology / methods. Statistics as Topic. Tissue Fixation

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  • (PMID = 21045378.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / von Willebrand Factor; 1HG84L3525 / Formaldehyde
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97. Hänninen MM, Haapasalo J, Haapasalo H, Fleming RE, Britton RS, Bacon BR, Parkkila S: Expression of iron-related genes in human brain and brain tumors. BMC Neurosci; 2009;10:36
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  • [Title] Expression of iron-related genes in human brain and brain tumors.
  • We investigated the mRNA levels of hepcidin (HAMP), HFE, neogenin (NEO1), transferrin receptor 1 (TFRC), transferrin receptor 2 (TFR2), and hemojuvelin (HFE2) in normal human brain, brain tumors, and astrocytoma cell lines.
  • The specimens included 5 normal brain tissue samples, 4 meningiomas, one medulloblastoma, 3 oligodendrocytic gliomas, 2 oligoastrocytic gliomas, 8 astrocytic gliomas, and 3 astrocytoma cell lines.
  • In most tumor types, the pattern of gene expression was diverse.
  • Notable findings include high expression of transferrin receptor 1 in the hippocampus and medulla oblongata compared to other brain regions, low expression of HFE in normal brain with elevated HFE expression in meningiomas, and absence of hepcidin mRNA in astrocytoma cell lines despite expression in normal brain and tumor specimens.
  • CONCLUSION: These results indicate that several iron-related genes are expressed in normal brain, and that their expression may be dysregulated in brain tumors.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Histocompatibility Antigens Class I / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antimicrobial Cationic Peptides / genetics. Antimicrobial Cationic Peptides / metabolism. Astrocytoma / genetics. Astrocytoma / metabolism. Cell Line, Tumor. Female. GPI-Linked Proteins. Hepcidins. Humans. Male. Meningioma / genetics. Meningioma / metabolism. Middle Aged. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. RNA, Messenger / analysis. Receptors, Transferrin / genetics. Receptors, Transferrin / metabolism. Statistics, Nonparametric. Young Adult

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  • [Cites] Histochem Cell Biol. 2001 Mar;115(3):195-203 [11326747.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Apr;290(4):G590-4 [16537971.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2213-21 [11489794.001]
  • [Cites] J Natl Cancer Inst. 2001 Sep 5;93(17):1337-43 [11535709.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] J Clin Invest. 2002 Oct;110(7):1037-44 [12370282.001]
  • [Cites] Biometals. 2003 Mar;16(1):63-75 [12572665.001]
  • [Cites] Blood. 2003 Aug 1;102(3):783-8 [12663437.001]
  • [Cites] Brain Res Bull. 2003 Aug 30;61(4):365-74 [12909279.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):343-54 [15122348.001]
  • [Cites] Nat Rev Neurosci. 2004 Nov;5(11):863-73 [15496864.001]
  • [Cites] J Neurosurg. 1990 Jun;72(6):941-5 [2159987.001]
  • [Cites] Nat Genet. 1996 Aug;13(4):399-408 [8696333.001]
  • [Cites] J Comp Neurol. 1996 Nov 25;375(4):675-92 [8930792.001]
  • [Cites] J Neurol Sci. 2004 Dec 15;227(1):27-33 [15546588.001]
  • [Cites] Science. 2004 Dec 17;306(5704):2090-3 [15514116.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Dev Comp Immunol. 2005;29(11):939-50 [15935472.001]
  • [Cites] J Biol Chem. 2005 Oct 7;280(40):33885-94 [16103117.001]
  • [Cites] BMC Neurol. 2006;6:24 [16824219.001]
  • [Cites] J Neurosci Res. 2006 Sep;84(4):790-800 [16933319.001]
  • [Cites] J Alzheimers Dis. 2006 Nov;10(2-3):215-22 [17119289.001]
  • [Cites] J Alzheimers Dis. 2006 Nov;10(2-3):267-76 [17119292.001]
  • [Cites] J Histochem Cytochem. 2007 Jan;55(1):85-96 [16982849.001]
  • [Cites] Eur J Haematol. 2007 Jan;78(1):1-10 [17042775.001]
  • [Cites] J Clin Invest. 2007 Jul;117(7):1926-32 [17557118.001]
  • [Cites] Retina. 2007 Oct;27(8):997-1003 [18040235.001]
  • [Cites] Blood. 2008 Jan 15;111(2):924-31 [17938254.001]
  • [Cites] Biochemistry. 2008 Apr 8;47(14):4237-45 [18335997.001]
  • [Cites] Cell Metab. 2008 Apr;7(4):288-90 [18396134.001]
  • [Cites] J Biol Chem. 2008 Jun 20;283(25):17494-502 [18445598.001]
  • [Cites] Nat Rev Cancer. 2008 Dec;8(12):967-75 [18987634.001]
  • [Cites] BMC Cancer. 2005;5:154 [16324219.001]
  • [Cites] Brain Pathol. 2005 Oct;15(4):297-310 [16389942.001]
  • [Cites] J Clin Oncol. 2006 Mar 10;24(8):1253-65 [16525180.001]
  • [Cites] J Biol Chem. 2001 Mar 16;276(11):7806-10 [11113131.001]
  • (PMID = 19386095.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antimicrobial Cationic Peptides; 0 / CD71 antigen; 0 / GPI-Linked Proteins; 0 / HAMP protein, human; 0 / HFE protein, human; 0 / HFE2 protein, human; 0 / Hepcidins; 0 / Histocompatibility Antigens Class I; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Transferrin; 0 / TFR2 protein, human; 0 / neogenin
  • [Other-IDs] NLM/ PMC2679039
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98. Hartmann C, Meyer J, Balss J, Capper D, Mueller W, Christians A, Felsberg J, Wolter M, Mawrin C, Wick W, Weller M, Herold-Mende C, Unterberg A, Jeuken JW, Wesseling P, Reifenberger G, von Deimling A: Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas. Acta Neuropathol; 2009 Oct;118(4):469-74
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  • [Title] Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas.
  • IDH2 encoding mitochondrial NADP+-dependent isocitrate dehydrogenase is also mutated in these tumors, albeit at much lower frequencies.
  • Preliminary data suggest an importance of IDH1 mutation for prognosis showing that patients with anaplastic astrocytomas, oligodendrogliomas and oligoastrocytomas harboring IDH1 mutations seem to fare much better than patients without this mutation in their tumors.
  • We report on an inverse association of IDH1 and IDH2 mutations in these gliomas and a non-random distribution of the mutation types within the tumor entities.
  • IDH1 mutations of the R132C type are strongly associated with astrocytoma, while IDH2 mutations predominantly occur in oligodendroglial tumors.
  • In addition, patients with anaplastic glioma harboring IDH1 mutations were on average 6 years younger than those without these alterations.
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Isocitrate Dehydrogenase / genetics
  • [MeSH-minor] Adult. Age Factors. Brain / pathology. Cell Differentiation. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Mutation. Prognosis. Tumor Cells, Cultured

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  • (PMID = 19554337.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase
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99. Jha P, Suri V, Jain A, Sharma MC, Pathak P, Jha P, Srivastava A, Suri A, Gupta D, Chosdol K, Chattopadhyay P, Sarkar C: O6-methylguanine DNA methyltransferase gene promoter methylation status in gliomas and its correlation with other molecular alterations: first Indian report with review of challenges for use in customized treatment. Neurosurgery; 2010 Dec;67(6):1681-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: O6-methylguanine methyltransferase (MGMT) promoter methylation in adult glioblastomas (glioblastoma multiforme) is considered a promising molecular alteration, predictive of better response to temozolomide therapy and longer overall survival.
  • OBJECTIVE: To look at the frequency of MGMT methylation in glial tumors of all grades and types, and correlate this alteration with loss of heterozygosity 1p/19q, TP53 gene mutations, epidermal growth factor receptor (EGFR) amplification, and isocitrate dehydrogenase 1 (IDH1) mutations.
  • RESULTS: There was an inverse correlation of MGMT promoter methylation frequency with tumor grade, observed in 79.4%, 70.8%, and 56.8% of grade II, grade III, and grade IV gliomas, respectively.
  • The difference was statistically significant in grade II vs IV tumors (P=.036).
  • In astrocytic tumors, there was no correlation of MGMT methylation with TP53 mutation or EGFR amplification.
  • [MeSH-major] Brain Neoplasms / genetics. DNA Methylation / genetics. Gene Expression Regulation, Neoplastic / genetics. Glioma / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adult. Antineoplastic Agents, Alkylating / therapeutic use. Chromosomes, Human, Pair 1 / genetics. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Designer Drugs. Female. Humans. India. Isocitrate Dehydrogenase / genetics. Isocitrate Dehydrogenase / metabolism. Male. Middle Aged. Mutation / genetics. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Retrospective Studies. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 21107199.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Designer Drugs; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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100. Sareddy GR, Panigrahi M, Challa S, Mahadevan A, Babu PP: Activation of Wnt/beta-catenin/Tcf signaling pathway in human astrocytomas. Neurochem Int; 2009 Sep;55(5):307-17
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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 Wnt/beta-catenin/Tcf signaling pathway in human astrocytomas.
  • Astrocytomas are the most common form of primary brain tumors.
  • Although, over activation of Wnt/beta-catenin/Tcf pathway is a hallmark of several forms of cancer, little is known about its role in human astrocytomas.
  • Here, we report the evidence that Wnt/beta-catenin/Tcf signaling pathway is constitutively activated in astrocytic tumors.
  • In the present study, human astrocytic tumors with different clinical grades were analyzed for mRNA expression of Dvl-1, Dvl-2, Dvl-3, beta-catenin, c-myc and cyclin D1 and protein levels of beta-catenin, Lef1, Tcf4, c-Myc, N-Myc, c-jun and cyclin D1.
  • Western blotting revealed upregulation of beta-catenin, Lef1, Tcf4 and their target proteins in the core tumor tissues in comparison to peritumor and normal brain tissues.
  • [MeSH-minor] Adolescent. Adult. Base Sequence. Blotting, Western. DNA Primers. Female. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult






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