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1. Hoffman S, Propp JM, McCarthy BJ: Temporal trends in incidence of primary brain tumors in the United States, 1985-1999. Neuro Oncol; 2006 Jan;8(1):27-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Data for the years 1985 through 1999 from six collaborating state cancer registries of the Central Brain Tumor Registry of the United States were used to determine incidence trends in the broad age groups 0-19, 20-64, and >or=65 years, overall and for selected histologies.
  • Specific histologies that were increasing included anaplastic astrocytomas in individuals aged >or=65 years, microscopically confirmed gliomas in both adult age groups, and microscopically confirmed glioma, not otherwise specified (NOS), in children.
  • Decreases were noted for astrocytoma, NOS, nonmicroscopically confirmed gliomas, and pituitary tumors.
  • Improvements in diagnosis and classification are likely reflected in the decreasing trends in unspecified glioma subgroups and the accompanying increasing trends in more specific glioma subgroups.

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  • [Cites] Neuroepidemiology. 2004 May-Jun;23(3):101-9 [15084778.001]
  • [Cites] Neuro Oncol. 2006 Jan;8(1):1-11 [16443943.001]
  • [Cites] N Engl J Med. 1985 Oct 3;313(14):859-64 [3897866.001]
  • [Cites] AJR Am J Roentgenol. 1986 Sep;147(3):453-5 [3488645.001]
  • [Cites] J Natl Cancer Inst. 1990 Oct 17;82(20):1621-4 [2213902.001]
  • [Cites] Am J Ind Med. 1991;19(4):421-31 [2035544.001]
  • [Cites] CMAJ. 1991 Dec 15;145(12):1583-91 [1742695.001]
  • [Cites] J Natl Cancer Inst. 1991 Nov 20;83(22):1679-81 [1749021.001]
  • [Cites] Cancer. 1992 Mar 1;69(5):1300-6 [1739929.001]
  • [Cites] J Natl Cancer Inst. 1992 Mar 18;84(6):442-5 [1538422.001]
  • [Cites] Neurosurgery. 1992 Jul;31(1):78-82 [1641113.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • [Cites] Br J Cancer. 1994 Nov;70(5):973-9 [7947107.001]
  • [Cites] Cancer. 1995 Jan 1;75(1 Suppl):330-7 [8001004.001]
  • [Cites] Ann Neurol. 1995 Jan;37(1):67-73 [7818260.001]
  • [Cites] Eur J Cancer. 1994;30A(10):1498-511 [7833109.001]
  • [Cites] IARC Sci Publ. 1994;(128):1-302 [7698823.001]
  • [Cites] Cancer. 1995 Nov 1;76(9):1634-42 [8635069.001]
  • [Cites] Cancer. 1996 Aug 1;78(3):532-41 [8697401.001]
  • [Cites] Paediatr Perinat Epidemiol. 1996 Jul;10(3):319-38 [8822774.001]
  • [Cites] Int J Epidemiol. 1995 Dec;24(6):1078-85 [8824847.001]
  • [Cites] Stat Med. 2000 Feb 15;19(3):335-51 [10649300.001]
  • [Cites] Cancer. 2000 May 15;88(10):2342-9 [10820357.001]
  • [Cites] N Engl J Med. 2001 Jan 11;344(2):79-86 [11150357.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Mar;60(3):248-62 [11245209.001]
  • [Cites] Neuro Oncol. 2001 Jul;3(3):141-51 [11465394.001]
  • [Cites] Neuro Oncol. 1999 Jan;1(1):14-25 [11554386.001]
  • [Cites] Brain Pathol. 2002 Apr;12(2):257-9 [11958379.001]
  • [Cites] Neurology. 2002 Apr 23;58(8):1304-6 [11971109.001]
  • [Cites] Cancer. 2002 Jul 1;95(1):193-202 [12115333.001]
  • [Cites] J Neurooncol. 2002 Oct;60(1):61-9 [12416547.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Feb;62(2):111-26 [12578221.001]
  • [Cites] Neuroepidemiology. 2003 Mar-Apr;22(2):124-9 [12629278.001]
  • [Cites] Int J Cancer. 2004 Jan 20;108(3):450-5 [14648713.001]
  • [Cites] Neuroepidemiology. 2004 Jan-Apr;23(1-2):85-93 [14739573.001]
  • [Cites] Am J Epidemiol. 2004 Feb 1;159(3):277-83 [14742288.001]
  • [Cites] Cancer. 1997 Apr 1;79(7):1381-93 [9083161.001]
  • [Cites] J Natl Cancer Inst. 1998 Sep 2;90(17):1269-77 [9731733.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 7;91(7):648-9 [10203289.001]
  • [Cites] AIDS. 1999 Jan 14;13(1):103-8 [10207551.001]
  • [Cites] Cancer. 1999 May 1;85(9):2077-90 [10223251.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 2;91(11):973-4 [10359552.001]
  • [Cites] J Natl Cancer Inst. 1999 Aug 18;91(16):1382-90 [10451443.001]
  • [Cites] Neurology. 1999 Sep 22;53(5):1141-3 [10496285.001]
  • [Cites] Cancer. 2004 Nov 15;101(10):2293-9 [15476282.001]
  • [Cites] Epidemiology. 2004 Nov;15(6):653-9 [15475713.001]
  • (PMID = 16443945.001).
  • [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
  • [Other-IDs] NLM/ PMC1871920
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2. Götze S, Wolter M, Reifenberger G, Müller O, Sievers S: Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas. Int J Cancer; 2010 Jun 1;126(11):2584-93
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  • [Title] Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas.
  • Recent studies suggested a role of Wnt signaling in gliomas, the most common primary brain tumors.
  • We investigated 70 gliomas of different malignancy grades for promoter hypermethylation in 8 genes encoding members of the secreted frizzled-related protein (SFRP1, SFRP2, SFRP4, SFRP5), dickkopf (DKK1, DKK3) and naked (NKD1, NKD2) families of Wnt pathway inhibitors.
  • While none of the tumors carried CTNNB1 mutations, we found frequent promoter hypermethylation of Wnt pathway inhibitor genes, with at least one of these genes being hypermethylated in 6 of 16 diffuse astrocytomas (38%), 4 of 14 anaplastic astrocytomas (29%), 7 of 10 secondary glioblastomas (70%) and 23 of 30 primary glioblastomas (77%).
  • Furthermore, SFRP1-hypermethylated gliomas showed significantly lower expression of the respective transcripts when compared with unmethylated tumors.
  • Taken together, our results suggest an important role of epigenetic silencing of Wnt pathway inhibitor genes in astrocytic gliomas, in particular, in glioblastomas, with distinct patterns of hypermethylated genes distinguishing primary from secondary glioblastomas.
  • [MeSH-major] Astrocytoma / genetics. DNA Methylation / genetics. Promoter Regions, Genetic. Wnt Proteins / genetics
  • [MeSH-minor] Carrier Proteins / genetics. Cell Line, Tumor. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Exons. Eye Proteins / genetics. Glioblastoma / genetics. Glioblastoma / secondary. Glioma / genetics. Glioma / pathology. Humans. Intercellular Signaling Peptides and Proteins / genetics. Membrane Proteins / genetics. Mutation. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. beta Catenin / genetics

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

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  • [Cites] Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):639-44 [12515857.001]
  • [Cites] J Clin Oncol. 2001 Sep 15;19(18 Suppl):41S-44S [11560970.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6962-70 [14583498.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Mar 1;58(3):972-5 [14967458.001]
  • [Cites] J Neuropathol Exp Neurol. 2004 Jul;63(7):700-7 [15290895.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178.001]
  • [Cites] Biometrika. 1965 Dec;52(3):650-3 [5858975.001]
  • [Cites] Cancer Res. 1984 Mar;44(3):1002-7 [6318979.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jun;87(11):4207-11 [1693434.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8602-6 [2236070.001]
  • [Cites] Cancer Res. 1991 Apr 15;51(8):2164-72 [2009534.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;22(1):225-30 [1309204.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2965-9 [1557402.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 May 15;89(10):4309-13 [1584765.001]
  • [Cites] Cancer Res. 1994 Feb 15;54(4):1008-15 [8313355.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3127-30 [8205529.001]
  • [Cites] Oncogene. 1994 Aug;9(8):2313-20 [8036013.001]
  • [Cites] Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182.001]
  • [Cites] Cancer Res. 1995 Dec 1;55(23):5536-9 [7585629.001]
  • [Cites] Cancer Res. 1996 Sep 1;56(17):3859-61 [8752145.001]
  • [Cites] Oncogene. 1996 Sep 5;13(5):1065-72 [8806696.001]
  • [Cites] Clin Cancer Res. 1998 Jan;4(1):215-22 [9516974.001]
  • [Cites] Oncol Res. 1997;9(11-12):581-7 [9563005.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Jul;57(7):684-9 [9690672.001]
  • [Cites] Int J Oncol. 1998 Oct;13(4):717-24 [9735401.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Dec;57(12):1138-45 [9862636.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1383-7 [10728703.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7503-8 [10852962.001]
  • [Cites] Cell. 2000 Oct 13;103(2):211-25 [11057895.001]
  • [Cites] Oncol Res. 2000;12(2):107-12 [11132923.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Feb;2(2):127-37 [11252954.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 15;93(16):1246-56 [11504770.001]
  • [Cites] Clin Cancer Res. 2003 Sep 15;9(11):4151-8 [14519639.001]
  • (PMID = 16133418.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / CRUK/ A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2815848; NLM/ UKMS2690
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4. Ritch PS, Carroll SL, Sontheimer H: Neuregulin-1 enhances survival of human astrocytic glioma cells. Glia; 2005 Aug 15;51(3):217-28
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  • [Title] Neuregulin-1 enhances survival of human astrocytic glioma cells.
  • Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.
  • In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.
  • Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.
  • We then verify receptor expression in a panel of human glioma cell lines.
  • Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.
  • Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.
  • Moreover, Nrg-1beta activates an inhibitor of apoptosis, Akt, implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas.
  • This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

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  • [Cites] Oncogene. 1992 Sep;7(9):1859-66 [1354348.001]
  • [Cites] Neurosurgery. 1993 Jul;33(1):106-15 [7689190.001]
  • [Cites] Mol Cell Biol. 1994 Jan;14(1):492-500 [8264617.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 1;91(3):1064-8 [8302832.001]
  • [Cites] Mol Cell Biol. 1994 Mar;14(3):1909-19 [7509448.001]
  • [Cites] Mol Cell Biol. 1994 Jun;14(6):3550-8 [7515147.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9387-91 [7937775.001]
  • [Cites] Biochim Biophys Acta. 1994 Dec 30;1198(2-3):165-84 [7819273.001]
  • [Cites] Oncogene. 1995 Apr 6;10(7):1403-11 [7731691.001]
  • [Cites] J Cell Biol. 1995 Jul;130(1):127-35 [7540614.001]
  • [Cites] J Biol Chem. 1995 Aug 11;270(32):19188-96 [7642587.001]
  • [Cites] Neuron. 1996 Aug;17(2):229-43 [8780647.001]
  • [Cites] Mol Cell Neurosci. 1996 Apr;7(4):247-62 [8793861.001]
  • [Cites] EMBO J. 1997 Apr 1;16(7):1647-55 [9130710.001]
  • [Cites] Nature. 1997 May 29;387(6632):509-12 [9168114.001]
  • [Cites] Nature. 1997 May 29;387(6632):512-6 [9168115.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):4007-14 [9199335.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9562-7 [9275162.001]
  • [Cites] J Neurochem. 1997 Nov;69(5):1859-63 [9349528.001]
  • [Cites] J Neurosci Res. 1997 Dec 1;50(5):755-68 [9418963.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):193-209 [9440020.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):223-48 [9440022.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):335-46 [9440030.001]
  • [Cites] Genes Dev. 1998 Jun 15;12(12):1825-36 [9637684.001]
  • [Cites] Biochem J. 1998 Aug 1;333 ( Pt 3):757-63 [9677338.001]
  • [Cites] Biochem J. 1998 Oct 1;335 ( Pt 1):1-13 [9742206.001]
  • [Cites] Can J Neurol Sci. 1998 Nov;25(4):267-81 [9827227.001]
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3675-85 [9851974.001]
  • [Cites] Eur J Neurosci. 1999 Mar;11(3):769-80 [10103071.001]
  • [Cites] Mol Cell Neurosci. 1999 Feb;13(2):79-94 [10192767.001]
  • [Cites] Oncogene. 1999 Apr 29;18(17):2681-9 [10348342.001]
  • [Cites] EMBO J. 1994 Jun 15;13(12):2831-41 [8026468.001]
  • [Cites] Adv Cancer Res. 2000;77:25-79 [10549355.001]
  • [Cites] Glia. 2000 Jan 15;29(2):104-11 [10625327.001]
  • [Cites] Toxicol Pathol. 2000 Jan-Feb;28(1):171-7 [10669005.001]
  • [Cites] Biochem J. 2000 Mar 15;346 Pt 3:561-76 [10698680.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3159-67 [10880430.001]
  • [Cites] J Neurosci. 2000 Oct 15;20(20):7622-30 [11027222.001]
  • [Cites] Bioessays. 2000 Nov;22(11):987-96 [11056475.001]
  • [Cites] Brain Res Dev Brain Res. 2000 Nov 30;124(1-2):93-9 [11113516.001]
  • [Cites] Annu Rev Neurosci. 2001;24:385-428 [11283316.001]
  • [Cites] Neuro Oncol. 2000 Apr;2(2):96-102 [11303626.001]
  • [Cites] Mol Cell Neurosci. 2001 Apr;17(4):761-7 [11312610.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2841-51 [11042203.001]
  • [Cites] J Biol Chem. 2001 Mar 9;276(10):7320-6 [11058599.001]
  • [Cites] Curr Opin Neurobiol. 2001 Jun;11(3):287-96 [11399426.001]
  • [Cites] J Neurooncol. 2001 Feb;51(3):245-64 [11407596.001]
  • [Cites] J Neurosci. 2001 Jul 1;21(13):4740-51 [11425901.001]
  • [Cites] Genes Dev. 2001 Aug 1;15(15):1913-25 [11485986.001]
  • [Cites] Curr Opin Neurol. 2001 Dec;14(6):683-8 [11723374.001]
  • [Cites] Fed Proc. 1983 Jun;42(9):2627-9 [6852276.001]
  • [Cites] Nature. 1985 Jan 10-18;313(5998):144-7 [2981413.001]
  • [Cites] Cell. 1985 Jul;41(3):697-706 [2860972.001]
  • [Cites] Science. 1985 Dec 6;230(4730):1132-9 [2999974.001]
  • [Cites] Cell. 1986 Jun 6;45(5):649-57 [2871941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903 [3477813.001]
  • [Cites] Cancer Res. 1988 Jul 15;48(14):3910-8 [2454731.001]
  • [Cites] Science. 1989 May 12;244(4905):707-12 [2470152.001]
  • [Cites] Neurosurgery. 1989 Nov;25(5):681-94 [2685640.001]
  • [Cites] J Neurosurg. 1991 Aug;75(2):284-93 [1649272.001]
  • [Cites] Ann N Y Acad Sci. 1991;633:35-47 [1789559.001]
  • [Cites] Cell. 1992 Apr 3;69(1):205-16 [1348215.001]
  • [Cites] J Neurosci Res. 1992 Jan;31(1):175-87 [1377283.001]
  • (PMID = 15812817.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247-010003; United States / NINDS NIH HHS / NS / R01 NS036692-05A1; United States / NCI NIH HHS / CA / CA097247-010003; United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50CA97247; United States / NINDS NIH HHS / NS / NS036692-05A1; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01-NS36692; United States / NINDS NIH HHS / NS / R01 NS036692-06; United States / NINDS NIH HHS / NS / NS036692-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuregulin-1; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS25075; NLM/ PMC2548407
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5. Meini A, Sticozzi C, Massai L, Palmi M: A nitric oxide/Ca(2+)/calmodulin/ERK1/2 mitogen-activated protein kinase pathway is involved in the mitogenic effect of IL-1beta in human astrocytoma cells. Br J Pharmacol; 2008 Apr;153(8):1706-17
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  • [Title] A nitric oxide/Ca(2+)/calmodulin/ERK1/2 mitogen-activated protein kinase pathway is involved in the mitogenic effect of IL-1beta in human astrocytoma cells.
  • EXPERIMENTAL APPROACH: In this study we used human astrocytoma U-373MG cells to investigate the role of nitric oxide (NO), intracellular Ca(2+) concentration ([Ca(2+)](i)), and extracellular signal-regulated protein kinase (ERK) in the signalling pathway mediating IL-1beta-induced astrocyte proliferation.
  • Pretreatment with the nonspecific NOS inhibitor, N-omega-nitro-l-arginine methyl ester (L-NAME) or the selective iNOS inhibitor, N-[[3-(aminomethyl)phenyl]methyl]-ethanimidamide dihydrochloride (1400W), antagonized ERK activation and cell proliferation induced by IL-1beta.
  • [MeSH-minor] Astrocytoma / metabolism. Calcium / metabolism. Calmodulin / metabolism. Cell Proliferation / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Mitosis / physiology. Nitric Oxide / metabolism. Time Factors

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  • [Cites] Korean J Ophthalmol. 2003 Jun;17(1):1-6 [12882501.001]
  • [Cites] J Neurosci Res. 2007 Jun;85(8):1694-703 [17465018.001]
  • [Cites] Eur J Neurosci. 2004 Jan;19(2):479-84 [14725643.001]
  • [Cites] J Neurosci. 2004 Mar 17;24(11):2837-45 [15028778.001]
  • [Cites] Curr Mol Med. 2004 Mar;4(2):193-205 [15032713.001]
  • [Cites] Prog Neurobiol. 2004 Feb;72(2):111-27 [15063528.001]
  • [Cites] Trends Neurosci. 2004 May;27(5):238-40 [15111002.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):19936-47 [14996842.001]
  • [Cites] J Cell Sci. 2004 Sep 15;117(Pt 20):4727-37 [15331636.001]
  • [Cites] Med Sci Monit. 2004 Sep;10(9):BR325-30 [15328477.001]
  • [Cites] J Cell Biol. 1982 Aug;94(2):325-34 [6980885.001]
  • [Cites] Science. 1985 Apr 26;228(4698):497-9 [3872478.001]
  • [Cites] Lymphokine Res. 1987 Spring;6(2):83-91 [3495709.001]
  • [Cites] Brain Res. 1988 Feb 1;466(2):201-10 [3359311.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Mar 30;167(3):1242-8 [2157429.001]
  • [Cites] Rev Physiol Biochem Pharmacol. 1992;119:67-121 [1604156.001]
  • [Cites] J Neurol Sci. 1992 Aug;111(1):92-103 [1403003.001]
  • [Cites] FEBS Lett. 2000 Apr 28;472(2-3):203-7 [10788611.001]
  • [Cites] Br J Pharmacol. 2000 Jun;130(4):891-9 [10864897.001]
  • [Cites] J Neurosci. 2000 Dec 15;20(24):8980-6 [11124973.001]
  • [Cites] Br J Pharmacol. 2001 Apr;132(7):1531-41 [11264247.001]
  • [Cites] Circulation. 2001 Sep 18;104(12 Suppl 1):I344-9 [11568080.001]
  • [Cites] Mol Neurobiol. 2002 Apr;25(2):133-47 [11936556.001]
  • [Cites] Cell Signal. 2002 Aug;14(8):649-54 [12020764.001]
  • [Cites] J Mol Cell Cardiol. 2002 May;34(5):583-96 [12056861.001]
  • [Cites] Neurosignals. 2002 Jul-Aug;11(4):175-90 [12393944.001]
  • [Cites] Neuroscientist. 2003 Feb;9(1):10-22 [12580336.001]
  • [Cites] Eur J Neurosci. 2003 Feb;17(4):692-700 [12603259.001]
  • [Cites] Nature. 1993 Jan 28;361(6410):315-25 [8381210.001]
  • [Cites] Prog Brain Res. 1992;94:353-65 [1337615.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Mar 15;191(2):327-34 [7681665.001]
  • [Cites] Neurosci Lett. 1994 Jun 20;174(2):123-6 [7526282.001]
  • [Cites] Nature. 1995 Aug 10;376(6540):524-7 [7637786.001]
  • [Cites] Eur J Pharmacol. 1995 Jul 25;281(1):97-9 [8566125.001]
  • [Cites] J Neurochem. 1996 Apr;66(4):1496-503 [8627304.001]
  • [Cites] Am J Pathol. 1996 Mar;148(3):889-96 [8774143.001]
  • [Cites] Br J Pharmacol. 1996 Aug;118(7):1705-10 [8842435.001]
  • [Cites] N Engl J Med. 1998 Jan 29;338(5):278-85 [9445407.001]
  • [Cites] Science. 1998 May 15;280(5366):1082-6 [9582122.001]
  • [Cites] Eur J Neurosci. 2005 May;21(9):2347-60 [15932594.001]
  • [Cites] Curr Opin Investig Drugs. 2005 Jul;6(7):700-3 [16044665.001]
  • [Cites] Nitric Oxide. 2006 May;14(3):238-46 [16300973.001]
  • [Cites] Eur J Neurosci. 2006 Apr;23(7):1690-700 [16623825.001]
  • [Cites] J Neurochem. 2006 Jun;97(6):1676-89 [16805776.001]
  • [Cites] Diabetes. 2006 Sep;55(9):2455-62 [16936193.001]
  • [Cites] Glia. 2003 Oct;44(1):47-56 [12951656.001]
  • (PMID = 18297103.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calmodulin; 0 / Interleukin-1beta; 31C4KY9ESH / Nitric Oxide; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2438268
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6. Komotar RJ, Carson BS, Rao C, Chaffee S, Goldthwaite PT, Tihan T: Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases. Neurosurgery; 2005 Jan 01;56(1):E206-E210

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

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  • (PMID = 28184642.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. Uno M, Oba-Shinjo SM, Wakamatsu A, Huang N, Avancini Ferreira Alves V, Rosemberg S, Pires de Aguiar PH, Leite C, Miura F, Marino J R, Scaff M, Nagahashi-Marie SK: Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas. Int J Biol Markers; 2006 Jan - Mar;21(1):50-57

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

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  • (PMID = 28207094.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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8. Fisher PG, Tihan T, Goldthwaite PT, Wharam MD, Carson BS, Weingart JD, Repka MX, Cohen KJ, Burger PC: Outcome analysis of childhood low-grade astrocytomas. Pediatr Blood Cancer; 2008 Aug;51(2):245-50
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  • [Title] Outcome analysis of childhood low-grade astrocytomas.
  • BACKGROUND: We aimed to determine the long-term natural history of low-grade astrocytomas (LGA) in children, with respect to pathology, and to evaluate influence of treatment on survival.
  • RESULTS: Two hundred seventy-eight children (160 males; mean age 9.1 years; tumor location: 77 cerebrum, 62 cerebellum, 51 hypothalamic, 30 thalamus, 9 ventricle, 40 brainstem, and 9 spine) were assessed.
  • Among 246 specimens reviewed, diagnoses were 135 pilocytic astrocytoma (PA), 27 diffuse astrocytoma (DA), 75 unclassifiable well-differentiated astrocytoma (NOS), and 9 subependymal giant cell astrocytoma.
  • Reviewed diagnoses were highly associated with OS (P < 0.0001), with 5-year OS for PA 96%, DA 48%, and NOS 86%; these differences remained significant when stratified by location or extent of resection.
  • Among patients with residual tumor after surgery, 5-year PFS was 48% with observation alone (n = 114), no different (P = 0.32) from that achieved with immediate irradiation (n = 86).
  • While tumor location and resection extent affect outcome, pathologic diagnosis when carefully interpreted significantly influences long-term survival.
  • [MeSH-major] Astrocytoma / mortality. Brain Neoplasms / mortality

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  • (PMID = 18386785.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Khattab AZ, Ahmed MI, Fouad MA, Essa WA: Significance of p53 and CD31 in astrogliomas. Med Oncol; 2009;26(1):86-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of p53 and CD31 in astrogliomas.
  • BACKGROUND: Astrogliomas are the most common primary brain tumor.
  • Its progression is the result of activation of oncogenes, inactivation of tumor suppressor genes (TSGs), and expression of various growth factors.
  • The angiogenesis and p53 in astrogliomas play an important role in its grading, treatment strategies, and hence its clinical outcome.
  • OBJECTIVES: To analyze the frequency of presentation and the possible co-expression of p53 and angiogenesis marker (CD31) and their clinical implications in astrogliomas.
  • MATERIAL AND METHODS: This retrograde study included 45 cases with astrocytomas in the form of paraffin blocks.
  • Sections were stained with hematoxylin and eosin to determine the type and histological grade according to WHO (2007) classification of CNS tumors.
  • RESULTS: Both p53 and CD31 expressions were correlated well with the histopathological grades of different subtypes of astrogliomas with good discrimination between low and high grades.
  • Overall, a highly significant statistical correlation was observed between the grades of astrocytomas and the p53 and CD31 labeling indices.
  • Obviously, these observations demonstrate that the co-expression and increased levels of p53 and CD31 in astrogliomas are increasing as the tumor grade is increasing.
  • Thus, the two markers can be used as adjunct to the diagnosis and stratification of the high grade from the low-grade intrinsic brain astrogliomas.
  • [MeSH-major] Antigens, CD31 / biosynthesis. Astrocytoma / metabolism. Biomarkers, Tumor. Brain Neoplasms / metabolism. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neoplasm Staging

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

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  • (PMID = 17146292.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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11. Desjardins A, Reardon DA, Gururangan S, Peters K, Threatt S, Friedman A, Friedman H, Vredenburgh J: Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG). J Clin Oncol; 2009 May 20;27(15_suppl):e13004

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

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  • (PMID = 27962751.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Karrasch M, Gillespie GY, Braz E, Liechty PG, Nabors LB, Lakeman AD, Palmer CA, Parker JN, Whitley RJ, Markert JM: Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results. J Clin Oncol; 2009 May 20;27(15_suppl):2042

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

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  • (PMID = 27964649.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Simonelli M, Banna G, Navarria P, Di Ieva A, Zucali P, De Vincenzo F, Gaetani P, Condorelli R, Rodriguez Y Baena R, Scorsetti M, Santoro A: Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13037

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

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  • (PMID = 27962859.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Abacioglu MU, Caglar HB, Yumuk PF, Akgun Z, Atasoy BM, Sengoz M: Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma. J Clin Oncol; 2009 May 20;27(15_suppl):e13018

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

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  • (PMID = 27962826.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Lassman AB, Oligodendroglioma Study Group: Retrospective analysis of outcomes among more than 1,000 patients with newly diagnosed anaplastic oligodendroglial tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2014

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

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  • (PMID = 27964586.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Franceschi E, Tosoni A, Ermani M, Spagnolli F, La Torre L, Galzio RJ, Pozzati E, Talacchi A, Benevento F, Brandes AA: Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13003

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

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  • (PMID = 27962754.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Rudnick JD, Phuphanich S, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Black KL, Wheeler C, Yu J: A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2033

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

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  • (PMID = 27964627.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Witt H, Korshunov A, Remke M, Janzarik WG, Gnekow A, Scheurlen W, Kulozik AE, Lichter P, Pfister S: DNA methylation pattern of brain stem pilocytic astrocytomas in children. J Clin Oncol; 2009 May 20;27(15_suppl):10021

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

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  • (PMID = 27962622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Ochsenbein AF, Schubert AD, Vassella E, Mariani L: Quantitative analysis of 0&lt;sup&gt;6&lt;/sup&gt;-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):2069

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

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  • (PMID = 27964685.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Herndon J 2nd, Vredenburgh J, Reardon D, Desjardins A, Peters K, Gururangan S, Norfleet J, Friedman A, Bigner D, Friedman HS: Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13016

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

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  • (PMID = 27962830.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Merrell RT, Lachance DH, Anderson SK: Seizures in patients with glioma treated with phenytoin and levetiracetam. J Clin Oncol; 2009 May 20;27(15_suppl):e13020

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

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  • (PMID = 27962817.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Potthast L, Chowdhary S, Pan E, Yu D, Zhu W, Brem S: The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2057

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

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  • (PMID = 27964663.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Tosoni A, Franceschi E, Ermani M, Bacci A, Volpin L, Lombardo L, Ravenna G, Pinna G, Poggi R, Brandes AA: MGMT methylation status as a prognostic factor in anaplastic astrocytomas. J Clin Oncol; 2009 May 20;27(15_suppl):2052

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

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  • (PMID = 27964674.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Lin Y, Jiang T, Li G: MGMT expression in low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13001

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

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  • (PMID = 27962757.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Dong L, Pu PY, Wang H, Wang GX, Kang CS, Jiao DR: [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):232-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].
  • OBJECTIVE: To study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas. METHODS:.
  • (1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.
  • RESULTS: The frequency of p53 mutation in diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas and secondary glioblastomas was 1/10, 4/19 (21.1%), 4/6 and 2/2, respectively and the frequency of EGFR overexpression was 5/10, 10/19 (52.6%), 5/6 and 2/2, respectively.
  • Both p53 accumulation and EGFR overexpression increased accompanied by a successive increase of degree of the glioma malignancy.
  • CONCLUSIONS: EGFR overexpression is not infrequently seen, however, p53 mutation is rarely seen in the low grade gliomas.
  • Consequently, EGFR overexpression and p53 gene mutation are not mutually exclusive in astrocytic gliomagenesis but synergistically to promote the glioma progression.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16776982.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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26. Lamoral-Theys D, Le Mercier M, Le Calvé B, Rynkowski MA, Bruyère C, Decaestecker C, Haibe-Kains B, Bontempi G, Dubois J, Lefranc F, Kiss R: Long-term temozolomide treatment induces marked amino metabolism modifications and an increase in TMZ sensitivity in Hs683 oligodendroglioma cells. Neoplasia; 2010 Jan;12(1):69-79
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  • Gliomas account for more than 50% of all primary brain tumors.
  • The worst prognosis is associated with gliomas of astrocytic origin, whereas gliomas with an oligodendroglial origin offer higher sensitivity to chemotherapy, especially when oligodendroglioma cells display 1p19q deletions.
  • Temozolomide (TMZ) provides therapeutic benefits and is commonly used with radiotherapy in highly malignant astrocytic tumors, including glioblastomas.
  • [MeSH-minor] Animals. Antineoplastic Agents, Alkylating / pharmacology. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Genomics / methods. HT29 Cells. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Proteomics / methods. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Xenograft Model Antitumor Assays

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  • [Cites] J Neuropathol Exp Neurol. 2001 Sep;60(9):863-71 [11556543.001]
  • [Cites] Cancer Res. 2008 Jul 15;68(14):5706-15 [18632623.001]
  • [Cites] APMIS. 2008 Jul-Aug;116(7-8):615-28 [18834406.001]
  • [Cites] Neoplasia. 2008 Dec;10(12):1383-92 [19048117.001]
  • [Cites] Cancer Res. 2009 Jan 15;69(2):458-65 [19147558.001]
  • [Cites] J Neurooncol. 2009 Mar;92(1):57-63 [19011763.001]
  • [Cites] Neuro Oncol. 2009 Feb;11(1):69-79 [18772354.001]
  • [Cites] Oncologist. 2009 Feb;14(2):155-63 [19182242.001]
  • [Cites] Neoplasia. 2009 Apr;11(4):377-87 [19308292.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):459-66 [19269895.001]
  • [Cites] Neoplasia. 2009 May;11(5):485-96 [19412433.001]
  • [Cites] Science. 2009 May 22;324(5930):1029-33 [19460998.001]
  • [Cites] Brain Pathol. 2010 Jan;20(1):39-49 [18947333.001]
  • [Cites] Oncol Res. 2007;16(9):405-13 [18074675.001]
  • [Cites] Mol Cancer. 2008;7:14 [18221502.001]
  • [Cites] PLoS One. 2008;3(4):e1936 [18398462.001]
  • [Cites] J Neuropathol Exp Neurol. 2008 May;67(5):456-69 [18431251.001]
  • [Cites] Glia. 2001 Dec;36(3):375-90 [11746774.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Jul;61(7):585-96 [12125737.001]
  • [Cites] Cancer. 2002 Aug 1;95(3):641-55 [12209758.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):619-33 [12667446.001]
  • [Cites] Cancer Res. 2003 Apr 1;63(7):1684-95 [12670923.001]
  • [Cites] Genome Biol. 2003;4(10):R70 [14519205.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):448-57 [14713959.001]
  • [Cites] Clin Cancer Res. 2004 Mar 15;10(6):1871-4 [15041700.001]
  • [Cites] J Neuropathol Exp Neurol. 1998 Aug;57(8):791-802 [9720494.001]
  • [Cites] FEBS Lett. 1999 Aug 27;457(2):255-61 [10471790.001]
  • [Cites] Adv Cancer Res. 2004;92:95-118 [15530558.001]
  • [Cites] FASEB J. 2005 Feb;19(2):240-2 [15545299.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Cancer Res. 2005 May 15;65(10):4101-17 [15899800.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Neoplasia. 2005 Oct;7(10):930-43 [16242076.001]
  • [Cites] Acta Neuropathol. 2006 May;111(5):475-82 [16598485.001]
  • [Cites] Oncol Rep. 2006 Jul;16(1):33-9 [16786120.001]
  • [Cites] Neoplasia. 2006 May;8(5):402-12 [16790089.001]
  • [Cites] Cancer Biol Ther. 2006 Jul;5(7):729-35 [16861922.001]
  • [Cites] Mol Cancer. 2006;5:67 [17140455.001]
  • [Cites] Oncogene. 2007 Jan 11;26(2):186-97 [16819506.001]
  • [Cites] Cell Death Differ. 2007 Mar;14(3):548-58 [16946731.001]
  • [Cites] Neoplasia. 2007 May;9(5):358-69 [17534441.001]
  • [Cites] Neuro Oncol. 2007 Jul;9(3):314-8 [17435180.001]
  • [Cites] PLoS One. 2007;2(6):e576 [17593975.001]
  • [Cites] J Clin Oncol. 2007 Sep 10;25(26):4127-36 [17827463.001]
  • [Cites] Neoplasia. 2007 Sep;9(9):766-76 [17898872.001]
  • [Cites] Pharmacol Res. 2007 Oct;56(4):275-87 [17897837.001]
  • [Cites] Cancer J. 2007 Sep-Oct;13(5):335-44 [17921733.001]
  • [Cites] Expert Rev Anticancer Ther. 2007 Nov;7(11):1581-90 [18020926.001]
  • [Cites] Annu Rev Pathol. 2006;1:97-117 [18039109.001]
  • [Cites] Toxicol Appl Pharmacol. 2008 Jun 1;229(2):172-83 [18313712.001]
  • [Cites] Biochem Pharmacol. 2008 Aug 1;76(3):303-11 [18573489.001]
  • [Cites] Exp Cell Res. 2008 Sep 10;314(15):2870-83 [18639545.001]
  • (PMID = 20072655.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Other-IDs] NLM/ PMC2805885
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27. Xu GW, Mymryk JS, Cairncross JG: Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin. J Neurooncol; 2005 Sep;74(2):141-9
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  • [Title] Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin.
  • p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.
  • In this report, we examined the effect of p53 inactivation on the chemosensitivity of two additional human astrocytic glioma cell lines, D54 and A172, in order to assess whether sensitization is a general property of astrocytic tumor cells.
  • Sensitization to both BCNU and TMZ was associated with failure of p21(WAF1) induction, lack of a sustained G2 cell cycle arrest and significant tumor cell death.
  • These findings suggest that enhanced sensitivity to BCNU and TMZ is a general property of human astrocytic glioma cells in which p53 was disrupted.
  • In contrast, p53 inactivation rendered D54 and U87MG cells significantly more resistant to cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which high-grade astrocytomas sometimes respond.
  • These results indicate that p53 status influences the chemosensitivity of astrocytic glioma cells in a drug-type specific manner, a finding that may have implications for the selection of drug treatments for patients with astrocytic gliomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Carmustine / therapeutic use. Cisplatin / therapeutic use. Dacarbazine / analogs & derivatives. Gene Silencing. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. Tumor Cells, Cultured. Tumor Stem Cell Assay

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  • (PMID = 16193384.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Tumor Suppressor Protein p53; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine
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28. Pareés I, Alonso J, Rovira A, Martínez E, Montalban X: [Diffuse astrocytoma presenting as an optic-spinal syndrome]. Rev Neurol; 2009 Apr 1-15;48(7):354-6
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  • [Title] [Diffuse astrocytoma presenting as an optic-spinal syndrome].
  • [Transliterated title] Síndrome opticomedular como forma de presentación de un astrocitoma difuso.
  • INTRODUCTION: Spinal cord involvement is a rare presentation of grade II astrocytomas.
  • Nevertheless, differentiation from inflammatory demyelinating diseases of the central nervous system can be challenging in some clinical situations.
  • A patient with an optic-spinal syndrome due to a fibrillary astrocytoma is described.
  • CASE REPORT: A 32 years-old man was admitted to the hospital because of a subacute spinal cord syndrome.
  • A new MRI with spectroscopy revealed an infiltrative lesion involving the right frontal lobe, optic chiasm, internal capsule, brainstem and cervical spinal cord, which was suggestive of low-grade astrocytoma.
  • Brain biopsy confirmed the diagnosis of diffuse fibrillary astrocytoma.
  • Brain biopsy is often necessary for a definite diagnosis.
  • [MeSH-major] Astrocytoma. Demyelinating Diseases. Optic Neuritis. Spinal Cord / pathology

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  • (PMID = 19319816.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Oligoclonal Bands
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29. Furnari FB, Fenton T, Bachoo RM, Mukasa A, Stommel JM, Stegh A, Hahn WC, Ligon KL, Louis DN, Brennan C, Chin L, DePinho RA, Cavenee WK: Malignant astrocytic glioma: genetics, biology, and paths to treatment. Genes Dev; 2007 Nov 1;21(21):2683-710
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  • [Title] Malignant astrocytic glioma: genetics, biology, and paths to treatment.
  • Malignant astrocytic gliomas such as glioblastoma are the most common and lethal intracranial tumors.
  • This progress is fueling new opportunities for understanding the fundamental basis for development of this devastating disease and also novel therapies that, for the first time, portend meaningful clinical responses.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Brain Neoplasms / therapy
  • [MeSH-minor] Animals. Animals, Genetically Modified. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Models, Animal. Gene Regulatory Networks. Humans. Models, Biological. Necrosis / chemically induced. Neoplasm Invasiveness. Neoplasm Staging. Neovascularization, Pathologic / drug therapy

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  • (PMID = 17974913.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA099041; United States / NCI NIH HHS / CA / CA95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 306
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30. Figarella-Branger D, Bouvier C: [Histological classification of human gliomas: state of art and controversies]. Bull Cancer; 2005 Apr;92(4):301-9
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  • [Title] [Histological classification of human gliomas: state of art and controversies].
  • [Transliterated title] Classification anatomopathologique des gliomes: faits et controverses.
  • The histological classification of human gliomas remains in 2005 a challenge.
  • The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.
  • Although the standard remains the WHO classification, this classification suffered from lack of reproducibility among pathologists.
  • In particular this classification does not take into account the intrinsic morphological heterogeneity of infiltrative gliomas and does not discriminate the tumour cells from the residual brain parenchyma.
  • According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).
  • Circumscribed gliomas mainly corresponds to pilocytic astrocytomas (grade I).
  • In contrast, the Sainte Anne classification takes into account the macroscopic informations provided by imaging techniques and the tumour growth patterns.
  • Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.
  • According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).
  • In the future the glioma classification has to be unique and should take into account clinical data, neuroradiological and histological features and results of molecular biology.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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  • (PMID = 15888386.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
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31. Tfelt-Hansen J: The role of calcium-sensing receptor and signalling pathways in the pathophysiology in two in vitro models of malignant hypercalcemia: the rat rice H-500 Leydig testis cancer and prostate cancer (PC-3) cells. Expression and regulation of pituitary tumor transforming gene in Leydig testis cancer and astrocyte and astrocytoma cells. Dan Med Bull; 2008 Feb;55(1):17-46
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  • [Title] The role of calcium-sensing receptor and signalling pathways in the pathophysiology in two in vitro models of malignant hypercalcemia: the rat rice H-500 Leydig testis cancer and prostate cancer (PC-3) cells. Expression and regulation of pituitary tumor transforming gene in Leydig testis cancer and astrocyte and astrocytoma cells.
  • The finding that the CaR is expressed on cancer cells has opened the door to a new understanding of the role of extracellular calcium as a promalignant stimulus through the CaR and its signaling apparatus as demonstrated in this thesis.
  • The growth rate of the tumor was also increased by stimulation of the CaR, as DNA synthesis and protection against apoptosis were enhanced.
  • The oncogene, pituitary tumor-transforming gene (PTTG), was found to be upregulated by the CaR in the H-500 cells, whereas calcium had no effect on PTTG expression in the U-87 astrocytoma cell line, but other proproliferative agents did upregulate PTTG in the U-87 cells.
  • Nitric oxide synthase (NOS) exists in three isoforms, and I found that the CaR upregulated the inducible NOS but not the two other isoforms.
  • [MeSH-minor] Animals. Apoptosis. Astrocytes. Astrocytoma. Cell Membrane. Hemostasis. In Vitro Techniques. Male. Nitric Oxide Synthase. Rats

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  • (PMID = 18321443.001).
  • [ISSN] 1603-9629
  • [Journal-full-title] Danish medical bulletin
  • [ISO-abbreviation] Dan Med Bull
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Receptors, Calcium-Sensing; EC 1.14.13.39 / Nitric Oxide Synthase; SY7Q814VUP / Calcium
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32. Xu P, Qiu M, Zhang Z, Kang C, Jiang R, Jia Z, Wang G, Jiang H, Pu P: The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo. J Neurooncol; 2010 Mar;97(1):41-51
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  • [Title] The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo.
  • Deregulation of Notch signaling has been implicated in some genetic diseases and tumorigenesis.
  • The function of Notch signaling in a variety of tumors can be either oncogenic or tumor-suppressive, depending on the cellular context.
  • In this study, Notch1 overexpression was observed in the majority of 45 astrocytic gliomas with different grades and in U251MG glioma cells.
  • Meanwhile, tumor growth was delayed in established subcutaneous gliomas in nude mice treated with Notch1 siRNA in vivo.
  • These results suggest that Notch1 plays an important oncogenic role in the development and progression of astrocytic gliomas.
  • [MeSH-major] Astrocytoma / genetics. Gene Expression Regulation, Neoplastic / physiology. Receptor, Notch1 / genetics
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Disease Models, Animal. Flow Cytometry / methods. Humans. In Situ Nick-End Labeling / methods. Matrix Metalloproteinase 9 / metabolism. Mice. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Transfection / methods

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  • (PMID = 19771395.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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33. Freitas MR, de Muzio SD, Pessoa RC, Stávale JN, Borges LR, Malheiros SM: [Diffuse bone marrow metastasis in cerebellar high-grade astrocytoma. A case report]. Rev Neurol; 2009 Mar 1-15;48(5):242-4
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  • [Title] [Diffuse bone marrow metastasis in cerebellar high-grade astrocytoma. A case report].
  • [Transliterated title] Metastasis difusa de la medula osea en un astrocitoma cerebeloso de alto grado. Un caso clinico.
  • INTRODUCTION: Cerebellar high-grade astrocytoma is uncommon.
  • Although more prone to present cerebrospinal fluid dissemination, the cerebellar location is not particularly related to the occurrence of extra-cranial metastases, which are also unusual in supratentorial malignant gliomas.
  • CASE REPORT: A 46 year-old man with cerebellar anaplastic astrocytoma who developed pancytopenia due to extensive bone marrow metastases.
  • CONCLUSION: Extraneural metastases of brain gliomas are rare and the spread to the bone marrow confers an extremely poor prognosis for these patients.
  • The expected improvement in glioma patients' survival due to the combination of more efficient therapies may lead to an increased incidence of this uncommon presentation, justifying a more rigorous follow-up of systemic manifestations.
  • [MeSH-major] Astrocytoma / pathology. Bone Marrow Neoplasms / secondary. Cerebellar Neoplasms / pathology

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  • (PMID = 19263392.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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34. Zhou YH, Hess KR, Liu L, Linskey ME, Yung WK: Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables. Neuro Oncol; 2005 Oct;7(4):485-94
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  • [Title] Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables.
  • The disparate lengths of survival among patients with malignant astrocytic gliomas (anaplastic astrocytomas [AAs] and glioblastoma multiforme [GBM]) cannot be adequately accounted for by clinical variables (patient age, histology, and recurrent status).
  • We previously explicated the expression and prognostic value of PAX6, PTEN, VEGF, and EGFR in these glioma tissues and established a comprehensive prognostic model (Zhou et al., 2003).
  • This study attempts to improve that model by including four additional genetic markers, which exhibited a differential expression (P < 0.001) among tumor grades and between tumor and normal tissues.
  • This finding suggests that the expression of IGFBP2 is associated with pathways activated specifically in GBMs that result in enhancing invasiveness and angiogenesis.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical

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  • [Cites] Cancer Res. 2003 Oct 15;63(20):6962-70 [14583498.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6613-25 [14583454.001]
  • [Cites] Cancer. 1988 Nov 15;62(10):2152-65 [3179928.001]
  • [Cites] Genes Chromosomes Cancer. 1992 Jul;5(1):75-82 [1384665.001]
  • [Cites] Genes Chromosomes Cancer. 1992 Nov;5(4):357-74 [1283325.001]
  • [Cites] Brain Pathol. 1993 Jan;3(1):19-26 [8269081.001]
  • [Cites] J Natl Cancer Inst. 1994 Jun 1;86(11):829-35 [8182763.001]
  • [Cites] Nature. 1994 Jul 7;370(6484):61-5 [8015608.001]
  • [Cites] Hum Pathol. 1995 Aug;26(8):846-51 [7543440.001]
  • [Cites] J Neurooncol. 1995 Oct;26(1):11-6 [8583240.001]
  • [Cites] Acta Neuropathol. 1996 Jul;92(1):70-4 [8811128.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Mar;56(3):291-300 [9056543.001]
  • [Cites] J Neurooncol. 1997 Oct;35(1):13-28 [9266437.001]
  • [Cites] Cancer Res. 1997 Dec 1;57(23):5254-7 [9393744.001]
  • [Cites] Oncogene. 1998 Jan 15;16(2):257-63 [9464544.001]
  • [Cites] Brain Pathol. 1998 Oct;8(4):655-67 [9804374.001]
  • [Cites] Invasion Metastasis. 1997;17(5):221-39 [9876217.001]
  • [Cites] Cancer Res. 1999 Apr 15;59(8):1820-4 [10213484.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4228-32 [10485462.001]
  • [Cites] J Neurooncol. 2005 Feb;71(3):223-9 [15735909.001]
  • [Cites] Br J Neurosurg. 2000 Feb;14(1):28-32 [10884881.001]
  • [Cites] Cancer Res. 2000 Dec 1;60(23):6617-22 [11118044.001]
  • [Cites] Neuro Oncol. 2000 Jul;2(3):164-73 [11302337.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 15;93(16):1246-56 [11504770.001]
  • [Cites] Curr Opin Cell Biol. 2001 Oct;13(5):534-40 [11544020.001]
  • [Cites] Oncogene. 2001 Nov 1;20(50):7437-46 [11704875.001]
  • [Cites] Oncogene. 2001 Oct 11;20(46):6669-78 [11709701.001]
  • [Cites] Bioinformatics. 2002 Mar;18(3):405-12 [11934739.001]
  • [Cites] Virchows Arch. 2003 Apr;442(4):329-35 [12684767.001]
  • [Cites] Neurochem Res. 2003 Jun;28(6):925-31 [12718447.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4315-21 [12907597.001]
  • [Cites] Clin Cancer Res. 2003 Aug 15;9(9):3369-75 [12960124.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):920-7 [14871821.001]
  • (PMID = 16212813.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ribosomal Proteins; 0 / ribosomal protein S9; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC1871729
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35. Haapasalo J, Hilvo M, Nordfors K, Haapasalo H, Parkkila S, Hyrskyluoto A, Rantala I, Waheed A, Sly WS, Pastorekova S, Pastorek J, Parkkila AK: Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas. Neuro Oncol; 2008 Apr;10(2):131-8
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  • [Title] Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas.
  • CA XII has been proposed to be involved in acidification of the extracellular milieu, creating an appropriate microenvironment for rapid tumor growth.
  • Because RNA sequence databases have indicated that two isoforms of CA XII might exist in human tissues, and because alternatively spliced protein forms have been linked to aggressive behavior of cancer cells, we designed a study to evaluate the presence of the two forms of CA XII in diffuse astrocytomas, a tumor type known for its aggressive and often noncurable behavior.
  • Reverse transcription PCR of tumor samples surprisingly revealed that CA XII present in diffuse astrocytomas is mainly encoded by a shorter mRNA variant.
  • We further showed by Western blotting that anti-CA XII antibody recognized both isoforms in the glioblastoma cell lines, and we then evaluated the expression of CA XII in astrocytomas using immunohistochemistry and correlated the results with various clinicopathological and molecular factors.
  • Of 370 diffusely infiltrating astrocytomas, 363 cases (98%) showed immunoreactions for CA XII.
  • From these results, we conclude that CA XII is commonly expressed in diffuse astrocytomas and that it might be used as a biomarker of poor prognosis.
  • The absence of 11 amino acids in the shorter isoform, which seems to be common in astrocytomas, may affect the normal quaternary structure and biological function of CA XII.
  • [MeSH-major] Astrocytoma / enzymology. Biomarkers, Tumor / analysis. Brain Neoplasms / enzymology. Carbonic Anhydrases / genetics. Carbonic Anhydrases / metabolism

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  • [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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36. Aguilar Moliner I, Costa Orvay JA, Juma K, Costa Clara JM, Cruz Martínez O, Pou Fernández J: [Optic pathway astrocytoma: an unusual cause of failure to thrive in infants]. An Pediatr (Barc); 2007 Jun;66(6):622-4
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  • [Title] [Optic pathway astrocytoma: an unusual cause of failure to thrive in infants].
  • [Transliterated title] Astrocitoma de vías ópticas: una causa infrecuente de retraso ponderal en el lactante.
  • We report a case of low-grade astrocytoma of the optic pathway in a 2-month-old child whose main symptoms at diagnosis were failure to thrive and anorexia.
  • Unfortunately, despite therapeutic efforts, the tumor showed local and metastatic progression refractory to chemotherapy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Failure to Thrive / etiology. Optic Nerve Glioma / diagnosis

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  • (PMID = 17583627.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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37. Elsir T, Eriksson A, Orrego A, Lindström MS, Nistér M: Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas. J Neuropathol Exp Neurol; 2010 Feb;69(2):129-38
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  • [Title] Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas.
  • PROX1 is a prospero-related transcription factor that plays a critical role in the development of various organs including the mammalian lymphatic and central nervous systems; it controls cell proliferation and differentiation through different transcription pathwaysand has both oncogenic and tumor-suppressive functions.
  • We investigated PROX1 expression patterns in 56 human astrocytic gliomas of different grades using immunohistochemistry.
  • An average of 79% of cells in World Health Organization Grade IV (glioblastoma, n = 15) and 57% of cells in World Health Organization Grade III (anaplastic astrocytoma, n = 13) were strongly PROX1 positive; low-grade diffuse astrocytomas (Grade II, n = 13) had 21% of cells that were strongly positive; Grade I tumors (n = 15) had 1.5%; and non-neoplastic brain tissue (n = 15) had 3.7% of cells that were PROX1 positive.
  • Analyses of coexpression with proliferation markers suggest that PROX1+ cells have a marginally lower rate of proliferation than other tumor cells but are still mitotically active.
  • We conclude that PROX1 may constitute a useful tool for the diagnosis and grading ofastrocytic gliomas and for distinguishing Grade III and Grade IV tumors from Grade I and Grade II tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Homeodomain Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Antigens, Nuclear / metabolism. Biomarkers / metabolism. Brain Diseases / metabolism. Cell Proliferation. Humans. Immunohistochemistry. Microtubule-Associated Proteins / metabolism. Microvessels / metabolism. Mitosis. Nerve Tissue Proteins / metabolism. Tubulin / metabolism

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  • (PMID = 20084020.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / neuronal nuclear antigen NeuN, human; 0 / prospero-related homeobox 1 protein
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38. Katsetos CD, Reddy G, Dráberová E, Smejkalová B, Del Valle L, Ashraf Q, Tadevosyan A, Yelin K, Maraziotis T, Mishra OP, Mörk S, Legido A, Nissanov J, Baas PW, de Chadarévian JP, Dráber P: Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines. J Neuropathol Exp Neurol; 2006 May;65(5):465-77
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  • [Title] Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines.
  • Centrosome amplification is a pivotal mechanism underlying tumorigenesis but its role in gliomas is underinvestigated.
  • The present study specifically examines the expression and distribution of the centrosome-associated cytoskeletal protein gamma-tubulin in 56 primary diffuse astrocytic gliomas (grades II-IV) and in 4 human glioblastoma cell lines (U87MG, U118MG, U138MG, and T98G).
  • In tumors in adults (n = 46), varying degrees of localization were detected in all tumor grades, but immunoreactivity was significantly increased in high-grade anaplastic astrocytomas and glioblastomas multiforme as compared to low-grade diffuse astrocytomas (p = 0.0001).
  • A similar trend was noted in diffuse gliomas in children but the sample of cases was too small as to be statistically meaningful.
  • Our results indicate that overexpression and ectopic cellular distribution of gamma-tubulin in astrocytic gliomas may be significant in the context of centrosome protein amplification and may be linked to tumor progression and anaplastic potential.
  • [MeSH-minor] Antigens / metabolism. Blotting, Northern / methods. Cell Line, Tumor. Humans. Immunohistochemistry / methods

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  • (PMID = 16772870.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
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39. Knizetova P, Darling JL, Bartek J: Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy. J Cell Mol Med; 2008 Jan-Feb;12(1):111-25
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  • [Title] Vascular endothelial growth factor in astroglioma stem cell biology and response to therapy.
  • Malignant astrogliomas are among the most aggressive, highly vascular and infiltrating tumours bearing a dismal prognosis, mainly due to their resistance to current radiation treatment and chemotherapy.
  • Efforts to identify and target the mechanisms that underlie astroglioma resistance have recently focused on candidate cancer stem cells, their biological properties, interplay with their local microenvironment or 'niche', and their role in tumour progression and recurrence.
  • Both paracrine and autocrine regulation of astroglioma cell behaviour by locally produced cytokines such as the vascular endothelial growth factor (VEGF) are emerging as key factors that determine astroglioma cell fate.
  • Here, we review these recent rapid advances in astroglioma research, with emphasis on the significance of VEGF in astroglioma stem-like cell biology.
  • Furthermore, we highlight the unique DNA damage checkpoint properties of the CD133-marker-positive astroglioma stem-like cells, discuss their potential involvement in astroglioma radioresistance, and consider the implications of this new knowledge for designing combinatorial, more efficient therapeutic strategies.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / therapy. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Neoplastic Stem Cells / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18031298.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 129
  • [Other-IDs] NLM/ PMC3823475
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40. Faria AV, Azevedo GC, Zanardi VA, Ghizoni E, Queiroz LS: Dissemination patterns of pilocytic astrocytoma. Clin Neurol Neurosurg; 2006 Sep;108(6):568-72
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  • [Title] Dissemination patterns of pilocytic astrocytoma.
  • Two patients with multifocal pilocytic astrocytoma diagnosed by magnetic resonance imaging (MRI) and confirmed by histopathological examination are reported.
  • They presented distinct sites and mechanisms of metastasis: to distant ventricles through the cerebral spinal fluid (CSF) in patient 1 and to contralateral parenchyma, possibly through white matter tracts, in patient 2, a pathway not so far reported in pilocytic astrocytoma.
  • Early detection of multifocal pilocytic astrocytoma by MRI may change treatment strategies and improve prognosis.
  • [MeSH-major] Astrocytoma / secondary. Brain Neoplasms / pathology


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

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  • (PMID = 16865689.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / APOD protein, human; 0 / ATP1B2 protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Apolipoproteins; 0 / Apolipoproteins D; 0 / Biomarkers, Tumor; 0 / Cation Transport Proteins; 0 / Cell Adhesion Molecules, Neuronal; 0 / DMXL1 protein, human; 0 / FAM107A protein, human; 0 / Glycoproteins; 0 / Hydroxamic Acids; 0 / Membrane Transport Proteins; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / PSD protein, human; 0 / Protein Synthesis Inhibitors; 0 / Proteins; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 3.5.1.98 / Histone Deacetylases; EC 3.5.1.98 / histone deacetylase 3; EC 3.6.1.- / Adenosine Triphosphatases; M801H13NRU / Azacitidine
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42. Korkolopoulou P, Perdiki M, Thymara I, Boviatsis E, Agrogiannis G, Kotsiakis X, Angelidakis D, Rologis D, Diamantopoulou K, Thomas-Tsagli E, Kaklamanis L, Gatter K, Patsouris E: Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX. Hum Pathol; 2007 Apr;38(4):629-38

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

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  • (PMID = 17367605.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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43. Hartmann C, Hentschel B, Wick W, Capper D, Felsberg J, Simon M, Westphal M, Schackert G, Meyermann R, Pietsch T, Reifenberger G, Weller M, Loeffler M, von Deimling A: Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas. Acta Neuropathol; 2010 Dec;120(6):707-18
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  • [Title] Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas.
  • WHO grading of human brain tumors extends beyond a strictly histological grading system by providing a basis predictive for the clinical behavior of the respective neoplasm.
  • For example, patients with glioblastoma WHO grade IV usually show a less favorable clinical course and receive more aggressive first-line treatment than patients with anaplastic astrocytoma WHO grade III.
  • Here we provide evidence that the IDH1 status is more prognostic for overall survival than standard histological criteria that differentiate high-grade astrocytomas.
  • We sequenced the isocitrate dehydrogenase 1 gene (IDH1) at codon 132 in 382 patients with anaplastic astrocytoma and glioblastoma from the NOA-04 trial and from a prospective translational cohort study of the German Glioma Network.
  • Patients with anaplastic astrocytomas carried IDH1 mutations in 60%, and patients with glioblastomas in 7.2%.
  • The sequence from more favorable to poorer outcome was (1) anaplastic astrocytoma with IDH1 mutation, (2) glioblastoma with IDH1 mutation, (3) anaplastic astrocytoma without IDH1 mutation and (4) glioblastoma without IDH1 mutation (p < 0.0001).
  • In this combined set of anaplastic astrocytomas and glioblastomas both, IDH1 mutation and IDH1 expression status were of greater prognostic relevance than histological diagnosis according to the current WHO classification system.
  • We propose to complement the current WHO classification and grading of high-grade astrocytic gliomas by the IDH1 mutation status and to use this combined histological and molecular classification in future clinical trials.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Glioma / classification. Glioma / genetics. Isocitrate Dehydrogenase / genetics. Mutation / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Cohort Studies. Female. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Young Adult


44. Yang Z, Wang Y, Fang J, Chen F, Liu J, Wu J, Wang Y, Song T, Zeng F, Rao Y: Downregulation of WIF-1 by hypermethylation in astrocytomas. Acta Biochim Biophys Sin (Shanghai); 2010 Jun 15;42(6):418-25
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  • [Title] Downregulation of WIF-1 by hypermethylation in astrocytomas.
  • Wnt inhibitory factor-1 (WIF-1) acts as a Wnt antagonist and tumor suppressor, but hypermethylation of WIF-1 gene promoter and low expression of WIF-1 activate Wnt signaling aberrantly and induce the development of several human tumors.
  • By using RT-PCR, immunohistochemistry and methylation-specific PCR, we analyzed the expression and methylation of WIF-1 in 4 normal brain tissues, 35 freshly resected astrocytoma tissues and 4 glioblastoma-derived cell lines.
  • Significant downregulation of WIF-1 mRNA and protein expression levels was observed in astrocytoma tissues compared with normal brain tissues.
  • Significant association between WIF-1 downregulation and pathological grade of astrocytomas was found.
  • WIF-1 gene aberrant methylation was observed in 19 of 35 (54.29%) tumor samples.
  • Our results suggested that the WIF-1 gene is frequently silenced in astrocytoma by aberrant promoter methylation.
  • This may be an important mechanism in astrocytoma carcinogenesis.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Astrocytoma / genetics. DNA Methylation. Repressor Proteins / genetics
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / metabolism. Cell Line, Tumor. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Promoter Regions, Genetic. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Wnt Proteins / genetics. beta Catenin / genetics

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

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  • [Cites] Oncogene. 2009 May 21;28(20):2119-23 [19363522.001]
  • [Cites] Acta Neuropathol. 2009 Jun;117(6):657-65 [19271226.001]
  • [Cites] Mol Carcinog. 2009 Aug;48(8):703-12 [19142899.001]
  • [Cites] Pediatr Blood Cancer. 2009 Sep;53(3):417-23 [19479971.001]
  • [Cites] J Clin Oncol. 2009 Aug 1;27(22):3691-7 [19581535.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12):1173-8 [19726761.001]
  • [Cites] Oncogene. 2009 Oct 1;28(39):3468-76 [19617900.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Jan;27(1):44-51 [10564585.001]
  • [Cites] Cancer. 2000 Oct 1;89(7):1569-76 [11013373.001]
  • [Cites] Pediatr Neurosurg. 2001 Dec;35(6):311-7 [11786699.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Curr Treat Options Oncol. 2001 Dec;2(6):529-36 [12057098.001]
  • [Cites] Nat Genet. 2002 Jul;31(3):306-10 [12068298.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1559-61 [12202832.001]
  • [Cites] J Neurooncol. 2002 Sep;59(2):107-15 [12241103.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14071-6 [12391318.001]
  • [Cites] J Neurosurg. 2003 Jun;98(6):1170-4 [12816259.001]
  • [Cites] J Clin Oncol. 2003 Aug 1;21(15):2968-73 [12885817.001]
  • [Cites] Neurosurgery. 2003 Sep;53(3):544-53; discussion 554-5 [12943571.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):846-51 [14520411.001]
  • [Cites] Neurology. 2004 Apr 27;62(8):1311-6 [15111667.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] J Neurosurg. 1988 Jan;68(1):41-7 [3335911.001]
  • [Cites] J Neurosurg. 1988 Aug;69(2):171-6 [3392563.001]
  • [Cites] Neurosurgery. 1992 Sep;31(3):413-8; discussion 419 [1407423.001]
  • [Cites] Science. 1996 Jun 14;272(5268):1668-71 [8658145.001]
  • [Cites] Cell. 1996 Jun 14;85(6):841-51 [8681379.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):842-5 [9041183.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2085-8 [9187099.001]
  • [Cites] Cancer Res. 1997 Jul 1;57(13):2581-5 [9205058.001]
  • [Cites] J Clin Oncol. 1997 Aug;15(8):2792-9 [9256121.001]
  • [Cites] J Neurooncol. 1998 Mar;37(1):9-16 [9525833.001]
  • [Cites] J Neurosurg. 1999 Feb;90(2):265-73 [9950497.001]
  • [Cites] Oncogene. 1999 Jan 21;18(3):833-6 [9989836.001]
  • [Cites] Neuropathol Appl Neurobiol. 1999 Apr;25(2):134-42 [10216001.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):5198-204 [16051961.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):839-45 [16424016.001]
  • [Cites] Dev Cell. 2006 Feb;10(2):187-97 [16459298.001]
  • [Cites] Curr Biol. 2007 Jan 23;17(2):165-72 [17196391.001]
  • [Cites] Childs Nerv Syst. 2007 May;23(5):543-7 [17226033.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Oncogene. 2007 Aug 23;26(39):5752-61 [17353902.001]
  • [Cites] Stem Cells. 2007 Oct;25(10):2524-33 [17628016.001]
  • [Cites] J Clin Invest. 2008 May;118(5):1739-49 [18398503.001]
  • [Cites] Pediatr Blood Cancer. 2008 Aug;51(2):245-50 [18386785.001]
  • [Cites] J Neuropathol Exp Neurol. 2008 Sep;67(9):878-87 [18716556.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8673-7 [18974108.001]
  • [Cites] Cancer Res. 2009 Feb 15;69(4):1284-92 [19190345.001]
  • [Cites] Trends Pharmacol Sci. 2009 Jun;30(6):303-12 [19443052.001]
  • (PMID = 20223881.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA068485; United States / NINDS NIH HHS / NS / K02NS053614
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Transcription Factors; 0 / patched receptors
  • [Other-IDs] NLM/ PMC2940682
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46. Villarejo F, de Diego JM, de la Riva AG: Prognosis of cerebellar astrocytomas in children. Childs Nerv Syst; 2008 Feb;24(2):203-10

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

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  • (PMID = 17710415.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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47. Lefranc F, Rynkowski M, DeWitte O, Kiss R: Present and potential future adjuvant issues in high-grade astrocytic glioma treatment. Adv Tech Stand Neurosurg; 2009;34:3-35
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  • [Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.
  • Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.
  • Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.
  • Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.
  • Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.
  • Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.
  • Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells.
  • The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy


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

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  • (PMID = 18061226.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Quaternary Ammonium Compounds; 660YQ98I10 / Potassium Chloride; SY7Q814VUP / Calcium
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49. Zscharnack K, Kessler R, Bleichert F, Warnke JP, Eschrich K: The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells. Neuropathol Appl Neurobiol; 2009 Dec;35(6):566-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells.
  • Here, we studied the role of the PFKFB3 splice variants in human astrocytic gliomas.
  • METHODS: We analysed the PFKFB3 splice variants in 48 astrocytic gliomas by RT-PCR and real-time PCR.
  • RESULTS: UBI2K5 and UBI2K6 are the predominant splice variants in rapidly proliferating high-grade astrocytomas while the expression of UBI2K3 and UBI2K4 is mainly restricted to low-grade astrocytomas and nonneoplastic brain tissue.
  • The UBI2K4 mRNA level is downregulated in astrocytic gliomas with increasing malignancy grade.
  • CONCLUSIONS: Our results demonstrate that the splice variant UBI2K4 impedes the tumour cell growth and might serve as a tumour suppressor in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Phosphofructokinase-2 / metabolism
  • [MeSH-minor] Brain / metabolism. Cell Count. Cell Line, Tumor. Cell Proliferation. Cell Survival. Down-Regulation. Humans. Neoplasm Staging. Polymerase Chain Reaction. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transfection

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  • (PMID = 19490427.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; EC 2.7.1.105 / PFKFB3 protein, human; EC 2.7.1.105 / Phosphofructokinase-2
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50. Shostak KO, Dmitrenko VV, Vudmaska MI, Naidenov VG, Beletskii AV, Malisheva TA, Semenova VM, Zozulya YP, Demotes-Mainard J, Kavsan VM: Patterns of expression of TSC-22 protein in astrocytic gliomas. Exp Oncol; 2005 Dec;27(4):314-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of expression of TSC-22 protein in astrocytic gliomas.
  • AIM: To evaluate expression patterns of protein product of putative tumor suppressor gene TSC-22 in human astrocytic tumors by immunohistochemical approach.
  • Immunohistochemical analysis of TSC-22 and GFAP expression with the use of anti-human-TSC-22- and anti-human-GFAP-antibodies was performed on histological slides of astrocytic tumors.
  • RESULTS: Immunohistochemical analysis has shown that the number of cells expressing TSC-22 was significantly lower in glioblastoma tissues than that in diffuse astrocytoma.
  • Double immunohistochemical staining of astrocytic tumors using anti-human-TSC-2- and anti-human-GFAP-antibodies showed that both TSC-22 and GFAP expression is co-localized in astrocytes.
  • In more aggressive forms of astrocytic tumors decreased expression of TSC-22 mRNA correlates with its lowered expression on protein level.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Repressor Proteins / biosynthesis
  • [MeSH-minor] Amino Acid Sequence. Astrocytes / metabolism. Base Sequence. Biomarkers, Tumor / analysis. Gene Expression Profiling. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Microglia / metabolism. Molecular Sequence Data. Recombinant Proteins / biosynthesis. Recombinant Proteins / genetics

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  • (PMID = 16404353.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / TSC22D1 protein, human
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51. Eskelin S, Tommila P, Palosaari T, Kivelä T: Photodynamic therapy with verteporfin to induce regression of aggressive retinal astrocytomas. Acta Ophthalmol; 2008 Nov;86(7):794-9

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

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

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

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  • (PMID = 17616049.001).
  • [ISSN] 0004-4849
  • [Journal-full-title] Boletín de la Asociación Médica de Puerto Rico
  • [ISO-abbreviation] Bol Asoc Med P R
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Puerto Rico
  • [Number-of-references] 18
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53. Raju GP, Urion DK, Sahin M: Neonatal subependymal giant cell astrocytoma: new case and review of literature. Pediatr Neurol; 2007 Feb;36(2):128-31
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  • [Title] Neonatal subependymal giant cell astrocytoma: new case and review of literature.
  • Subependymal giant cell astrocytomas are one of the three major intracranial lesions found in tuberous sclerosis complex.
  • Subependymal giant cell astrocytomas are typically slow-growing tumors of mixed glioneuronal lineage which can become aggressive and cause obstructive hydrocephalus usually in older children and adolescents.
  • Neonatal subependymal giant cell astrocytomas are extremely rare, and their natural history and prognosis are poorly understood.
  • This report investigates an extremely large neonatal subependymal giant cell astrocytoma which was initially identified in utero at 19 weeks of gestation in a high-risk pregnancy with no family history of tuberous sclerosis complex.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Imaging

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  • (PMID = 17275668.001).
  • [ISSN] 0887-8994
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 16
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54. Giannopoulou E, Ravazoula P, Kalofonos H, Makatsoris T, Kardamakis D: Expression of HIF-1alpha and iNOS in astrocytic gliomas: a clinicopathological study. In Vivo; 2006 May-Jun;20(3):421-5

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

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  • (PMID = 16724682.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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55. Kim SH, Kang SS, Jung TY, Jung S: Juvenile pilomyxoid astrocytoma in the opticohypothalamus. J Korean Neurosurg Soc; 2010 Nov;48(5):445-7

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

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  • [Cites] Anticancer Res. 2009 Mar;29(3):919-26 [19414328.001]
  • [Cites] J Neurooncol. 1998 May;37(3):263-70 [9524084.001]
  • [Cites] Clin Neuropathol. 2001 Nov-Dec;20(6):256-62 [11758781.001]
  • [Cites] J Neurosurg. 2003 Aug;99(2):416-20 [12924720.001]
  • [Cites] Neurosurgery. 2003 Sep;53(3):544-53; discussion 554-5 [12943571.001]
  • [Cites] Neurosurgery. 2004 Jan;54(1):72-9; discussion 79-80 [14683543.001]
  • [Cites] AJNR Am J Neuroradiol. 2008 Nov;29(10):1861-6 [18701580.001]
  • [Cites] Cancer. 1993 May 15;71(10):3165-72 [8490847.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Jan;58(1):46-53 [10068313.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Oct;58(10):1061-8 [10515229.001]
  • [Cites] Pediatr Neurosurg. 2000 Apr;32(4):214-9 [10940774.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4572-8 [14673044.001]
  • [Cites] Neuropathology. 2006 Feb;26(1):89-93 [16521485.001]
  • [Cites] J Neurosurg. 1978 Aug;49(2):179-84 [671072.001]
  • (PMID = 21286484.001).
  • [ISSN] 1598-7876
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC3030087
  • [Keywords] NOTNLM ; Adjuvant chemotherapy / Opticohypothalamus / Pilomyxoid astrocytoma
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56. Guan Y, Mizoguchi M, Yoshimoto K, Hata N, Shono T, Suzuki SO, Araki Y, Kuga D, Nakamizo A, Amano T, Ma X, Hayashi K, Sasaki T: MiRNA-196 is upregulated in glioblastoma but not in anaplastic astrocytoma and has prognostic significance. Clin Cancer Res; 2010 Aug 15;16(16):4289-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MiRNA-196 is upregulated in glioblastoma but not in anaplastic astrocytoma and has prognostic significance.
  • They are implicated in tumorigenesis and function both as tumor suppressors and as oncogenes.
  • The clinical significance of miRNA expression profiles in malignant gliomas remains unclear.
  • EXPERIMENTAL DESIGN: In this study, we examined the expression levels of 365 mature human miRNAs in 12 malignant gliomas, including 8 glioblastomas and 4 anaplastic astrocytomas, using TaqMan real-time quantitative PCR arrays.
  • A validation study was done to corroborate a subset of the results, including expression levels of miR-196a, -196b, -21, and -15b, by analyzing 92 malignant gliomas by conventional real-time PCR.
  • RESULTS: Expression profiles in glioblastomas and anaplastic astrocytomas suggested that 16 miRNAs were candidate markers associated with the malignant progression of gliomas.
  • Both miRNAs showed increased expression levels in glioblastomas relative to both anaplastic astrocytomas and normal brains in the validation study.
  • CONCLUSIONS: Our results suggest that miR-196 may play a role in the malignant progression of gliomas and may be a prognostic predictor in glioblastomas.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Glioblastoma / genetics. MicroRNAs / genetics

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

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

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

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

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

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  • (PMID = 18945545.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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62. Kunitz A, Wolter M, van den Boom J, Felsberg J, Tews B, Hahn M, Benner A, Sabel M, Lichter P, Reifenberger G, von Deimling A, Hartmann C: DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas. Brain Pathol; 2007 Oct;17(4):363-70
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  • [Title] DNA hypermethylation and aberrant expression of the EMP3 gene at 19q13.3 in Human Gliomas.
  • Allelic losses on 19q are found in the majority of oligodendroglial tumors and approximately one-third of diffuse astrocytomas.
  • However, the tumor suppressor genes (TSG) on 19q are still elusive.
  • In line with this, other authors reported EMP3 as being epigenetically silenced in neuroblastomas and astrocytomas.
  • To further investigate EMP3 as a TSG candidate on 19q13.3, we performed molecular analysis of this gene in 162 human gliomas.
  • Mutation analysis did not reveal EMP3 alteration in 132 gliomas.
  • In astrocytomas, EMP3 hypermethylation was also paralleled by reduced expression but was independent of the 19q status.
  • EMP3 hypermethylation was detected in more than 80% of diffuse, anaplastic astrocytomas and secondary glioblastomas.
  • Our data corroborate that oligodendroglial and astrocytic gliomas often show EMP3 hypermethylation and aberrant expression.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic / genetics. Glioma / genetics. Membrane Glycoproteins / genetics
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / metabolism. Astrocytoma / physiopathology. Gene Expression Profiling. Gene Silencing / physiology. Genetic Predisposition to Disease / genetics. Humans. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / physiopathology. Oligonucleotide Array Sequence Analysis

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  • (PMID = 17610521.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / EMP3 protein, human; 0 / Membrane Glycoproteins
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63. Oka F, Yamashita Y, Kumabe T, Tominaga T: Total resection of a hemorrhagic tectal pilocytic astrocytoma--case report. Neurol Med Chir (Tokyo); 2007 May;47(5):219-21
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  • [Title] Total resection of a hemorrhagic tectal pilocytic astrocytoma--case report.
  • A 21-year-old man presented with a hemorrhagic pilocytic astrocytoma of the tectal plate manifesting as sudden onset of severe headache, vertigo, nausea, and vomiting.
  • Magnetic resonance (MR) imaging revealed a dorsally exophytic tectal tumor as hypointense on the T(1)-weighted image and hyperintense on the T(2)-weighted image with contrast enhancement.
  • Radical resection of the tumor was selected because of the unusual aggressive clinical course with hemorrhage and suspicion of malignant components.
  • The tumor was totally resected via an occipital transtentorial approach using a neuronavigation system without surgical complications.
  • The histological diagnosis was pilocytic astrocytoma.
  • Tectal plate pilocytic astrocytoma is rarely associated with hemorrhage but should be considered in the differential diagnosis of intracranial hemorrhage with acute presentation.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery. Intracranial Hemorrhages / etiology. Tectum Mesencephali

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

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  • (PMID = 17471019.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Transcription Factor AP-2
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65. Xiao A, Yin C, Yang C, Di Cristofano A, Pandolfi PP, Van Dyke T: Somatic induction of Pten loss in a preclinical astrocytoma model reveals major roles in disease progression and avenues for target discovery and validation. Cancer Res; 2005 Jun 15;65(12):5172-80
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  • [Title] Somatic induction of Pten loss in a preclinical astrocytoma model reveals major roles in disease progression and avenues for target discovery and validation.
  • High-grade astrocytomas are invariably deadly and minimally responsive to therapy.
  • Pten is frequently mutated in aggressive astrocytoma but not in low-grade astrocytoma.
  • However, the Pten astrocytoma suppression mechanisms are unknown.
  • Here we introduced conditional null alleles of Pten (Pten(loxp/loxp)) into a genetically engineered mouse astrocytoma model [TgG(deltaZ)T121] in which the pRb family proteins are inactivated specifically in astrocytes.
  • Depletion of Pten function in adult astrocytoma cells alleviated the apoptosis evoked by pRb family protein inactivation and also induced tumor cell invasion.
  • Thus, we show that Pten deficiency in pRb-deficient astrocytoma cells contributes to tumor progression via multiple mechanisms, including suppression of apoptosis, increased cell invasion, and angiogenesis, all of which are hallmarks of high-grade astrocytoma.
  • These studies not only provide mechanistic insight into the role of Pten in astrocytoma suppression but also describe a valuable animal model for preclinical testing that is coupled with a primary cell-based system for target discovery and drug screening.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Protein Tyrosine Phosphatases / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Alleles. Animals. Apoptosis / genetics. Disease Models, Animal. Disease Progression. Female. Genes, Tumor Suppressor. Male. Mice. Mice, Transgenic. Neoplasm Invasiveness. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / pathology. PTEN Phosphohydrolase. Retinoblastoma Protein / deficiency. Retinoblastoma Protein / physiology

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  • (PMID = 15958561.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01-CA84314
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Proteins; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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66. Dashti SR, Robinson S, Rodgers M, Cohen AR: Pineal region giant cell astrocytoma associated with tuberous sclerosis: case report. J Neurosurg; 2005 Apr;102(3 Suppl):322-5
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  • [Title] Pineal region giant cell astrocytoma associated with tuberous sclerosis: case report.
  • Tuberous sclerosis complex is a genetic disorder characterized by the development of hamartomas in multiple organs including the brain, skin, eye, kidney, and heart.
  • Subependymal giant cell astrocytomas, typically located adjacent to the foramen of Monro, can enlarge and cause symptomatic ventricular obstruction.
  • The authors describe the case of a 3-year-old boy with a history of tuberous sclerosis and retinal lesions who presented with an enlarging enhancing pineal region mass.
  • Pathological examination showed a giant cell astrocytoma.
  • To the authors' knowledge, this is the first reported case of tuberous sclerosis associated with a giant cell astrocytoma of the pineal region.
  • [MeSH-major] Astrocytoma / complications. Astrocytoma / surgery. Pinealoma / complications. Pinealoma / surgery. Tuberous Sclerosis / complications

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  • (PMID = 15881760.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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67. Hamlat A, Saikali S, Diabira S, Messerer M, Riffaud L: Diagnosis of childhood astrocytomas. Expert Opin Med Diagn; 2009 Sep;3(5):501-22

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

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

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

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

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  • (PMID = 20809042.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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70. Matsuda K, Sakurada K, Mouri W, Saino M, Sato S, Saito S, Kayama T, Nakazato Y: [Operative case of isomorphic astrocytoma]. Brain Nerve; 2007 Aug;59(8):881-6
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  • [Title] [Operative case of isomorphic astrocytoma].
  • Diffuse astrocytomas are classified as WHO Grade II tumors.
  • Recently, a subtype presenting with better prognosis has been proposed, and it is known as "isomorphic astrocytoma."
  • A clinical case that we encountered was believed to be categorized as this subtype; it has been presented in this report.
  • The tumor was resected under awake surgery.
  • The pathological diagnosis was diffuse astrocytoma, but this tumor was considered to be the isomorphic subtype.
  • Some parts of the tumor showed a relatively high MIB-1 labeling index (LI) of 9.2%, and additional 50-Gy radiotherapy was performed.
  • Isomorphic astrocytoma is characterized by prolonged epileptic seizures, a low MIB-1 LI, and better prognosis.
  • In our case, since the MIB-1 LI was higher in some parts of the tumor, the appropriate therapy for WHO Grade II tumors was performed.
  • However, this case was considered representative of isomorphic astrocytoma.
  • No reports of this tumor subtype have been previously described in Japan.
  • Therefore, this report is the first case of isomorphic astrocytoma reported to Japanese literature.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery

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  • (PMID = 17713125.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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71. Hernández-Hernández OT, Rodríguez-Dorantes M, González-Arenas A, Camacho-Arroyo I: Progesterone and estradiol effects on SRC-1 and SRC-3 expression in human astrocytoma cell lines. Endocrine; 2010 Feb;37(1):194-200
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  • [Title] Progesterone and estradiol effects on SRC-1 and SRC-3 expression in human astrocytoma cell lines.
  • In this study, we determined progesterone and estrogen receptor isoform expression in two human astrocytoma cell lines with different evolution grade (U373, grade III; and D54, grade IV) by Western Blot.
  • Our data suggest that SRC-1 and SRC-3 expression is differentially regulated by sex steroid hormones in astrocytomas and that P(4) regulates SRC-1 expression depending on the evolution grade of human astrocytoma cells.
  • [MeSH-major] Astrocytoma / metabolism. Estradiol / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. Nuclear Receptor Coactivator 1 / metabolism. Nuclear Receptor Coactivator 3 / metabolism. Progesterone / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Humans. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Receptors, Estradiol / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors

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  • (PMID = 20963570.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Estradiol; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / NCOA3 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1; EC 2.3.1.48 / Nuclear Receptor Coactivator 3
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72. Jakubowicz-Gil J, Langner E, Wertel I, Piersiak T, Rzeski W: Temozolomide, quercetin and cell death in the MOGGCCM astrocytoma cell line. Chem Biol Interact; 2010 Oct 6;188(1):190-203
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  • [Title] Temozolomide, quercetin and cell death in the MOGGCCM astrocytoma cell line.
  • The aim of the present study was to investigate the effect of Temozolomide (an alkylating chemotherapeutic agent) and quercetin (natural flavonoid) on cell death in the human astrocytoma cell line MOGGCCM (WHO grade III).
  • We demonstrated for the first time that combinations of both drugs were much more effective in programmed cell death induction in glioma cells.
  • Temozolomide administered with quercetin seems to be a potent and promising combination which might be useful in glioma therapy.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Death / drug effects. Dacarbazine / analogs & derivatives. Quercetin / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Fluorescent Antibody Technique, Indirect. Humans

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20654599.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9IKM0I5T1E / Quercetin
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73. Dong L, Witkowski CM, Craig MM, Greenwade MM, Joseph KL: Cytotoxicity effects of different surfactant molecules conjugated to carbon nanotubes on human astrocytoma cells. Nanoscale Res Lett; 2009;4(12):1517-23
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  • [Title] Cytotoxicity effects of different surfactant molecules conjugated to carbon nanotubes on human astrocytoma cells.
  • Phase contrast and epifluorescence microscopy were utilized to monitor morphological changes in human astrocytoma cells during a time-course exposure to single-walled carbon nanotube (SWCNT) conjugates with different surfactants and to investigate sub-cellular distribution of the nanotube conjugates, respectively.

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  • [Cites] Nat Nanotechnol. 2007 Jan;2(1):47-52 [18654207.001]
  • [Cites] Exp Mol Pathol. 2009 Jun;86(3):215-23 [19186176.001]
  • [Cites] Bioorg Med Chem. 2009 Apr 15;17(8):2950-62 [19299149.001]
  • [Cites] J Pharm Sci. 1998 Nov;87(11):1305-7 [9811481.001]
  • [Cites] J Phys Chem B. 2005 Jul 14;109(27):13148-53 [16852637.001]
  • [Cites] Mol Pharm. 2004 Nov-Dec;1(6):399-405 [16028351.001]
  • [Cites] Nat Nanotechnol. 2006 Oct;1(1):60-5 [18654143.001]
  • [Cites] Cell Tissue Res. 2009 Jan;335(1):75-96 [18633647.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3357-62 [16492781.001]
  • [Cites] Nat Neurosci. 2006 Feb;9(2):260-7 [16388306.001]
  • [Cites] Nat Rev Neurosci. 2006 Jan;7(1):41-53 [16371949.001]
  • [Cites] J Am Chem Soc. 2005 Apr 27;127(16):6021-6 [15839702.001]
  • [Cites] Environ Sci Technol. 2005 Mar 1;39(5):1378-83 [15787380.001]
  • [Cites] J Am Chem Soc. 2004 Dec 8;126(48):15638-9 [15571374.001]
  • [Cites] J Am Chem Soc. 2004 Jun 9;126(22):6850-1 [15174838.001]
  • [Cites] Nat Biotechnol. 2003 Oct;21(10):1166-70 [14520401.001]
  • [Cites] Toxicol Sci. 2004 Jan;77(1):117-25 [14514968.001]
  • [Cites] Toxicol Sci. 2004 Jan;77(1):126-34 [14514958.001]
  • [Cites] Bioessays. 2003 Sep;25(9):888-96 [12938178.001]
  • [Cites] Toxicol Lett. 2006 Aug 1;165(1):88-100 [16527436.001]
  • [Cites] Science. 2002 Jul 26;297(5581):593-6 [12142535.001]
  • [Cites] Adv Drug Deliv Rev. 2001 Mar 23;47(1):65-81 [11251246.001]
  • [Cites] Annu Rev Physiol. 2001;63:795-813 [11181976.001]
  • [Cites] Science. 2003 May 2;300(5620):775-8 [12730595.001]
  • (PMID = 20652100.001).
  • [ISSN] 1931-7573
  • [Journal-full-title] Nanoscale research letters
  • [ISO-abbreviation] Nanoscale Res Lett
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Astrocytoma cells / Blood–brain barrier / Brain tumors / Carbon nanotubes / Central nervous system / Cytotoxicity / Gene therapy / Non-viral gene vector / Surfactants
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74. Quick Q, Skalli O: Alpha-actinin 1 and alpha-actinin 4: contrasting roles in the survival, motility, and RhoA signaling of astrocytoma cells. Exp Cell Res; 2010 Apr 15;316(7):1137-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-actinin 1 and alpha-actinin 4: contrasting roles in the survival, motility, and RhoA signaling of astrocytoma cells.
  • Here, we have examined whether the two highly homologous non-muscle alpha-actinin isoforms 1 and 4 exhibit functional differences in astrocytoma cells.
  • The protein levels of these isoforms were differentially regulated during the development and progression of astrocytomas, as alpha-actinin 1 was higher in astrocytomas compared to normal brains whereas alpha-actinin 4 was elevated in high-grade astrocytomas compared to normal brains and low grade astrocytomas.
  • RNAi demonstrated contrasted contributions of alpha-actinin 1 and 4 to the malignant behavior of U-373, U-87 and A172 astrocytoma cells.
  • While alpha-actinin 1 appeared to favor the expansion of U-373, U-87 and A172 astrocytoma cell populations, alpha-actinin 4 played this role only for U-373 cells.
  • Finally, in the three astrocytoma cell lines examined, alpha-actinin 1 and 4 had contrasted biochemical properties as alpha-actinin 4 was significantly more abundant in the actin cytoskeleton than alpha-actinin 1.
  • Collectively, these findings suggest that alpha-actinin 1 and 4 are differentially regulated during the development and progression of astrocytomas because each of these isoforms uniquely contributes to distinct malignant properties of astrocytoma cells.
  • [MeSH-major] Actinin / physiology. Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Movement / genetics. rhoA GTP-Binding Protein / physiology
  • [MeSH-minor] Brain / metabolism. Cell Proliferation. Cell Survival / genetics. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Signal Transduction / genetics. Signal Transduction / physiology. Time Factors. Tumor Cells, Cultured

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 20156433.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ACTN1 protein, human; 0 / ACTN4 protein, human; 11003-00-2 / Actinin; EC 3.6.5.2 / rhoA GTP-Binding Protein
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75. Sexton M, Woodruff G, Cudaback E, Kreitzer FR, Xu C, Lin YH, Möller T, Bai M, Manning HC, Bornhop D, Stella N: Binding of NIR-conPK and NIR-6T to astrocytomas and microglial cells: evidence for a protein related to TSPO. PLoS One; 2009 Dec 18;4(12):e8271
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  • [Title] Binding of NIR-conPK and NIR-6T to astrocytomas and microglial cells: evidence for a protein related to TSPO.
  • NIR-6T is a DAA1106 analogue also conjugated to IRDye 800CW.We found that NIR-6T competed for [(3)H]-PK 11195 binding in astrocytoma cell homogenates with nanomolar affinity, but did not exhibit specific binding in intact astrocytoma cells in culture, indicating that NIR-6T is unlikely to constitute a useful MI agent for monitoring TSPO expression in intact cells.
  • Conversely, we found that NIR-conPK did not compete for [(3)H]-PK 11195 binding in astrocytoma cell homogenate, but exhibited specific binding in intact astrocytoma cells in culture with nanomolar affinity, suggesting that NIR-conPK binds to a protein distinct, but related to, TSPO.
  • Accordingly, treating intact astrocytoma cells and microglia in culture with cytokines led to significant changes in the amount of NIR-conPK specific binding without corresponding change in TSPO expression.
  • Remarkably, the cytokine-induced changes in the protein targeted by NIR-conPK in intact microglia were selective, since IFN-gamma (but not TNFalpha and TGFbeta) increased the amount of NIR-conPK specific binding in these cells.Together these results suggest that NIR-conPK binds to a protein that is related to TSPO, and expressed by astrocytomas and microglia.
  • Our results also suggest that the expression of this protein is increased by specific cytokines, and thus allows for the monitoring of a particular subtype of microglia activation.

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  • [Cites] Brain. 2000 Nov;123 ( Pt 11):2321-37 [11050032.001]
  • [Cites] Bioorg Med Chem Lett. 2007 Mar 15;17(6):1667-70 [17251020.001]
  • [Cites] AJR Am J Roentgenol. 2001 Apr;176(4):1016-8 [11264101.001]
  • [Cites] Jpn J Exp Med. 1967 Oct;37(5):461-74 [4301953.001]
  • [Cites] Brain Res. 1984 Jul 23;306(1-2):283-91 [6466977.001]
  • [Cites] J Neurosurg. 1989 Jul;71(1):113-8 [2544689.001]
  • [Cites] J Neuroimmunol. 1990 May;27(2-3):229-37 [2110186.001]
  • [Cites] Am J Physiol. 1993 Nov;265(5 Pt 1):L421-9 [8238529.001]
  • [Cites] Mol Cancer Res. 2007 Apr;5(4):341-9 [17426249.001]
  • [Cites] J Mol Cell Cardiol. 2007 May;42(5):1001-7 [17362986.001]
  • [Cites] Nucl Med Biol. 2007 May;34(4):439-46 [17499734.001]
  • [Cites] Curr Pharm Des. 2007;13(23):2385-405 [17692008.001]
  • [Cites] Exp Neurol. 2007 Sep;207(1):118-27 [17658516.001]
  • [Cites] J Neurochem. 2007 Sep;102(6):2118-31 [17555551.001]
  • [Cites] Bioconjug Chem. 2007 Nov-Dec;18(6):2018-23 [17979225.001]
  • [Cites] J Neuroimmune Pharmacol. 2006 Jun;1(2):127-37 [18040779.001]
  • [Cites] Anal Sci. 2008 Jan;24(1):51-3 [18187849.001]
  • [Cites] Br J Pharmacol. 2008 Jan;153(2):299-308 [17982478.001]
  • [Cites] Pharmacol Ther. 2008 Apr;118(1):1-17 [18374421.001]
  • [Cites] Radiology. 2008 Sep;248(3):925-35 [18647846.001]
  • [Cites] Neurochem Int. 2009 Jan;54(1):28-36 [18984021.001]
  • [Cites] J Fluoresc. 2009 Mar;19(2):277-84 [18758925.001]
  • [Cites] Brain. 2001 Oct;124(Pt 10):2014-27 [11571219.001]
  • [Cites] Brain Pathol. 2002 Jan;12(1):108-16 [11771519.001]
  • [Cites] Org Lett. 2002 Apr 4;4(7):1075-8 [11922786.001]
  • [Cites] J Biol Chem. 2002 Jun 7;277(23):20869-76 [11916961.001]
  • [Cites] Eur Radiol. 2003 Jan;13(1):195-208 [12541130.001]
  • [Cites] Nat Rev Drug Discov. 2003 Feb;2(2):151-4 [12563306.001]
  • [Cites] Cancer Res. 2003 Apr 1;63(7):1602-7 [12670911.001]
  • [Cites] Ann N Y Acad Sci. 2003 May;992:39-47 [12794045.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Jun;85(2-5):275-83 [12943713.001]
  • [Cites] Clin Biochem. 2004 Jan;37(1):61-6 [14675564.001]
  • [Cites] Neurobiol Dis. 2003 Dec;14(3):417-24 [14678758.001]
  • [Cites] Bioorg Med Chem. 2004 Jan 15;12(2):423-38 [14723961.001]
  • [Cites] Curr Opin Investig Drugs. 2004 Jan;5(1):29-33 [14983970.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3214-9 [14976257.001]
  • [Cites] J Clin Invest. 2004 Apr;113(7):981-9 [15057304.001]
  • [Cites] Synapse. 2004 Jun 15;52(4):283-91 [15103694.001]
  • [Cites] Brain. 2004 Jun;127(Pt 6):1379-92 [15069023.001]
  • [Cites] Vet J. 2004 Nov;168(3):230-7 [15501140.001]
  • [Cites] Mol Pharmacol. 1994 Feb;45(2):255-61 [7906855.001]
  • [Cites] Biochem Pharmacol. 1994 Aug 3;48(3):583-6 [8068045.001]
  • [Cites] J Pharmacol Exp Ther. 1995 May;273(2):721-7 [7752076.001]
  • [Cites] J Neurosci Res. 1997 Oct 15;50(2):345-53 [9373043.001]
  • [Cites] Neurosci Lett. 1998 Jan 23;241(1):53-6 [9502214.001]
  • [Cites] Eur J Pharmacol. 1998 Mar 26;345(3):339-42 [9592035.001]
  • [Cites] Int Rev Immunol. 1998;16(5-6):457-99 [9646173.001]
  • [Cites] Eur J Pharmacol. 1999 Apr 29;371(2-3):197-204 [10357257.001]
  • [Cites] Ann Neurol. 2004 Dec;56(6):894-7 [15562429.001]
  • [Cites] Neuroimage. 2005 Jan 15;24(2):591-5 [15627603.001]
  • [Cites] Biochem Pharmacol. 2005 Mar 1;69(5):819-30 [15710359.001]
  • [Cites] Neurobiol Dis. 2005 Nov;20(2):550-61 [15916899.001]
  • [Cites] Oncogene. 2005 Nov 17;24(51):7503-13 [16091749.001]
  • [Cites] Mol Pharmacol. 2006 Jan;69(1):37-44 [16189298.001]
  • [Cites] Bioconjug Chem. 2006 May-Jun;17(3):735-40 [16704212.001]
  • [Cites] Trends Pharmacol Sci. 2006 Aug;27(8):402-9 [16822554.001]
  • [Cites] Prog Neurobiol. 2006 Dec;80(6):308-22 [17156911.001]
  • [Cites] Neurology. 2000 Oct 10;55(7):1052-4 [11061271.001]
  • (PMID = 20020060.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA014486; United States / NIDA NIH HHS / DA / DA14486; United States / PHS HHS / / T32ATO-0815-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Extracts; 0 / Chemokines; 0 / Fluorescent Dyes; 0 / Indoles; 0 / NIR-6T; 0 / NIR-conPK; 0 / RNA, Messenger; 0 / Receptors, GABA-A
  • [Other-IDs] NLM/ PMC2792720
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76. Moshel YA, Elliott RE, Monoky DJ, Wisoff JH: Role of diffusion tensor imaging in resection of thalamic juvenile pilocytic astrocytoma. J Neurosurg Pediatr; 2009 Dec;4(6):495-505
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  • [Title] Role of diffusion tensor imaging in resection of thalamic juvenile pilocytic astrocytoma.
  • OBJECT: The choice of surgical approach during resection of a thalamic juvenile pilocytic astrocytoma (JPA) is dictated by the location of the displaced normal thalamus and posterior limb of the internal capsule (PLIC).
  • Diffusion tensor (DT) imaging and white matter tractography can identify the location of the PLIC in relation to the tumor and may be useful in planning the operative trajectory.
  • Gross-total resection of all cystic and solid tumor components was confirmed on postoperative imaging in all cases.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / surgery. Brain Neoplasms / diagnosis. Brain Neoplasms / surgery. Diffusion Tensor Imaging / standards. Microsurgery. Thalamus / pathology. Thalamus / surgery


77. Benes V 3rd, Barsa P, Benes V Jr, Suchomel P: Prognostic factors in intramedullary astrocytomas: a literature review. Eur Spine J; 2009 Oct;18(10):1397-422

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors in intramedullary astrocytomas: a literature review.
  • Astrocytomas affect a significant portion of patients with intramedullary tumors.
  • Only tumor grade was consistently reported as the major factor affecting prognosis.
  • The influence of other clinical factors (age, gender, history length, functional status, tumor location or extent, syrinx or cyst presence) can be speculated upon, but cannot be assessed adequately from the available literature.
  • For both low- and high-grade (HG) astrocytomas, maximal safe tumor resection should be the primary treatment objective but is often not feasible in contrast to other intramedullary and spinal neoplasms.
  • Since the biological nature of spinal cord HG glioma is identical to that of the brain, the same treatment algorithm of maximal safe resection followed by concomitant radio- and chemotherapy would be sensible to implement.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / therapy. Spinal Cord / pathology. Spinal Cord Neoplasms / diagnosis. Spinal Cord Neoplasms / therapy
  • [MeSH-minor] Drug Therapy / methods. Humans. Neoplasm Invasiveness / pathology. Neurosurgical Procedures / methods. Prognosis. Radiotherapy / methods

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  • [Cites] J Neurooncol. 2001 May;53(1):61-6 [11678433.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Feb 1;52(2):316-24 [11872276.001]
  • [Cites] Neuro Oncol. 2003 Jul;5(3):208-13 [12816727.001]
  • [Cites] Neurosurgery. 2003 Jul;53(1):110-20; discussion 120-2 [12823880.001]
  • [Cites] Cancer. 2003 Aug 1;98(3):554-61 [12879473.001]
  • [Cites] Am J Roentgenol Radium Ther Nucl Med. 1969 Mar;105(3):659-64 [5775022.001]
  • [Cites] Cancer. 1975 Jun;35(6):1558-62 [1148990.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1976 Mar;39(3):290-6 [932744.001]
  • [Cites] Paraplegia. 1977 Nov;15(3):262-73 [201902.001]
  • [Cites] Cancer. 1978 May;41(5):1751-60 [417797.001]
  • [Cites] Radiology. 1980 May;135(2):473-9 [7367644.001]
  • [Cites] J Neurosurg. 1981 Mar;54(3):323-30 [7463133.001]
  • [Cites] Pediatr Neurosurg. 1997 Jul;27(1):34-9 [9486834.001]
  • [Cites] Childs Nerv Syst. 1998 Jul;14(7):317-21 [9726582.001]
  • [Cites] Cancer. 1998 Dec 1;83(11):2391-9 [9840540.001]
  • [Cites] Radiat Oncol Investig. 1998;6(6):276-80 [9885944.001]
  • [Cites] Childs Nerv Syst. 1999 Jan;15(1):17-28 [10066016.001]
  • [Cites] Pediatr Neurosurg. 1999 Jan;30(1):1-5 [10202299.001]
  • [Cites] Am J Clin Oncol. 1999 Aug;22(4):344-51 [10440187.001]
  • [Cites] J Neurosurg Spine. 2005 Mar;2(3):249-55 [15796348.001]
  • [Cites] Neurosurgery. 2005 May;56(5):972-81; discussion 972-81 [15854245.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Sep 1;63(1):91-100 [16111576.001]
  • [Cites] Lancet. 2005 Sep 17-23;366(9490):985-90 [16168780.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Mar 15;64(4):1060-71 [16373081.001]
  • [Cites] Spinal Cord. 2006 Dec;44(12):740-5 [16670687.001]
  • [Cites] Acta Neurochir (Wien). 2008 Apr;150(4):371-9; discussion 379 [18176774.001]
  • [Cites] Eur Spine J. 2008 Mar;17(3):327-35 [18026865.001]
  • [Cites] Spinal Cord. 2008 Apr;46(4):282-6 [17909556.001]
  • [Cites] Neurosurgery. 2008 Apr;62(4):753-64; discussion 264-6 [18496181.001]
  • [Cites] Neurosurgery. 2008 Jul;63(1):55-60; discussion 60-1 [18728568.001]
  • [Cites] Pediatr Neurosurg. 1997 Jul;27(1):12-8 [9486831.001]
  • [Cites] Br J Cancer. 1999 Nov;81(5):835-40 [10555754.001]
  • [Cites] J Clin Neurosci. 2000 Jan;7(1):20-3 [10847645.001]
  • [Cites] J Neurosurg. 2000 Oct;93(2 Suppl):183-93 [11012047.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Oct 1;48(3):837-42 [11020582.001]
  • [Cites] J Neurooncol. 2001 Mar;52(1):85-94 [11451207.001]
  • [Cites] Cancer. 1982 Aug 15;50(4):732-5 [7093908.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1982 May;8(5):925-9 [7107424.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1982 Jun;8(6):999-1003 [7107442.001]
  • [Cites] J Neurosurg. 1982 Nov;57(5):685-9 [7131070.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1985 Nov;11(11):1933-9 [2997089.001]
  • [Cites] J Neurosurg. 1985 Nov;63(5):669-75 [4056869.001]
  • [Cites] Adv Tech Stand Neurosurg. 1986;13:135-69 [3510623.001]
  • [Cites] J Neurosurg. 1987 Apr;66(4):621-5 [3031241.001]
  • [Cites] Childs Nerv Syst. 1987;3(2):89-92 [3040249.001]
  • [Cites] J Neurosurg. 1989 Jan;70(1):50-4 [2909688.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1989 Jun;16(6):1397-403 [2542194.001]
  • [Cites] J Neurosurg. 1989 Dec;71(6):842-5 [2585075.001]
  • [Cites] Neurosurgery. 1989 Dec;25(6):855-9 [2601814.001]
  • [Cites] J Neurosurg. 1990 Apr;72(4):523-32 [2319309.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Jul;19(1):3-8 [2380091.001]
  • [Cites] Neurosurgery. 1990 Aug;27(2):193-6 [2385335.001]
  • [Cites] Neurosurgery. 1991 Nov;29(5):651-6; discussion 656-7 [1961392.001]
  • [Cites] Neurosurgery. 1992 Apr;30(4):490-3 [1584345.001]
  • [Cites] J Neurosurg. 1992 Sep;77(3):355-9 [1506881.001]
  • [Cites] Clin Neurosurg. 1992;39:361-87 [1458751.001]
  • [Cites] J Neurosurg. 1993 Aug;79(2):204-9 [8331401.001]
  • [Cites] Br J Neurosurg. 1993;7(5):473-81 [8267886.001]
  • [Cites] Radiother Oncol. 1993 Dec;29(3):294-300 [8127979.001]
  • [Cites] J Neurosurg. 1994 Oct;81(4):507-12 [7931582.001]
  • [Cites] Neurosurgery. 1994 Jul;35(1):69-74; discussion 74-6 [7936155.001]
  • [Cites] Neurosurgery. 1994 Nov;35(5):865-73; discussion 873 [7838335.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Sep 30;33(2):323-8 [7673019.001]
  • [Cites] J Neurosurg. 1995 Oct;83(4):590-5 [7674006.001]
  • [Cites] Eur Spine J. 1996;5(4):243-50 [8886736.001]
  • [Cites] J Neurosurg. 1996 Dec;85(6):1036-43 [8929492.001]
  • [Cites] Childs Nerv Syst. 1996 Dec;12(12):776-80 [9118146.001]
  • [Cites] Childs Nerv Syst. 1997 Feb;13(2):108-12 [9105749.001]
  • [Cites] Clin Neurol Neurosurg. 1997 Feb;99(1):1-5 [9107459.001]
  • [Cites] J Neurooncol. 1997 Jul;33(3):205-11 [9195492.001]
  • [Cites] Childs Nerv Syst. 1997 Jul;13(7):375-82 [9298273.001]
  • [Cites] Pediatr Neurosurg. 1997 May;26(5):247-54 [9440494.001]
  • [Cites] J Neurosurg. 1998 Feb;88(2):215-20 [9452226.001]
  • (PMID = 19562388.001).
  • [ISSN] 1432-0932
  • [Journal-full-title] European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society
  • [ISO-abbreviation] Eur Spine J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 76
  • [Other-IDs] NLM/ PMC2899373
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78. Hänninen MM, Haapasalo J, Haapasalo H, Fleming RE, Britton RS, Bacon BR, Parkkila S: Expression of iron-related genes in human brain and brain tumors. BMC Neurosci; 2009;10:36
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  • BACKGROUND: Defective iron homeostasis may be involved in the development of some diseases within the central nervous system.
  • We investigated the mRNA levels of hepcidin (HAMP), HFE, neogenin (NEO1), transferrin receptor 1 (TFRC), transferrin receptor 2 (TFR2), and hemojuvelin (HFE2) in normal human brain, brain tumors, and astrocytoma cell lines.
  • The specimens included 5 normal brain tissue samples, 4 meningiomas, one medulloblastoma, 3 oligodendrocytic gliomas, 2 oligoastrocytic gliomas, 8 astrocytic gliomas, and 3 astrocytoma cell lines.
  • In most tumor types, the pattern of gene expression was diverse.
  • Notable findings include high expression of transferrin receptor 1 in the hippocampus and medulla oblongata compared to other brain regions, low expression of HFE in normal brain with elevated HFE expression in meningiomas, and absence of hepcidin mRNA in astrocytoma cell lines despite expression in normal brain and tumor specimens.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antimicrobial Cationic Peptides / genetics. Antimicrobial Cationic Peptides / metabolism. Astrocytoma / genetics. Astrocytoma / metabolism. Cell Line, Tumor. Female. GPI-Linked Proteins. Hepcidins. Humans. Male. Meningioma / genetics. Meningioma / metabolism. Middle Aged. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. RNA, Messenger / analysis. Receptors, Transferrin / genetics. Receptors, Transferrin / metabolism. Statistics, Nonparametric. Young Adult

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  • [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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79. Haris M, Husain N, Singh A, Husain M, Srivastava S, Srivastava C, Behari S, Rathore RK, Saksena S, Gupta RK: Dynamic contrast-enhanced derived cerebral blood volume correlates better with leak correction than with no correction for vascular endothelial growth factor, microvascular density, and grading of astrocytoma. J Comput Assist Tomogr; 2008 Nov-Dec;32(6):955-65
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  • [Title] Dynamic contrast-enhanced derived cerebral blood volume correlates better with leak correction than with no correction for vascular endothelial growth factor, microvascular density, and grading of astrocytoma.
  • OBJECTIVE: To look for the impact of leak correction on correlation of perfusion indices with microvessel density (MVD) and vascular endothelial growth factor (VEGF) in astrocytomas.
  • METHODS: Dynamic contrast-enhanced magnetic resonance imaging was performed in 64 patients with varying grades of astrocytoma.
  • MVD and VEGF-expressing cells were quantified from the excised tumor tissues and were correlated with perfusion metrics.
  • RESULTS: Perfusion indices showed significant difference among the astrocytoma grades.
  • The corrected rCBV correlated (r = 0.853, P = <0.001) strongly, whereas the uncorrected rCBV (r = 0.592, P = <0.001) and k(trans) (r = 0.498, P = 0.001) correlated moderately with tumor grade.
  • The corrected rCBV discriminated 100% low-grade from high-grade astrocytoma, while uncorrected rCBV did this in 95.5% low-grade and 71.4% high-grade astrocytoma.
  • CONCLUSIONS: Corrected rCBV better correlates with grade and is more accurate in discriminating low-grade from high-grade astrocytoma compared with uncorrected rCBV.
  • [MeSH-major] Artifacts. Astrocytoma / pathology. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Gadolinium DTPA. Image Interpretation, Computer-Assisted / methods. Magnetic Resonance Imaging / methods. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 19204461.001).
  • [ISSN] 1532-3145
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Vascular Endothelial Growth Factor A; K2I13DR72L / Gadolinium DTPA
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80. Hamir AN, Picton R, Blythe LL, Heidel JR: Diagnostic exercise: astrocytoma with involvement of medulla oblongata, spinal cord, and spinal nerves in a raccoon (Procyon lotor). Vet Pathol; 2008 Nov;45(6):949-51
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  • [Title] Diagnostic exercise: astrocytoma with involvement of medulla oblongata, spinal cord, and spinal nerves in a raccoon (Procyon lotor).
  • Described are clinical signs and pathologic and immunohistochemical findings in an adult female raccoon (Procyon lotor) with an astrocytoma that involved medulla, cervical spinal cord, and roots of the cervical spinal nerves.
  • This appears to be the only reported case of astrocytoma that involved multiple anatomic sites in the central nervous system of this raccoon.
  • [MeSH-major] Astrocytoma / veterinary. Central Nervous System Neoplasms / veterinary. Medulla Oblongata / pathology. Raccoons. Spinal Cord / pathology. Spinal Nerves / pathology

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  • (PMID = 18984803.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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81. Reddy PS, Umesh S, Thota B, Tandon A, Pandey P, Hegde AS, Balasubramaniam A, Chandramouli BA, Santosh V, Rao MR, Kondaiah P, Somasundaram K: PBEF1/NAmPRTase/Visfatin: a potential malignant astrocytoma/glioblastoma serum marker with prognostic value. Cancer Biol Ther; 2008 May;7(5):663-8
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  • [Title] PBEF1/NAmPRTase/Visfatin: a potential malignant astrocytoma/glioblastoma serum marker with prognostic value.
  • Malignant astrocytomas comprise anaplastic astrocytoma (AA; grade III) and Glioblastoma (GBM; grade IV).
  • Using cDNA microarray based expression profiling of different grades of astrocytomas, we identified several fold increased levels of PBEF1 transcripts in GBM samples.
  • Further validation using real time RT-qPCR on an independent set of tumor samples (n=91) and normal brain samples (n=9), GBM specific higher expression of PBEF1 was confirmed.
  • Immunohistochemical staining for PBEF1 on a subset of the above samples largely reinforced our finding.
  • We carried out ELISA analysis on serum samples of astrocytoma patients to determine whether this protein levels would correlate with the presence of tumor and tumor grade.
  • Statistical analysis of these data indicates that in patients with astrocytoma, serum PBEF1 levels correlate with tumor grade and is highest in GBM.
  • Immunohistochemical analysis of an independent set of 51 retrospective GBM cases with known survival data revealed that PBEF1 expression in the tumor tissue along with its co-expression with p53 was associated with poor survival.
  • Thus, we have identified PBEF1 as a potential malignant astrocytoma serum marker and prognostic indicator among GBMs.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor. Brain / metabolism. Brain Neoplasms / metabolism. Cytokines / physiology. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. Nicotinamide Phosphoribosyltransferase / metabolism
  • [MeSH-minor] Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry / methods. Oligonucleotide Array Sequence Analysis. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18728403.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / Tumor Suppressor Protein p53; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
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82. Tehrani M, Friedman TM, Olson JJ, Brat DJ: Intravascular thrombosis in central nervous system malignancies: a potential role in astrocytoma progression to glioblastoma. Brain Pathol; 2008 Apr;18(2):164-71
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  • [Title] Intravascular thrombosis in central nervous system malignancies: a potential role in astrocytoma progression to glioblastoma.
  • The presence of necrosis within a diffuse glioma is a powerful predictor of poor prognosis, yet little is known of its origins.
  • Intravascular thrombosis is a frequent finding in glioblastoma [GBM; World Health Organization (WHO) grade IV] specimens and could potentially be involved in astrocytoma progression to GBM or represent a surrogate marker of GBM histology.
  • We investigated whether intravascular thrombosis was more frequent or prominent in GBM than other central nervous system (CNS) malignancies and considered its prognostic significance in anaplastic astrocytoma (AA; WHO grade III), which lacks necrosis.
  • Histologic sections were examined for thrombosis, necrosis and microvascular hyperplasia from each of 297 CNS tumors, including 103 GBMs, 46 AAs, 20 diffuse astrocytoma (DAs; WHO grade II), eight anaplastic oligodendrogliomas (AOs; WHO grade III), 20 oligodendrogliomas (ODs; WHO grade II), 49 metastatic carcinomas (METs), 31 primary central nervous system lymphomas (PCNSLs) and 20 medulloblastomas (MBs).

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  • [Cites] J Neuropathol Exp Neurol. 2005 Jun;64(6):479-89 [15977639.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2584-91 [16510576.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Jun;65(6):529-39 [16783163.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Sep;65(9):846-54 [16957578.001]
  • [Cites] Cancer Res. 2006 Nov 15;66(22):10643-6 [17108099.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 May;62(2):126-36 [17293122.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Proc Staff Meet Mayo Clin. 1949 Feb 2;24(3):71-5 [18111063.001]
  • [Cites] Cancer. 2000 Jun 1;88(11):2606-18 [10861440.001]
  • [Cites] J Neuropathol Exp Neurol. 2001 Mar;60(3):248-62 [11245209.001]
  • [Cites] Thromb Res. 2001 Jun 15;102(6):V215-24 [11516455.001]
  • [Cites] Curr Opin Pulm Med. 2001 Sep;7(5):326-31 [11584184.001]
  • [Cites] J Neurosurg. 1991 Mar;74(3):480-6 [1899696.001]
  • [Cites] Nature. 1992 Oct 29;359(6398):845-8 [1279432.001]
  • [Cites] Neurosurgery. 1995 Feb;36(2):375-80; discussion 380-1 [7731519.001]
  • [Cites] Cancer. 1996 Mar 15;77(6):1161-6 [8635139.001]
  • [Cites] Noshuyo Byori. 1996 Nov;13(2):115-8 [8958516.001]
  • [Cites] J Pathol Bacteriol. 1954 Jul;68(1):231-3 [13212575.001]
  • [Cites] Acta Pathol Microbiol Scand. 1950;27(1):51-64 [15406242.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1406-13 [15735028.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Neuro Oncol. 2005 Apr;7(2):122-33 [15831231.001]
  • [Cites] Trends Mol Med. 2002;8(4 Suppl):S62-7 [11927290.001]
  • [Cites] Clin Biochem. 2002 Jun;35(4):321-5 [12135696.001]
  • [Cites] Neurosurgery. 2002 Jul;51(1):2-12; discussion 12-3 [12182418.001]
  • [Cites] Ann Intern Med. 2003 Apr 15;138(8):659-68 [12693889.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):920-7 [14871821.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Mar 15;58(4):1147-52 [15001257.001]
  • [Cites] Lab Invest. 2004 Apr;84(4):397-405 [14990981.001]
  • [Cites] Cancer. 1983 Aug 1;52(3):550-4 [6305479.001]
  • [Cites] Cancer. 1987 May 1;59(9):1617-25 [3030531.001]
  • [Cites] Cancer. 1988 Nov 15;62(10):2152-65 [3179928.001]
  • (PMID = 18093251.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS053727-01; United States / NINDS NIH HHS / NS / R01 NS053727; United States / NINDS NIH HHS / NS / NS053727; United States / NINDS NIH HHS / NS / R01 NS053727-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ NIHMS82090; NLM/ PMC2610479
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83. Hlobilkova A, Ehrmann J, Sedlakova E, Krejci V, Knizetova P, Fiuraskova M, Kala M, Kalita O, Kolar Z: Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression? Neoplasma; 2007;54(4):334-41
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  • [Title] Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression?
  • The most frequent alterations found in astrocytomas are two major groups of signaling proteins: the cell cycle and the growth factor-regulated signaling pathways.
  • The aim of our study was to detect changes in expression of the following proteins: the tumor suppressors PTEN, p53, and p21Waf1/Cip1, glial fibrillary acidic protein (GFAP, as a marker of astroglial differentiation), the phosphorylated form of protein kinase B/Akt (PKB/Akt), which is downstream to the epidermal growth factor receptor (EGFR), and MDM2, which degrades p53.
  • Paraffin-embedded astrocytoma tissue samples from 89 patients were divided into low grade (grade I-II; 42 samples) and high grade astrocytomas (grade III-IV; 47 samples).
  • EGFR protein was detected in 29 % of low grade and in 60 % of high grade astrocytomas.
  • The expression of phosphorylated PKB/Akt was found in roughly the same proportions: in 86% of low grade and in 79% of high grade astrocytomas.
  • PTEN was not found in most of astrocytomas, 64% of low grade and 74% of high grade tumors showed no PTEN staining.
  • Overexpression of the mutated form of p53 or loss of p53 expression, however, was found in about 63% in both groups of astrocytomas with no differences between them.
  • GFAP expression was decreased in tumor astrocytes compared to normal astrocytes and this decreased with grading.
  • GFAP positive tumor cells were detected in only 50% of low grade, and 32% of high grade astrocytomas.
  • We conclude that EGFR expression increases with astrocytoma grading.
  • PTEN defects may also participate in aggressive tumor behaviour through activation of the PKB/Akt pathway.
  • The alteration of p53 supports the finding that the cell cycle regulation is also disrupted during development of astrocytomas.
  • EGFR is one of the factors, which drives the progression of astrocytomas from low to high grade stage.
  • [MeSH-major] Astrocytoma / metabolism. Cell Cycle. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Mutation / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / pathology. PTEN Phosphohydrolase / metabolism. Phosphorylation. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17822324.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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84. Josan V, Smith P, Kornberg A, Rickert C, Maixner W: Development of a pilocytic astrocytoma in a dysembryoplastic neuroepithelial tumor. Case report. J Neurosurg; 2007 Jun;106(6 Suppl):509-12
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  • [Title] Development of a pilocytic astrocytoma in a dysembryoplastic neuroepithelial tumor. Case report.
  • The authors report on a patient in whom a pilocytic astrocytoma developed within a DNET, raising questions regarding the classification of these lesions and the need for lifelong clinical and imaging surveillance.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Cerebral Cortex. Magnetic Resonance Imaging. Neoplasms, Second Primary / diagnosis. Neuroectodermal Tumors, Primitive / diagnosis


85. Rovin RA, Winn R: Expression of O6-methylguanine-deoxyribose nucleic acid methyltransferase and temozolomide response in a patient with a malignant spinal cord astrocytoma. Case report. J Neurosurg Spine; 2007 May;6(5):447-50
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  • [Title] Expression of O6-methylguanine-deoxyribose nucleic acid methyltransferase and temozolomide response in a patient with a malignant spinal cord astrocytoma. Case report.
  • The authors report the case of a 28-year-old woman with a high-grade spinal cord astrocytoma.
  • Treatment using surgery, radiation, and temozolomide (TMZ) led to functional recovery and regression of the residual tumor as demonstrated on serial magnetic resonance images.
  • Genetic testing revealed that this tumor did not express the DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT).
  • This is the first report in the literature correlating MGMT expression with the clinical response of a high-grade spinal cord astrocytoma treated using TMZ.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / metabolism. Dacarbazine / analogs & derivatives. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Spinal Cord Neoplasms / drug therapy. Spinal Cord Neoplasms / metabolism

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  • (PMID = 17542512.001).
  • [ISSN] 1547-5654
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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86. Lee WH, Jin JS, Tsai WC, Chen YT, Chang WL, Yao CW, Sheu LF, Chen A: Biological inhibitory effects of the Chinese herb danggui on brain astrocytoma. Pathobiology; 2006;73(3):141-8
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  • [Title] Biological inhibitory effects of the Chinese herb danggui on brain astrocytoma.
  • In nude mice, the growth of the tumor was inhibited by 30% by AS-CH or AS-AC (20 mg/kg; p < 0.05) and by 60% by AS-CH or AS-AC (60 mg/kg; p < 0.05).
  • CONCLUSIONS: Danggui may inhibit tumor growth by reducing the level of VEGF and the proapoptotic protein, cathepsin B.
  • Thus, danggui may be useful in the treatment of high-grade astrocytomas.
  • [MeSH-major] Angelica sinensis / chemistry. Antineoplastic Agents / pharmacology. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Drugs, Chinese Herbal / pharmacology. Phytotherapy
  • [MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cathepsin B / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Female. Formazans / metabolism. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Plant Extracts / pharmacology. Tetrazolium Salts / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17085958.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Chinese Herbal; 0 / Formazans; 0 / Plant Extracts; 0 / Tetrazolium Salts; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 23305-68-2 / MTT formazan; EC 3.4.22.1 / Cathepsin B
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87. Butowski NA, Sneed PK, Chang SM: Diagnosis and treatment of recurrent high-grade astrocytoma. J Clin Oncol; 2006 Mar 10;24(8):1273-80
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  • [Title] Diagnosis and treatment of recurrent high-grade astrocytoma.
  • High-grade gliomas represent a significant source of cancer-related death, and usually recur despite treatment.
  • In this analysis of current brain tumor medicine, we review diagnosis, standard treatment, and emerging therapies for recurrent astrocytomas.
  • Difficulties in interpreting radiographic evidence, especially with regard to differentiating between tumor and necrosis, present a formidable challenge.
  • The most accurate diagnoses come from tissue confirmation of recurrent tumor, but a combination of imaging techniques, such as magnetic resonance spectroscopy imaging, may also be relevant for diagnosis.
  • We describe the use of conventional radiotherapy, intensity-modulated radiotherapy, brachytherapy, radiosurgery, and photodynamic therapy for recurrent high-grade glioma.
  • The treatment of this devastating disease has so far been met with limited success, but emerging knowledge of neuroscience and the development of novel therapeutic agents will likely give patients new options and require the neuro-oncology community to redefine clinical trial design and strategy continually.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / therapy. Central Nervous System Neoplasms / diagnosis. Central Nervous System Neoplasms / therapy. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Glioma / diagnosis. Glioma / therapy. Humans. Radiotherapy

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  • (PMID = 16525182.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 87
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88. Henson JW, Hobbs W, Chakravarti A, Louis DN: Alterations in p53, p21, and MIB-1 labeling index in primary human astrocytomas following radiation therapy. J Neurooncol; 2005 Sep;74(2):151-4
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  • [Title] Alterations in p53, p21, and MIB-1 labeling index in primary human astrocytomas following radiation therapy.
  • Little is known about the cellular and genetic changes that occur in human astrocytomas following radiation therapy (RT).
  • Experimental studies would suggest that early effects include induction of p53 and p21 expression, cell cycle arrest, and selection of tumor cells with molecular changes that correlate with radiation resistance.
  • Unfortunately, tissue sampling of primary human astrocytomas closely following radiation therapy is uncommon, hindering comparative assessment of primary human tumors.
  • Through local databases, we were able to collect eight cases in which tissue was resected within 8 weeks of RT because of bulky residual disease: two patients with grade II diffuse astrocytomas (LGA) and 6 patients with high-grade astrocytomas (HGA; 1 anaplastic astrocytoma, 5 glioblastomas).
  • Only one tumor (52d post-RT) showed prominent radiation-induced histopathologic changes. p53 expression was detected in two tumors pre-RT and in six tumors post-RT.
  • The results of this unique series document that some primary human astrocytomas increase expression of p53 and p21 and decrease proliferation in response to RT.
  • However, the small size of the series argues for further studies of radiation induced molecular changes in primary human astrocytoma tissue.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / radiotherapy. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Ki-67 Antigen / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16193385.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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89. Saunders DE, Phipps KP, Wade AM, Hayward RD: Surveillance imaging strategies following surgery and/or radiotherapy for childhood cerebellar low-grade astrocytoma. J Neurosurg; 2005 Mar;102(2 Suppl):172-8
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  • [Title] Surveillance imaging strategies following surgery and/or radiotherapy for childhood cerebellar low-grade astrocytoma.
  • OBJECT: The authors sought to evaluate surveillance strategies for the detection and monitoring of residual and recurrent disease in children with cerebellar low-grade astrocytomas (CLGAs) treated surgically or with radiotherapy.
  • (2) those with residual disease with no immediate adjuvant therapy; and (3) those who received radiotherapy for residual/recurrent disease.
  • Eighty-four children were followed for a mean period of 73 months (range 2-159 months).
  • Following an incomplete resection, radiologically detected tumor progression leading to further treatment was detected at 7, 9, 12, 13, and 20 months, respectively, and an additional six tumors regressed or stablized.
  • For follow up of residual tumor, 6-month interval imaging for at least 3 years, yearly images for another 2 years, and subsequent 2-year imaging is recommended.
  • [MeSH-major] Astrocytoma / diagnosis. Cerebellar Neoplasms / diagnosis. Magnetic Resonance Imaging. Neoplasm, Residual / diagnosis. Tomography, X-Ray Computed
  • [MeSH-minor] Adolescent. Cerebellum / pathology. Cerebellum / radiography. Cerebellum / surgery. Child. Child, Preschool. Disease Progression. Female. Follow-Up Studies. Humans. Infant. Male. Neoplasm Recurrence, Local / epidemiology. Neoplasm Staging. Postoperative Care. Remission, Spontaneous. Time Factors

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  • (PMID = 16156227.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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90. Scott IS, Morris LS, Rushbrook SM, Bird K, Vowler SL, Burnet NG, Coleman N: Immunohistochemical estimation of cell cycle entry and phase distribution in astrocytomas: applications in diagnostic neuropathology. Neuropathol Appl Neurobiol; 2005 Oct;31(5):455-66
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  • [Title] Immunohistochemical estimation of cell cycle entry and phase distribution in astrocytomas: applications in diagnostic neuropathology.
  • Paraffin-embedded sections of intracerebral gliomas (n = 48), consisting of diffuse astrocytoma (n = 9), anaplastic astrocytoma (n = 8) and glioblastoma (n = 31), were analysed by immunohistochemistry using markers of cell cycle entry, Mcm-2 and Ki67, and putative markers of cell cycle phase, cyclins D1 (G1-phase), cyclin A (S-phase), cyclin B1 (G2-phase) and phosphohistone H3 (Mitosis).
  • There was a significant increase in Mcm-2 (P < 0.0001), Ki67 (P < 0.0001), cyclin A (P < 0.0001) and cyclin B1 (P = 0.002) expression with increasing grade from diffuse astrocytoma through anaplastic astrocytoma to glioblastoma, suggesting that any of these four markers has potential as a marker of tumour grade.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Cell Cycle / physiology. Immunohistochemistry / methods

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  • (PMID = 16150117.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCNB1 protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Histones; 136601-57-5 / Cyclin D1
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91. Maris C, Rorive S, Sandras F, D'Haene N, Sadeghi N, Bièche I, Vidaud M, Decaestecker C, Salmon I: Tenascin-C expression relates to clinicopathological features in pilocytic and diffuse astrocytomas. Neuropathol Appl Neurobiol; 2008 Jun;34(3):316-29
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  • [Title] Tenascin-C expression relates to clinicopathological features in pilocytic and diffuse astrocytomas.
  • AIMS: Tenascin-C (TN-C) is an extracellular matrix brain glycoprotein for which conflicting in vitro and in vivo results are reported in the literature dealing with its involvement in astrocytoma aggressiveness, in particular astrocytoma invasion.
  • In view of these conflicting results and the lack of data available on low-grade astrocytomas, the present study focuses on pilocytic World Health Organization (WHO) grade I, and diffuse WHO grade II astrocytomas, that is, two histological entities associated with very different invasive abilities.
  • METHODS: Using real-time reverse transcription polymerase chain reaction and immunohistochemistry, we analysed the TN-C expression in normal brain tissue as well as in a series of 54 pilocytic and 53 grade II astrocytomas.
  • Paralleling these observations, we showed that TN-C expression in low-grade astrocytomas similarly varies according to tumour site.
  • Cox regression analysis evidenced that TN-C provided an independent prognostic value which is enhanced in the case of grade II astrocytomas for which positive TN-C expression is associated with a higher risk of recurrence.
  • We also analysed TN-C expression specifically in vascular areas of low-grade astrocytomas without demonstrating any prognostic value for this additional feature.
  • RESULTS: Similarly to normal brain, low-grade astrocytomas exhibit variations in TN-C expression with site, and this expression is associated with an independent prognostic value in terms of recurrence.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Tenascin / biosynthesis
  • [MeSH-minor] Adult. Age Factors. Biomarkers, Tumor / analysis. Child. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Neoplasm Recurrence, Local / pathology. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Spinal Cord Neoplasms / metabolism. Spinal Cord Neoplasms / mortality. Spinal Cord Neoplasms / pathology

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  • (PMID = 17983425.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tenascin
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92. Zajdel A, Wilczok A, Slowinski J, Orchel J, Mazurek U: Aldehydic lipid peroxidation products in human brain astrocytomas. J Neurooncol; 2007 Sep;84(2):167-73
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  • [Title] Aldehydic lipid peroxidation products in human brain astrocytomas.
  • We explored whether these aldehydes and histone H3 mRNA levels could serve as biomarkers of malignancy and predictive factor in human brain astrocytomas.
  • Aldehydic lipid peroxidation products were determined as their dinitrophenylhydrazone derivatives in specimens obtained from 26 adult patients with brain astrocytomas.
  • H3 mRNA, 2-hydroxyhexanal, and 4-hydroxynonenal levels were higher in high-grade astrocytomas compared to low-grade astrocytomas and showed negative correlation with survival.
  • Higher levels of 2-hydroxyhexanal and 4-hydroxynonenal, and lower levels of n-hexanal were associated with poorer patient prognosis.
  • Our data suggest that tissue concentrations of aldehydic lipid peroxidation products can assist grading and predicting the clinical outcome in patients with astrocytic brain tumors.
  • Possibly, this parameter will enhance optimal selection of patients for individualized treatment protocols, tailored to unique biochemical and molecular profile of the tumor.
  • [MeSH-major] Aldehydes / analysis. Astrocytoma / metabolism. Brain Chemistry / physiology. Brain Neoplasms / metabolism. Lipid Peroxidation / physiology

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

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  • (PMID = 16187021.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / RNA, Messenger; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / PTPN13 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 13; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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94. Krueger DA, Care MM, Holland K, Agricola K, Tudor C, Mangeshkar P, Wilson KA, Byars A, Sahmoud T, Franz DN: Everolimus for subependymal giant-cell astrocytomas in tuberous sclerosis. N Engl J Med; 2010 Nov 4;363(19):1801-11
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  • [Title] Everolimus for subependymal giant-cell astrocytomas in tuberous sclerosis.
  • BACKGROUND: Neurosurgical resection is the standard treatment for subependymal giant-cell astrocytomas in patients with the tuberous sclerosis complex.
  • METHODS: Patients 3 years of age or older with serial growth of subependymal giant-cell astrocytomas were eligible for this open-label study.
  • The primary efficacy end point was the change in volume of subependymal giant-cell astrocytomas between baseline and 6 months.
  • Everolimus therapy was associated with a clinically meaningful reduction in volume of the primary subependymal giant-cell astrocytoma, as assessed on independent central review (P<0.001 for baseline vs. 6 months), with a reduction of at least 30% in 21 patients (75%) and at least 50% in 9 patients (32%).
  • There were no new lesions, worsening hydrocephalus, evidence of increased intracranial pressure, or necessity for surgical resection or other therapy for subependymal giant-cell astrocytoma.
  • CONCLUSIONS: Everolimus therapy was associated with marked reduction in the volume of subependymal giant-cell astrocytomas and seizure frequency and may be a potential alternative to neurosurgical resection in some cases, though long-term studies are needed. (Funded by Novartis; ClinicalTrials.gov number, NCT00411619.).
  • [MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Seizures / drug therapy. Sirolimus / analogs & derivatives. Tuberous Sclerosis / drug therapy


95. Rorive S, Lopez XM, Maris C, Trepant AL, Sauvage S, Sadeghi N, Roland I, Decaestecker C, Salmon I: TIMP-4 and CD63: new prognostic biomarkers in human astrocytomas. Mod Pathol; 2010 Oct;23(10):1418-28
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  • [Title] TIMP-4 and CD63: new prognostic biomarkers in human astrocytomas.
  • Based on the molecular profiling of astrocytomas, we previously identified a series of genes involved in astrocytoma invasion.
  • Of these, tissue inhibitor of metalloproteinase-4 (TIMP-4) was found to be overexpressed in pilocytic astrocytomas relative to diffuse astrocytomas of any histological grade.
  • Although some data suggest that TIMP-4 may be an anti-tumoral actor in astrocytomas, recent findings challenge this concept.
  • The present study aims to investigate the diagnostic and prognostic values of TIMP-4 and its putative partner CD63 in human astrocytomas.
  • Tissue microarray and image analysis were first carried out to quantitatively analyze the immunohistochemical expression of these proteins in 471 gliomas including 354 astrocytomas.
  • Pathological semi-quantitative scores of both markers' expression were then established and correlated to astrocytoma diagnosis and patient prognosis.
  • TIMP-4 and CD63 expressions were both overexpressed in astrocytomas compared with oligodendrogliomas (P<0.001) and in pilocytic astrocytomas compared with grade II diffuse astrocytomas (P<0.001).
  • In conclusion, this work provides the first evidence of a TIMP-4/CD63 association in astrocytoma tumor cells.
  • It identifies TIMP-4 and CD63 as markers of the astrocytic phenotype in patients with gliomas.
  • [MeSH-major] Antigens, CD / biosynthesis. Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Platelet Membrane Glycoproteins / biosynthesis. Tissue Inhibitor of Metalloproteinases / biosynthesis

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  • (PMID = 20693981.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD63; 0 / Biomarkers, Tumor; 0 / CD63 protein, human; 0 / Platelet Membrane Glycoproteins; 0 / Tissue Inhibitor of Metalloproteinases; 0 / tissue inhibitor of metalloproteinase-4
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96. Yan B, Omar FM, Das K, Ng WH, Lim C, Shiuan K, Yap CT, Salto-Tellez M: Characterization of Numb expression in astrocytomas. Neuropathology; 2008 Oct;28(5):479-84
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  • [Title] Characterization of Numb expression in astrocytomas.
  • Numb has also been reported to function as a tumor suppressor in breast cancers and medulloblastomas.
  • Given its role in maintaining neural progenitor pools in animal models and its reported role as a tumor suppressor, Numb could potentially contribute to astrocytoma oncogenesis.
  • We characterized Numb expression in both human astrocytoma tissue samples and glioblastoma cell lines.
  • We found that Numb is expressed in all grades of astrocytomas, being predominantly cytoplasmic in higher-grade astrocytomas but nuclear in pilocytic astrocytomas.
  • Numb expression in astrocytomas recapitulates that of progenitor cells during neurodevelopment, and suggests a role for Numb in astrocytoma oncogenesis.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Membrane Proteins / biosynthesis. Nerve Tissue Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Child. Child, Preschool. Female. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Neuroglia / metabolism. Neurons / metabolism

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  • (PMID = 18384513.001).
  • [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 / Glial Fibrillary Acidic Protein; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Numb protein, human
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97. Tsutsumi S, Higo T, Kondo A, Abe Y, Yasumoto Y, Ito M: Atypical cervical astrocytoma manifesting as occipitalgia. Neurol Med Chir (Tokyo); 2007 Aug;47(8):371-4
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  • [Title] Atypical cervical astrocytoma manifesting as occipitalgia.
  • Cervical MR imaging revealed a cervical intramedullary tumor.
  • Intraoperatively the subpial tumor was found to stretch the 3rd-5th dorsal nerve roots posteriorly, which was thought to cause the intolerable headache.
  • Total tumor resection was achieved without requiring myelotomy using electrophysiological monitoring with somatosensory and motor evoked potentials.
  • Histological examination identified diffuse astrocytoma.
  • Cervical astrocytoma of subpial location is a very rare cause of headache in adults.
  • [MeSH-major] Astrocytoma / complications. Astrocytoma / pathology. Headache / etiology. Spinal Cord / pathology. Spinal Cord Neoplasms / complications. Spinal Cord Neoplasms / pathology

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  • (PMID = 17721055.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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98. Tsutsumi S, Abe Y, Yasumoto Y, Ito M: Anaplastic pleomorphic xanthoastrocytoma with a component of anaplastic astrocytoma presenting as skull base tumor followed by downward extracranial extension. Case report. Neurol Med Chir (Tokyo); 2010;50(12):1108-12
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  • [Title] Anaplastic pleomorphic xanthoastrocytoma with a component of anaplastic astrocytoma presenting as skull base tumor followed by downward extracranial extension. Case report.
  • The patient underwent subtotal tumor resection.
  • Most of the tumor was located extraaxially, but a part of the tumor had invaded the temporal lobe, and had tightly adhered to the middle cerebral artery and its perforating vessels.
  • Histological examination revealed cellular pleomorphism with mitotic activity, focal necrosis, but lacking endothelial proliferation, consistent with anaplastic pleomorphic xanthoastrocytoma (PXA) with component of anaplastic astrocytoma.
  • Postoperatively, the patient underwent local irradiation and temozolomide administration, but the tumor relapsed 13 months later.
  • Second tumor resection was performed followed by gamma knife radiosurgery, but the residual tumor progressively grew, extending into the contralateral hemisphere, and formed an enormous mass in the left frontal lobe at 17 months.
  • Magnetic resonance imaging performed at 18 months revealed extracranial infiltration of the frontal tumor, through the cribriform plate, with enormous extension into the paranasal sinuses, nasal cavity, and orbit during the next month.
  • PXA with anaplastic appearance may have a component of anaplastic astrocytoma with more aggressive behavior.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Skull Base Neoplasms / pathology

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  • (PMID = 21206189.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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99. Yeh S, Fine HA, Smith JA: Corneal verticillata after dual anti-epidermal growth factor receptor and anti-vascular endothelial growth factor receptor 2 therapy (vandetanib) for anaplastic astrocytoma. Cornea; 2009 Jul;28(6):699-702
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  • [Title] Corneal verticillata after dual anti-epidermal growth factor receptor and anti-vascular endothelial growth factor receptor 2 therapy (vandetanib) for anaplastic astrocytoma.
  • PURPOSE: To describe a patient with a history of epithelial basement membrane dystrophy who developed symptomatic corneal verticillata after vandetanib therapy for anaplastic astrocytoma.
  • RESULTS: A 48-year-old female patient with a history of anaplastic astrocytoma status post resection, external beam radiation, and chemotherapy presented with glare symptoms, decreased contrast sensitivity, and increased lacrimation after approximately 12 months of therapy with the anti-epidermal growth factor receptor (EGFR) and anti-vascular endothelial growth factor receptor 2 protein tyrosine kinase inhibitor, vandetanib.
  • The patient remained under surveillance for tumor recurrence.
  • [MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Corneal Diseases / chemically induced. Neoplasm Recurrence, Local / drug therapy. Piperidines / adverse effects. Quinazolines / adverse effects. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors

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  • (PMID = 19512898.001).
  • [ISSN] 1536-4798
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Ointments; 0 / Piperidines; 0 / Quinazolines; 451W47IQ8X / Sodium Chloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.2.1.4 / Cellulase; EC 3.2.1.4 / carboxymethylcellulase
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100. Neyns B, Chaskis C, Joosens E, Menten J, D'Hondt L, Branle F, Sadones J, Michotte A: A multicenter cohort study of dose-dense temozolomide (21 of 28 days) for the treatment of recurrent anaplastic astrocytoma or oligoastrocytoma. Cancer Invest; 2008 Apr-May;26(3):269-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicenter cohort study of dose-dense temozolomide (21 of 28 days) for the treatment of recurrent anaplastic astrocytoma or oligoastrocytoma.
  • This multicenter cohort study enrolled 19 patients (15 anaplastic astrocytoma, 4 anaplastic oligoastrocytoma) who received temozolomide (100 mg/m2/day for 21 consecutive days every 28-day cycle) at first recurrence, either until disease progression or 12 cycles.
  • Among 15 evaluable patients, 2 had a complete or partial response, and 10 had stable disease.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Cohort Studies. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Survival Analysis






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