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51. Balosso S, Ravizza T, Perego C, Peschon J, Campbell IL, De Simoni MG, Vezzani A: Tumor necrosis factor-alpha inhibits seizures in mice via p75 receptors. Ann Neurol; 2005 Jun;57(6):804-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor-alpha inhibits seizures in mice via p75 receptors.
  • Brain inflammatory reactions have been described in various neurological disorders, including epilepsy.
  • Although there is clear evidence that cytokines affect neuroglial functions and blood-brain barrier permeability, scarce information is available on the functional consequences of brain inflammation on seizures.
  • We studied the role of tumor necrosis factor-alpha (TNF)-alpha and its p55 and p75 receptors in seizure modulation.
  • Transgenic mice with a perturbed TNF-alpha system showed profound alterations in seizure susceptibility: astrocytic overexpression of TNF-alpha was associated with reduced seizures, whereas mice lacking TNF-alpha p75 or both p55 and p75, receptors showed prolonged seizures.
  • Our findings show that increased brain levels of TNF-alpha result in significant inhibition of seizures in mice, and this action is mediated by neuronal p75 receptors.
  • This evidence highlights a novel function of TNF-alpha in brain and indicates a new system for anticonvulsive intervention.
  • [MeSH-major] Anticonvulsants / pharmacology. Epilepsy / drug therapy. Epilepsy / physiopathology. Receptors, Tumor Necrosis Factor, Type II / genetics. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Electroencephalography. Excitatory Amino Acid Agonists. Gene Expression. Hippocampus / physiology. Kainic Acid. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Receptors, Tumor Necrosis Factor, Type I / genetics. Receptors, Tumor Necrosis Factor, Type I / metabolism

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  • (PMID = 15852477.001).
  • [ISSN] 0364-5134
  • [Journal-full-title] Annals of neurology
  • [ISO-abbreviation] Ann. Neurol.
  • [Language] eng
  • [Grant] Italy / Telethon / / GP0285Y01; United States / NIDA NIH HHS / DA / DA12444
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Excitatory Amino Acid Agonists; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; SIV03811UC / Kainic Acid
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52. Alaraj A, Chan M, Oh S, Michals E, Valyi-Nagy T, Hersonsky T: Astroblastoma presenting with intracerebral hemorrhage misdiagnosed as dural arteriovenous fistula: review of a rare entity. Surg Neurol; 2007 Mar;67(3):308-13
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  • Immunohistochemically, the tumor cells show diffuse strong positivity for GFAP, S-100 protein, vimentin, as well as neuron-specific enolase and focal positivity for EMA.
  • A 4-vessel cerebral angiogram revealed a dural AVF in the left posterior temporal area.
  • Because of its high degree of proliferation, the presence of astroblastic pseudorosettes, prominent perivascular hyalinization, regional hyaline changes, and pushing borders with regard to the adjacent brain, the tumor was considered anaplastic.
  • CONCLUSIONS: Astroblastoma is a rare pure pathologic entity--a distinct form of astrocytic gliomas.
  • The diagnosis of astroblastoma is often difficult because of the astroblastic aspects that can be found in astrocytic tumors, in ependymomas, and in nonneuroepithelial tumors.
  • [MeSH-major] Central Nervous System Vascular Malformations / diagnosis. Cerebral Hemorrhage. Diagnostic Errors. Neoplasms, Neuroepithelial
  • [MeSH-minor] Adult. Cerebral Angiography. Diagnosis, Differential. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging

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  • (PMID = 17320647.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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53. Janardhanan R, Banik NL, Ray SK: N-(4-Hydroxyphenyl)retinamide induced differentiation with repression of telomerase and cell cycle to increase interferon-gamma sensitivity for apoptosis in human glioblastoma cells. Cancer Lett; 2008 Mar 8;261(1):26-36
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  • Glioblastoma is the most malignant and prevalent brain tumor in humans.
  • N-(4-Hydroxyphenyl)retinamide (4-HPR) induced astrocytic differentiation and increased sensitivity to interferon-gamma (IFN-gamma) for apoptosis in human glioblastoma A172, LN18, and SNB19 cells.

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  • (PMID = 18164543.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS057811-03; United States / NCI NIH HHS / CA / CA091460-04; United States / NCI NIH HHS / CA / R01 CA-91460; United States / NCI NIH HHS / CA / R01 CA091460-04; United States / NCI NIH HHS / CA / R01 CA091460; United States / NINDS NIH HHS / NS / R01 NS057811-03; United States / NINDS NIH HHS / NS / R01 NS-57811; United States / NINDS NIH HHS / NS / R01 NS057811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 187EJ7QEXL / Fenretinide; 82115-62-6 / Interferon-gamma; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS43293; NLM/ PMC3103940
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4. Bannykh SI, Stolt CC, Kim J, Perry A, Wegner M: Oligodendroglial-specific transcriptional factor SOX10 is ubiquitously expressed in human gliomas. J Neurooncol; 2006 Jan;76(2):115-27
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  • The two most common types of gliomas: astrocytoma and oligodendroglioma are distinguished based on their morphologic similarities to mature astrocytes and oligodendroglia.
  • We applied immunohistochemistry to analyze whether the expression of SOX10 can differentiate astrocytoma and oligodendroglioma.
  • High levels of expression were also found in pilocytic astrocytoma, consistent with recent studies suggesting that pilocytic astrocytomas have greater overlap with oligodendroglial than astrocytic tumors.
  • [MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. Glioma / metabolism. High Mobility Group Proteins / biosynthesis. Oligodendroglia / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytes / metabolism. Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / metabolism. Biomarkers, Tumor / metabolism. Blotting, Western. Child. Child, Preschool. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nerve Tissue Proteins / metabolism. SOXE Transcription Factors

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  • (PMID = 16205963.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / Nerve Tissue Proteins; 0 / OLIG1 protein, human; 0 / OLIG2 protein, human; 0 / SOX10 protein, human; 0 / SOXE Transcription Factors; 0 / Transcription Factors
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55. Froger N, Orellana JA, Cohen-Salmon M, Ezan P, Amigou E, Sáez JC, Giaume C: Cannabinoids prevent the opposite regulation of astroglial connexin43 hemichannels and gap junction channels induced by pro-inflammatory treatments. J Neurochem; 2009 Dec;111(6):1383-97
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  • Brain injuries as well as neurodegenerative diseases, are associated with neuro-inflammation characterized by astroglial and microglial activation and/or proliferation.
  • This opposite regulation is mediated by two pro-inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, released from activated microglia.
  • We observed that CBs inhibited the LPS-induced release of interleukin-1 beta and tumor necrosis factor-alpha from microglia.
  • Pharmacological characterizations of CB actions on astrocytic connexin43 channels revealed that these effects were mainly mediated through CB1 receptors activation, although non-CB1/CB2 receptors seemed to mediate the action of the methanandamide.
  • [MeSH-minor] Analgesics / pharmacology. Animals. Animals, Newborn. Arachidonic Acids / pharmacology. Benzoxazines / pharmacology. Cells, Cultured. Cerebral Cortex / cytology. Culture Media, Conditioned / pharmacology. Cyclohexanols / pharmacology. Drug Interactions. Enzyme-Linked Immunosorbent Assay / methods. Ethidium / metabolism. Gene Expression Regulation / drug effects. Interleukin-1beta / metabolism. Maximum Tolerated Dose. Mice. Microglia / chemistry. Morpholines / pharmacology. Naphthalenes / pharmacology. Piperidines / pharmacology. Pyrazoles / pharmacology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20050288.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Analgesics; 0 / Arachidonic Acids; 0 / Benzoxazines; 0 / Cannabinoids; 0 / Connexin 43; 0 / Connexins; 0 / Culture Media, Conditioned; 0 / Cyclohexanols; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Morpholines; 0 / Naphthalenes; 0 / Piperidines; 0 / Pyrazoles; 0 / Tumor Necrosis Factor-alpha; 134959-51-6 / Win 55212-2; 150314-39-9 / methanandamide; 158681-13-1 / rimonabant; 83003-12-7 / 3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol; EN464416SI / Ethidium
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56. Li M, Jia ZZ, Gu HM, Zhou XJ, Tang LM: [Application of apparent diffusion coefficient and fractional anisotropy in identification of tumor component and grading of brain astrocytoma]. Zhonghua Yi Xue Za Zhi; 2008 Dec 23;88(47):3352-5
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  • [Title] [Application of apparent diffusion coefficient and fractional anisotropy in identification of tumor component and grading of brain astrocytoma].
  • OBJECTIVE: To evaluate the value of apparent diffusion coefficient (ADC) and fractional anisotropy (FA) in identification of tumor element and grading of brain astrocytoma.
  • METHODS: Thirty-three patients with histologically confirmed astrocytoma underwent diffusion weighted imaging (DWI), diffusion tensor imaging (DTI), and conventional MRI before operation.
  • The values of ADC and FA of different regions in the same tumor and of astrocytoma of different grades were measured and compared.
  • RESULTS: The ADC values of the tumor parenchyma, necrotic region, peritumoral edema region were (1.28 +/- 0.44), (1.97 +/- 0.53), and (1.74 +/- 0.47) respectively, all significantly higher than that of the corresponding normal brain tissues [(0.80 +/- 0.18), P = 0.009, P = 0.000, P = 0.000] with significantly differences between the tumor parenchyma and necrotic region and peritumoral edema region (both P < 0.05), however, there was not significant difference between the necrotic region and peritumoral edema region.
  • The FA values of the tumor parenchyma, necrotic region, and peritumoral edema region were (0.18 +/- 0.07), (0.14 +/- 0.05), and (0.16 +/- 0.05) respectively, all significantly higher than that of the corresponding normal brain tissues [(0.58 +/- 0.10), all P = 0.000], without significant differences among the former 3 groups.
  • There were no significant differences in the ADC and FA values among the tumors at different grades, however, there was a tendency of ADC to decrease and of FA to increase along the increase of grade of tumor, although not significantly.
  • CONCLUSION: ADC value plays an important part in distinguishing tumor components and determining tumor boundary, and plays a certain role in judging the grade of astrocytomas.
  • FA value is vital to determine the tumor boundary, and has certain value in differentiating high-grade from low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Anisotropy. Female. Humans. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 19257968.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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57. Mortazavi H, Abedini R, Sadri F, Soori T, Vasheghani-Farahani A: Crusted scabies in a patient with brain astrocytoma: report of a case. Int J Infect Dis; 2010 Jun;14(6):e526-7
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  • [Title] Crusted scabies in a patient with brain astrocytoma: report of a case.
  • He suffered from a brain tumor (astrocytoma) and was immunosuppressed because he was receiving systemic steroids and chemo-radiation therapy.
  • He also had psychomotor retardation and behavior changes due to the pressure effect of his brain tumor.
  • The diagnosis of crusted scabies was established based on direct positive skin smears from the lesions.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Sarcoptes scabiei. Scabies / diagnosis
  • [MeSH-minor] Adult. Animals. Diagnosis, Differential. Fatal Outcome. Humans. Immunocompromised Host. Male. Pruritus / pathology

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  • [Copyright] Copyright 2009 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 19700360.001).
  • [ISSN] 1878-3511
  • [Journal-full-title] International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
  • [ISO-abbreviation] Int. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
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58. Monnet-Tschudi F, Hazekamp A, Perret N, Zurich MG, Mangin P, Giroud C, Honegger P: Delta-9-tetrahydrocannabinol accumulation, metabolism and cell-type-specific adverse effects in aggregating brain cell cultures. Toxicol Appl Pharmacol; 2008 Apr 1;228(1):8-16
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  • [Title] Delta-9-tetrahydrocannabinol accumulation, metabolism and cell-type-specific adverse effects in aggregating brain cell cultures.
  • The quantification of 11-OH-THC and of THC-COOH showed that brain aggregates were capable of THC metabolism.
  • Only the GABAergic marker was affected after the single treatment, whereas the GABAergic, cholinergic and astrocytic markers were decreased after the repeated treatments.
  • [MeSH-major] Brain / pathology. Dronabinol / metabolism. Dronabinol / toxicity
  • [MeSH-minor] Animals. Cannabinoids / metabolism. Cell Aggregation / drug effects. Cells, Cultured. Choline O-Acetyltransferase / metabolism. Chromatography, High Pressure Liquid. Female. GTP Phosphohydrolases / metabolism. Glutamate Decarboxylase / metabolism. Interleukin-6 / biosynthesis. L-Lactate Dehydrogenase / metabolism. Mass Spectrometry. Neuroglia / drug effects. Neurons / drug effects. Pregnancy. Rats. Receptor, Cannabinoid, CB1 / agonists. Receptor, Cannabinoid, CB2 / agonists. Reference Standards. Reverse Transcriptase Polymerase Chain Reaction. Solvents. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 18083204.001).
  • [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 / Cannabinoids; 0 / Interleukin-6; 0 / Receptor, Cannabinoid, CB1; 0 / Receptor, Cannabinoid, CB2; 0 / Solvents; 0 / Tumor Necrosis Factor-alpha; 7J8897W37S / Dronabinol; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.3.1.6 / Choline O-Acetyltransferase; EC 3.6.1.- / GTP Phosphohydrolases; EC 4.1.1.15 / Glutamate Decarboxylase
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59. Anan'eva II, Malkarov MS, Korsakova NA, Balkanov AS, Dorofeev AE, Kachkov IA, Suchkov SV: [Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition]. Arkh Patol; 2007 Jan-Feb;69(1):54-60
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  • [Title] [Glial tumors of the brain: current aspects of their classification and bases for genetic predisposition].
  • Malignant astrocytic gliomas account for 50% of all primary brain tumors.
  • Cells of origin are unknown for the majority of brain tumors: CNS tumors have frequently in their content many histological forms and their classification will depend on what the parts of neoplasm that will be clearly identified at the material taking and further investigation.
  • Current immunohistochemical studies may determine the antigenic structure of a tumor cell, compare it with the antigens expressed by a certain cell type and, thus, classify the tumor by its origin, but there are no antibodies which would correctly identify different types of tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / classification. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Genetic Predisposition to Disease
  • [MeSH-minor] Antigens, Neoplasm / biosynthesis. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Gene Expression Regulation, Neoplastic / genetics. Humans

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  • (PMID = 19385137.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
  • [Number-of-references] 45
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60. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • In addition, we summarize the key genetic alterations that have been attributed to astrocytoma patho-genesis and progression.
  • Also, the first steps have been taken in refining classical histopathological diagnosis by use of molecular predictive markers, for example, MGMT promoter hypermethylation in glioblastomas.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • [MeSH-major] Brain Neoplasms / genetics
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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61. Santel T, Pflug G, Hemdan NY, Schäfer A, Hollenbach M, Buchold M, Hintersdorf A, Lindner I, Otto A, Bigl M, Oerlecke I, Hutschenreuther A, Sack U, Huse K, Groth M, Birkemeyer C, Schellenberger W, Gebhardt R, Platzer M, Weiss T, Vijayalakshmi MA, Krüger M, Birkenmeier G: Curcumin inhibits glyoxalase 1: a possible link to its anti-inflammatory and anti-tumor activity. PLoS One; 2008;3(10):e3508
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  • [Title] Curcumin inhibits glyoxalase 1: a possible link to its anti-inflammatory and anti-tumor activity.
  • METHODOLOGY/PRINCIPAL FINDINGS: Cultures of whole blood cells and tumor cell lines (PC-3, JIM-1, MDA-MD 231 and 1321N1) were set up to investigate the effect of selected polyphenols, including curcumin, on the LPS-induced cytokine production (cytometric bead-based array), cell proliferation (WST-1 assay), cytosolic Glo1 and Glo2 enzymatic activity, apoptosis/necrosis (annexin V-FITC/propidium iodide staining; flow cytometric analysis) as well as GSH and ATP content.
  • Moreover, whereas curcumin was found to hamper the growth of breast cancer (JIMT-1, MDA-MB-231), prostate cancer PC-3 and brain astrocytoma 1321N1 cells, no effect on growth or vitality of human primary hepatocytes was elucidated.
  • Curcumin decreased D-lactate release by tumor cells, another clue for inhibition of intracellular Glo1.
  • This may account for curcumin's potency as an anti-inflammatory and anti-tumor agent.

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  • [ErratumIn] PLoS One. 2011;6(7). doi:10.1371/annotation/0eb2b9f3-1006-4dcd-ad61-367310a2686a. Hutschenreuter, Antje [corrected to Hutschenreuther, Antje]
  • (PMID = 18946510.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Phenols; 0 / Polyphenols; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 4.4.1.5 / Lactoylglutathione Lyase; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2567432
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62. Brozzi F, Arcuri C, Giambanco I, Donato R: S100B Protein Regulates Astrocyte Shape and Migration via Interaction with Src Kinase: IMPLICATIONS FOR ASTROCYTE DEVELOPMENT, ACTIVATION, AND TUMOR GROWTH. J Biol Chem; 2009 Mar 27;284(13):8797-811
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  • [Title] S100B Protein Regulates Astrocyte Shape and Migration via Interaction with Src Kinase: IMPLICATIONS FOR ASTROCYTE DEVELOPMENT, ACTIVATION, AND TUMOR GROWTH.
  • We show here that reducing S100B levels in the astrocytoma cell line GL15 and the Müller cell line MIO-M1 by small interference RNA technique results in a rapid disassembly of stress fibers, collapse of F-actin onto the plasma membrane and reduced migration, and acquisition of a stellate shape.
  • These results suggest that S100B might contribute to reduce the differentiation potential of cells of the astrocytic lineage and participate in the astrocyte activation process in the case of brain insult and in invasive properties of glioma cells.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Cell Movement. Cell Shape. Nerve Growth Factors / metabolism. S100 Proteins / metabolism. src-Family Kinases / metabolism
  • [MeSH-minor] Animals. Bucladesine / pharmacology. Cell Line, Tumor. Glycogen Synthase Kinase 3 / genetics. Glycogen Synthase Kinase 3 / metabolism. Humans. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Rats. S100 Calcium Binding Protein beta Subunit. Stress Fibers / genetics. Stress Fibers / metabolism. Stroke / genetics. Stroke / metabolism. rac1 GTP-Binding Protein / genetics. rac1 GTP-Binding Protein / metabolism. rhoA GTP-Binding Protein / genetics. rhoA GTP-Binding Protein / metabolism

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  • (PMID = 19147496.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nerve Growth Factors; 0 / RAC1 protein, human; 0 / RNA, Small Interfering; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human; 0 / S100b protein, rat; 124671-05-2 / RHOA protein, human; 63X7MBT2LQ / Bucladesine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.6.1.- / Rac1 protein, rat; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / rhoA GTP-Binding Protein
  • [Other-IDs] NLM/ PMC2659238
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63. Nakamura M, Ishida E, Shimada K, Kishi M, Nakase H, Sakaki T, Konishi N: Frequent LOH on 22q12.3 and TIMP-3 inactivation occur in the progression to secondary glioblastomas. Lab Invest; 2005 Feb;85(2):165-75
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  • Frequent allelic losses on the long arm of chromosome 22 (22q) in gliomas indicate the presence of tumor suppressor gene (TSG) at this location.
  • However, the target gene(s) residing in this chromosome are still unknown and their putative roles in the development of astrocytic tumors, especially in secondary glioblastoma, have not yet been defined.
  • To compile a precise physical map for the region of common deletions in astrocytic tumors, we performed a high-density loss of heterozygosity (LOH) analysis using 31 polymorphic microsatellite markers spanning 22q in a series of grade II diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas, and secondary glioblastomas that had evolved from lower grade astrocytomas.
  • This epigenetic change was significantly correlated to poor survival in eight patients with grade II diffuse astrocytoma.
  • Our results suggest that a 957 kb locus, located at 22q12.3, may contain the putative TSG, TIMP-3, that appears to be relevant to progression to secondary glioblastoma and subsequently to the prognosis of grade II diffuse astrocytoma.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 22. Glioblastoma / genetics. Loss of Heterozygosity. Tissue Inhibitor of Metalloproteinase-3 / genetics
  • [MeSH-minor] Adult. Alleles. DNA Methylation. Disease Progression. Epigenesis, Genetic. Gene Deletion. Gene Expression Regulation, Neoplastic. Genetic Markers. Humans. Immunohistochemistry. Microsatellite Repeats. Neoplasm Metastasis. Neoplasm Staging. Physical Chromosome Mapping. Polymorphism, Genetic. Prognosis. Promoter Regions, Genetic. Survival Analysis

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  • (PMID = 15592495.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Tissue Inhibitor of Metalloproteinase-3
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64. Hayashi S, Yamamoto M, Tachibana K, Ueno Y, Bu G, Fukushima T: Mechanism of photofrin-enhanced ultrasound-induced human glioma cell death. Anticancer Res; 2009 Mar;29(3):897-905
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  • BACKGROUND: Low-intensity ultrasound showed tumor cell killing by a non-thermal effect in human leukemia cells.
  • The aim of our study was to investigate the efficacy of low-intensity ultrasound on malignant astrocytic tumor cells with the photosensitizer, Photofrin, which is taken up by the cell surface receptor, low density lipoprotein receptor-related protein/alpha2-macroglobulin receptor (LRP/alpha2MR).
  • RESULTS: Ultrasound alone induced instant cell killing immediately after sonication in both U251MG and U105MG malignant gliomas cells.
  • CONCLUSION: This is the first report to demonstrate the usefulness of low-intensity ultrasound for the cell killing of malignant glioma cells.
  • [MeSH-major] Brain Neoplasms / therapy. Cell Survival / drug effects. Dihematoporphyrin Ether / therapeutic use. Glioma / therapy. Photosensitizing Agents / therapeutic use. Ultrasonic Therapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Low Density Lipoprotein Receptor-Related Protein-1 / genetics. Low Density Lipoprotein Receptor-Related Protein-1 / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. alpha-Macroglobulins / genetics. alpha-Macroglobulins / metabolism

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  • (PMID = 19414325.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Low Density Lipoprotein Receptor-Related Protein-1; 0 / Photosensitizing Agents; 0 / RNA, Messenger; 0 / alpha-Macroglobulins; 97067-70-4 / Dihematoporphyrin Ether
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65. Lee FY, Jan YJ, Wen MC, Li MC, Wang J, Wen-Hsien C: A 32-year-old man with a fourth ventricular mass. Brain Pathol; 2009 Apr;19(2):333-6
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  • Our case is in the fourth ventricle of a 32 year-old man.Many areas showed tumor cells with a signet-ring appearance and focally formed perivascular arrangements.
  • There was strong positive immunoreactivity to GFAP and S-100 protein, even in those vacuolated tumor cells.The proliferation index was less than 10%.
  • These findings confirm that the vacuoles were lipid droplets in astrocytic tumor cells.
  • The features noted are suggestive of a probable better prognosis in this variant of low-grade astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Cerebral Ventricle Neoplasms / pathology

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  • (PMID = 19291000.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / S100 Proteins
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66. Zarkovic K, Juric G, Waeg G, Kolenc D, Zarkovic N: Immunohistochemical appearance of HNE-protein conjugates in human astrocytomas. Biofactors; 2005;24(1-4):33-40
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  • Those of astrocytic origin are the most widespread of primary brain tumors and account for more then 60% of all CNS neoplasms.
  • The current state of knowledge on the associations between tumor etiology and oxidative stress suggests that environmental factors that cause oxidative stress could also induce and promote cancer, especially in case of hereditary predisposition.
  • The aim of present study was to investigate by immunohistochemistry the presence of HNE-modified proteins in different types of astrocytoma.
  • Our study comprised 45 astrocytic tumors.
  • Slides of paraffin-embedded tumor tissue were stained with hematoxylin-eosin or were prepared for immunohistochemistry with monoclonal antibodies to HNE-histidine conjugate.
  • Lowest intensity of HNE immunopositivity was present in tumor cells of almost all DA, predominantly around blood vessels.
  • In malignant variants of astrocytoma, AA and GB, HNE positivity was moderate to strong, and diffusely distributed in all tumors.
  • [MeSH-major] Aldehydes / analysis. Aldehydes / metabolism. Astrocytoma / chemistry. Immunohistochemistry. Proteins / analysis. Proteins / metabolism
  • [MeSH-minor] Antibodies, Monoclonal. Blood Vessels / chemistry. Brain Neoplasms / blood supply. Brain Neoplasms / chemistry. Brain Neoplasms / pathology. Endothelium, Vascular / chemistry. Humans

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  • (PMID = 16403961.001).
  • [ISSN] 0951-6433
  • [Journal-full-title] BioFactors (Oxford, England)
  • [ISO-abbreviation] Biofactors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antibodies, Monoclonal; 0 / Proteins; 29343-52-0 / 4-hydroxy-2-nonenal
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67. Crespo-Rodríguez AM, Smirniotopoulos JG, Rushing EJ: MR and CT imaging of 24 pleomorphic xanthoastrocytomas (PXA) and a review of the literature. Neuroradiology; 2007 Apr;49(4):307-15
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  • INTRODUCTION: The aim of our study was to review the imaging appearance of PXA, a rare and usually low-grade, astrocytic tumor that typically occurs in young adults.
  • [MeSH-major] Astrocytoma / diagnosis. Magnetic Resonance Imaging / methods. Supratentorial Neoplasms / diagnosis. Tomography, X-Ray Computed / methods

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  • (PMID = 17205313.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 44
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68. Bisland SK, Goebel EA, Hassanali NS, Johnson C, Wilson BC: Increased expression of mitochondrial benzodiazepine receptors following low-level light treatment facilitates enhanced protoporphyrin IX production in glioma-derived cells in vitro. Lasers Surg Med; 2007 Sep;39(8):678-84
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  • BACKGROUND AND OBJECTIVES: This study investigates whether low-level light treatment (LLLT) can enhance the expression of peripheral-type mitochondrial benzodiazepine receptors (PBRs) on glioma-derived tumor cells, and by doing so promote the synthesis of protoporphyrin IX (PpIX) and increase the photodynamic therapy (PDT)-induced cell kill using 5-aminolevulinic acid (ALA).
  • Cells of astrocytic derivation within the brain express PBRs, while neurons express the central-type of benzodiazepine receptor.
  • STUDY DESIGN: Astrocytoma-derived CNS-1 cells were exposed to a range of differing low-level light protocols immediately prior to PDT.
  • CONCLUSIONS: These data suggest that by selectively increasing PBR expression in tumor cells, LLLT facilitates enhanced tumor cell kill using ALA-PDT.
  • This may further improve the selectivity and efficacy of PDT treatment of brain tumors.
  • [MeSH-minor] Astrocytoma. Cell Cycle. Cell Survival. In Vitro Techniques. Microscopy, Confocal. Spectrometry, Fluorescence

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17886284.001).
  • [ISSN] 0196-8092
  • [Journal-full-title] Lasers in surgery and medicine
  • [ISO-abbreviation] Lasers Surg Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-43892
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protoporphyrins; 0 / Receptors, GABA; 0 / TSPO protein, human; 553-12-8 / protoporphyrin IX
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69. Dim DC, Lingamfelter DC, Taboada EM, Fiorella RM: Papillary glioneuronal tumor: a case report and review of the literature. Hum Pathol; 2006 Jul;37(7):914-8
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  • [Title] Papillary glioneuronal tumor: a case report and review of the literature.
  • Papillary glioneuronal tumor is a recently described central nervous system neoplasm that almost always occurs adjacent to the lateral ventricle.
  • We present a case of this rare entity, representing the 21st case of this lesion, which exhibits a mixed astrocytic and neuronal differentiation.
  • Histologic evaluation after surgical removal showed a cystic tumor consisting of 2 distinct components: a unique pseudopapillary architecture admixed with foci of solid areas.
  • The combination of cytologic benignity, lack of necrosis, and low proliferative index as evidenced by immunohistochemistry using antibody to Ki-67 confirmed the low malignant potential of this tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Carcinoma, Papillary / pathology. Ganglioglioma / pathology

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  • (PMID = 16784993.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Neurofilament Proteins; 0 / S100 Proteins; 0 / Synaptophysin
  • [Number-of-references] 12
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70. Anan M, Inoue R, Ishii K, Abe T, Fujiki M, Kobayashi H, Goya T, Nakazato Y: A rosette-forming glioneuronal tumor of the spinal cord: the first case of a rosette-forming glioneuronal tumor originating from the spinal cord. Hum Pathol; 2009 Jun;40(6):898-901
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  • [Title] A rosette-forming glioneuronal tumor of the spinal cord: the first case of a rosette-forming glioneuronal tumor originating from the spinal cord.
  • Rosette-forming glioneuronal tumors of the fourth ventricle are rare brain tumors, and only 19 such lesions have been previously reported.
  • Magnetic resonance imaging demonstrated a mass in the cervicothoracic spinal cord that suggested an intramedullary spinal tumor.
  • A total gross resection of the tumor was performed.
  • As is typical of rosette-forming glioneuronal tumors of the fourth ventricle, this spinal cord example manifested neurocytic and astrocytic components.
  • The astrocytic component showed characteristic features of a pilocytic astrocytoma, as is often the case in the fourth ventricle examples.
  • [MeSH-major] Cerebral Ventricle Neoplasms / pathology. Fourth Ventricle / pathology. Spinal Cord / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Adult. Astrocytoma / pathology. Female. Humans. Rosette Formation

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  • [CommentIn] Hum Pathol. 2009 Oct;40(10):1510; author reply 1510 [19616823.001]
  • (PMID = 19269010.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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71. Takenaga K, Nygren J, Zelenina M, Ohira M, Iuchi T, Lukanidin E, Sjöquist M, Kozlova EN: Modified expression of Mts1/S100A4 protein in C6 glioma cells or surrounding astrocytes affects migration of tumor cells in vitro and in vivo. Neurobiol Dis; 2007 Mar;25(3):455-63
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  • [Title] Modified expression of Mts1/S100A4 protein in C6 glioma cells or surrounding astrocytes affects migration of tumor cells in vitro and in vivo.
  • The calcium-binding Mts1/S100A4 protein plays an important role in motility and metastatic activity of tumor cells.
  • To investigate if Mts1/S100A4 has a significant role on brain tumor progression, we made quantitative RT-PCR analysis for the expression of S100A4/Mts1 in various grades of astrocytic tumors.
  • Our data showed that high-grade glioblastomas express higher amount of S100A4/Mts1 than low-grade astrocytic tumors.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Movement. S100 Proteins / metabolism
  • [MeSH-minor] Animals. Astrocytes / metabolism. Astrocytes / pathology. Cell Communication. Cell Line, Tumor. Corpus Callosum / metabolism. Corpus Callosum / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. In Vitro Techniques. Metalloproteases / metabolism. Neoplasm Invasiveness. Neoplasm Transplantation. Nerve Fibers, Myelinated / metabolism. Nerve Fibers, Myelinated / pathology. RNA, Small Interfering. Rats

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  • (PMID = 17223348.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / S100 Proteins; 0 / S100a4 protein, rat; 142662-27-9 / S100A4 protein, human; EC 3.4.- / Metalloproteases
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72. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Alterations in dipeptidyl peptidase-IV (DPP-IV) enzymatic activity are characteristic of malignant transformation.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • This is the first report showing that non-malignant brain tissue contains a DPP-IV-like enzymatic activity attributable mostly to DPP-8/9, while the substantial part of the activity in glioma is due to increased DPP-IV/CD26, localized in both the vascular and parenchymal compartments.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-major] Astrocytoma / enzymology. Astrocytoma / genetics. Dipeptidyl Peptidase 4 / genetics. Dipeptidyl Peptidase 4 / metabolism. Gene Expression Regulation, Enzymologic / physiology
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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73. Tan G, Sun SQ, Yuan DL: Expression of Kir 4.1 in human astrocytic tumors: correlation with pathologic grade. Biochem Biophys Res Commun; 2008 Mar 21;367(4):743-7
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  • [Title] Expression of Kir 4.1 in human astrocytic tumors: correlation with pathologic grade.
  • In this study, we investigated the expression of Kir 4.1 mRNA and protein in 80 cases of human astrocytic tumors by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry, respectively.
  • The correlation between Kir 4.1 expression and pathologic grade of astrocytic tumors was further analyzed.
  • Therefore, Kir 4.1 may be a new biomarker for astrocytic tumors.
  • It may also be an attractive therapy target for human astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism. Potassium Channels, Inwardly Rectifying / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Statistics as Topic. Tumor Cells, Cultured

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  • (PMID = 18191638.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Kcnj10 (channel); 0 / Neoplasm Proteins; 0 / Potassium Channels, Inwardly Rectifying
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74. Jin YH, Jung S, Jin SG, Jung TY, Moon KS, Kim IY: GRIM-19 Expression and Function in Human Gliomas. J Korean Neurosurg Soc; 2010 Jul;48(1):20-30
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  • OBJECTIVE: We determined whether the expression of GRIM-19 is correlated with pathologic types and malignant grades in gliomas, and determined the function of GRIM-19 in human gliomas.
  • METHODS: Tumor tissues were isolated and frozen at -80 just after surgery.
  • The tissues consisted of normal brain tissue (4), astrocytomas (2), anaplastic astrocytomas (2), oligodendrogliomas (13), anaplastic oligodendrogliomas (11), and glioblastomas (16).
  • To profile tumor-related genes, we applied RNA differential display using a Genefishing DEG kit, and validated the tumor-related genes by reverse transcription polymerase chain reaction (RT-PCR).
  • RESULTS: Based on RT-PCR analysis, the expression of GRIM-19 was higher in astrocytic tumors than oligodendroglial tumors.
  • The expression of GRIM-19 was higher in high-grade tumors than low-grade tumors or normal brain tissue; glioblastomas showed the highest expression.

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  • (PMID = 20717508.001).
  • [ISSN] 1598-7876
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2916144
  • [Keywords] NOTNLM ; Cell line / GRIM-19 / Gene Fishing / Glioblastoma / Human glioma
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75. Martínez C, Molina JA, Alonso-Navarro H, Jiménez-Jiménez FJ, Agúndez JA, García-Martín E: Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma. BMC Neurol; 2010;10:71
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  • [Title] Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma.
  • Aiming to identify genetic variations related to the risk of developing brain tumors, we investigated the putative association between common nonsynonymous PON1 polymorphisms and the risk of developing astrocytoma and meningioma.
  • METHODS: Seventy one consecutive patients with brain tumors (43 with astrocytoma grade II/III and 28 with meningioma) with ages ranging 21 to 76 years, and 220 healthy controls subjects were analyzed for the frequency of the nonsynonymous PON1 genotypes L55M rs854560 and Q192R rs662.
  • RESULTS: The frequencies of the PON1 genotypes and allelic variants of the polymorphisms PON1 L55M and PON1 Q192R did not differ significantly between patients with astrocytoma and meningioma and controls.
  • The minor allele frequencies were as follows: PON1 55L, 0.398, 0.328 and 0.286 for patients with astrocytoma, meningioma and control individuals, respectively; PON1 192R, 0.341, 0.362 and 0.302 for patients with astrocytoma, meningioma and control individuals, respectively.
  • Haplotype association analyses did not identify any significant association with the risk of developing astrocytoma or meningioma.
  • CONCLUSIONS: Common nonsynonymous PON1 polymorphisms are not related with the risk of developing astrocytoma and meningioma.
  • [MeSH-major] Aryldialkylphosphatase / genetics. Astrocytoma / genetics. Brain Neoplasms / genetics. Meningeal Neoplasms / genetics. Meningioma / genetics

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  • (PMID = 20723250.001).
  • [ISSN] 1471-2377
  • [Journal-full-title] BMC neurology
  • [ISO-abbreviation] BMC Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.8.1 / Aryldialkylphosphatase; EC 3.1.8.1 / PON1 protein, human
  • [Other-IDs] NLM/ PMC2936881
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76. Hsuchou H, Pan W, Barnes MJ, Kastin AJ: Leptin receptor mRNA in rat brain astrocytes. Peptides; 2009 Dec;30(12):2275-80
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  • [Title] Leptin receptor mRNA in rat brain astrocytes.
  • We recently reported that mouse astrocytes express leptin receptors (ObR), and that obesity induces upregulation of astrocytic ObR.
  • To provide further evidence of the importance of astrocytic ObR expression, we performed double-labeling fluorescent in situ hybridization (FISH) and immunohistochemistry in the rat hypothalamus.
  • Laser confocal microscopic image analysis showed that ObR mRNA was present in glial fibrillary acidic protein (+) cells that show distinctive astrocytic morphology as well as in neurons.
  • In cultured rat C6 astrocytoma cells treated with different doses of lipopolysaccharide for 6h, the mRNA for ObRa or ObRb did not show significant changes, as measured by quantitative RT-PCR.
  • However, the protein expression of both ObRa and ObRb, determined by Western blotting, was increased after the C6 cells were treated with either lipopolysaccharide or tumor necrosis factor-alpha.
  • The results indicate that astrocytic ObR expression is present in rats as well as mice, and that it probably plays a role in the neuroinflammatory response.

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  • (PMID = 19747514.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS045751-06; United States / NIDDK NIH HHS / DK / DK54880; United States / NINDS NIH HHS / NS / R01 NS062291-02; United States / NINDS NIH HHS / NS / NS062291-02; United States / NINDS NIH HHS / NS / R01 NS045751; United States / NINDS NIH HHS / NS / R01 NS062291; United States / NINDS NIH HHS / NS / NS045751-06; United States / NIDDK NIH HHS / DK / R01 DK054880; United States / NINDS NIH HHS / NS / NS62291; United States / NINDS NIH HHS / NS / NS45751; United States / NIDDK NIH HHS / DK / R56 DK054880
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Receptors, Leptin; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS144773; NLM/ PMC2787995
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77. Bellavance MA, Blanchette M, Fortin D: Recent advances in blood-brain barrier disruption as a CNS delivery strategy. AAPS J; 2008;10(1):166-77
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  • [Title] Recent advances in blood-brain barrier disruption as a CNS delivery strategy.
  • The blood-brain barrier (BBB) is a complex functional barrier composed of endothelial cells, pericytes, astrocytic endfeets and neuronal cells.
  • We also summarize recent clinical series highlighting promising results in the application of this procedure to maximize delivery of chemotherapy in the treatment of brain tumor patients.
  • [MeSH-major] Blood-Brain Barrier / metabolism. Central Nervous System / metabolism. Pharmaceutical Preparations / administration & dosage. Pharmaceutical Preparations / metabolism

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  • (PMID = 18446517.001).
  • [ISSN] 1550-7416
  • [Journal-full-title] The AAPS journal
  • [ISO-abbreviation] AAPS J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pharmaceutical Preparations
  • [Number-of-references] 64
  • [Other-IDs] NLM/ PMC2751463
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78. Wegrzynowicz M, Hilgier W, Dybel A, Oja SS, Saransaari P, Albrecht J: Upregulation of cerebral cortical glutathione synthesis by ammonia in vivo and in cultured glial cells: the role of cystine uptake. Neurochem Int; 2007 Jun;50(7-8):883-9
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  • [Title] Upregulation of cerebral cortical glutathione synthesis by ammonia in vivo and in cultured glial cells: the role of cystine uptake.
  • Glutathione (GSH) is a major antioxidant in the brain and ammonia neurotoxicity is associated with oxidative stress.
  • In this study, we show that intracerebral administration of ammonium chloride ("ammonia", final concentration 5mM) via a microdialysis probe, increases by 80% the glutathione content in cerebral cortical microdialysates, and tends to increase its content in striatal microdialysates.
  • Treatment with ammonia in vitro dose-dependently increased the glutathione content in cultured cerebral cortical astrocytes and a C6 glioma cell line.
  • In our hands, cystine, the precursor for astrocytic glutathione synthesis, was transported to astrocytes almost exclusively by system X(AG)-, while in C6 cells the transport engaged both system x(c)- (approximately 60% of uptake) and X(AG)- (approximately 40% of uptake).
  • The results are consistent with the concept of increased astrocytic glutathione synthesis as an adaptive response of the brain to ammonia challenge, and emphasize upregulation of cystine uptake as a factor contributing to this response.
  • [MeSH-major] Ammonia / pharmacology. Cerebral Cortex / metabolism. Cystine / metabolism. Glutathione / biosynthesis. Neuroglia / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Biological Transport. Bucladesine / pharmacology. Cell Differentiation / drug effects. Cell Line, Tumor. Cells, Cultured. Corpus Striatum / drug effects. Corpus Striatum / metabolism. Glioma. Male. Microdialysis. Prefrontal Cortex / drug effects. Prefrontal Cortex / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar

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  • (PMID = 17239489.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 48TCX9A1VT / Cystine; 63X7MBT2LQ / Bucladesine; 7664-41-7 / Ammonia; GAN16C9B8O / Glutathione
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79. Stukel JM, Caplan MR: Targeted drug delivery for treatment and imaging of glioblastoma multiforme. Expert Opin Drug Deliv; 2009 Jul;6(7):705-18
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  • Glioblastoma multiforme is a grade IV astrocytic tumor with a very high mortality rate.
  • Although current treatment often includes surgical resection, this rarely removes all primary tumor cells, so is usually followed by radiation and/or chemotherapy.
  • Remaining migratory tumor cells invade surrounding healthy tissue and contribute to secondary and tertiary tumor recurrence; therefore, despite significant research into glioma removal and treatment, prognosis remains poor.
  • As systemic delivery is limited by molecules larger than approximately 500 Da being unable to cross the blood-brain barrier (BBB), therapeutic concentrations are difficult to attain; thus, localized delivery options relying on diffusion and CED have been used to circumvent the BBB.
  • [MeSH-minor] Animals. Blood-Brain Barrier / metabolism. Combined Modality Therapy. Humans. Models, Theoretical. Tissue Distribution

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  • (PMID = 19538036.001).
  • [ISSN] 1744-7593
  • [Journal-full-title] Expert opinion on drug delivery
  • [ISO-abbreviation] Expert Opin Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 118
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80. Banerjee HN, Zhang L: Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy. Mol Cell Biochem; 2007 Jan;295(1-2):237-40
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  • [Title] Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy.
  • To explore the biochemical differences between brain cancer cells Astrocytoma and normal cells Astrocyte, we investigated the Raman spectra of single cell from these two cell types and analyzed the difference in spectra and intensity.
  • The Raman spectra of brain cancer cells was similar to those of normal cells, but the Raman intensity of cancer cells was much higher than that of normal cells.
  • The Raman spectra of brain cancer Astrocytoma shows that the structural changes of cancer cells happen so that many biological functions of these cells are lost.
  • The results indicate that Raman spectra can offer the experimental basis for the cancer diagnosis and treatment.
  • [MeSH-major] Astrocytes / chemistry. Astrocytoma / chemistry. Brain Neoplasms / chemistry. Spectroscopy, Near-Infrared. Spectrum Analysis, Raman

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  • (PMID = 16924417.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / G11HD 34280-05
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
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81. Akimoto J, Fukami S, Tsutsumi M, Hashimoto T, Miki T, Haraoka J, Kudo M: Radiopathological characteristics of cerebellar malignant glioma in adults. Brain Tumor Pathol; 2009;26(2):59-68
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  • [Title] Radiopathological characteristics of cerebellar malignant glioma in adults.
  • Our aim was to extract the radiopathological features of cerebellar malignant glioma in adults from the four cases we encountered.
  • Initially, these patients were given a diagnosis of cerebellar infarction or cavernous angioma, or had faint abnormalities in the cerebellum that were overlooked.
  • These patients were followed up for 2-14 months (mean, 6 months), and the tumor was detected when their clinical symptoms deteriorated.
  • The tumor was located in the hemisphere in one patient and in the vermis in three patients.
  • All patients underwent subtotal tumor resection, followed by postoperative radiochemotherapy.
  • The pathological features were typical of malignant glioma, partially presenting the features of low-grade glioma, such as pilocytic, astrocytic, or oligodendroglial components.
  • At the onset of cerebellar malignant glioma, diagnostic imaging shows few signs of brain tumor.
  • Because cerebellar malignant glioma is a rare disease, it is difficult to differentiate it from metastatic brain tumors and primary central nervous system lymphoma by preoperative imaging.
  • Some patho logical features suggesting malignant transformation from low-grade glioma were detected.
  • [MeSH-minor] Aged. Aged, 80 and over. Fatal Outcome. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Staining and Labeling. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19856216.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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82. Newton HB: Molecular neuro-oncology and the development of targeted therapeutic strategies for brain tumors. Part 4: p53 signaling pathway. Expert Rev Anticancer Ther; 2005 Feb;5(1):177-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular neuro-oncology and the development of targeted therapeutic strategies for brain tumors. Part 4: p53 signaling pathway.
  • Brain tumors are a diverse group of malignancies that remain refractory to conventional treatment approaches.
  • Molecular neuro-oncology has now begun to clarify the transformed phenotype of brain tumors and identify oncogenic pathways that might be amenable to targeted therapy.
  • Loss of the tumor suppressor gene p53 and its encoded protein are the most common genetic events in human cancer and are a frequent occurrence in brain tumors. p53 functions as a transcription factor and is responsible for the transactivation and repression of key genes involved in cell growth, apoptosis and the cell cycle.
  • Mutation of the p53 gene or dysfunction of its signaling pathway are early events in the transformation process of astrocytic gliomas.
  • Further development of targeted therapies designed to restore or enhance p53 function, and evaluation of these new agents in clinical trials, will be needed to improve survival and quality of life for patients with brain tumors.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / genetics. Genes, p53. Signal Transduction. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 15757449.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
  • [Number-of-references] 111
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83. Demuth T, Reavie LB, Rennert JL, Nakada M, Nakada S, Hoelzinger DB, Beaudry CE, Henrichs AN, Anderson EM, Berens ME: MAP-ing glioma invasion: mitogen-activated protein kinase kinase 3 and p38 drive glioma invasion and progression and predict patient survival. Mol Cancer Ther; 2007 Apr;6(4):1212-22
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  • Although astrocytic brain tumors do not metastasize systemically, during tumorigenesis glioma cells adopt an invasive phenotype that is poorly targeted by conventional therapies; hence, glioma patients die of recurrence from the locally invasive tumor population.
  • Cell-based assays and ex vivo brain slice invasion studies were used for functional validation.
  • We further report that these members of the MAPK family are strong promoters of tumor invasion, progression, and poor patient survival.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Astrocytoma / enzymology. Astrocytoma / pathology. Biomarkers / metabolism. Cell Line, Tumor. Collagen Type I / metabolism. Disease Progression. Enzyme Activation / drug effects. Gene Expression Profiling. Humans. Male. Neoplasm Invasiveness. Phosphorylation / drug effects. Prognosis. Protein Kinase Inhibitors / pharmacology. Rats. Rats, Wistar. Survival Analysis. Up-Regulation / drug effects. Up-Regulation / genetics

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  • (PMID = 17406030.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA085139; United States / NINDS NIH HHS / NS / NS042262
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Collagen Type I; 0 / Protein Kinase Inhibitors; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 3
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84. Hartmann C, Bartels G, Gehlhaar C, Holtkamp N, von Deimling A: PIK3CA mutations in glioblastoma multiforme. Acta Neuropathol; 2005 Jun;109(6):639-42
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  • Glioblastoma multiforme WHO grade IV is the most common and malignant variant of astrocytic tumors.
  • Loss of heterozygosity of chromosome 10 and mutations in the tumor suppressor gene PTEN on 10q are molecular hallmarks of glioblastomas.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Phosphatidylinositol 3-Kinases / genetics


85. Walton NM, Snyder GE, Park D, Kobeissy F, Scheffler B, Steindler DA: Gliotypic neural stem cells transiently adopt tumorigenic properties during normal differentiation. Stem Cells; 2009 Feb;27(2):280-9
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  • An increasing body of evidence suggests that astrocytic gliomas of the central nervous system may be derived from gliotypic neural stem cells.
  • To identify any hallmark signs of cancer in neural stem cells or their progeny, we cultured subventricular zone-derived tissue in a unique in vitro model that temporally and phenotypically recapitulates adult neurogenesis.

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  • (PMID = 18988710.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070143; United States / NICHD NIH HHS / HD / T32 HD043730; United States / NINDS NIH HHS / NS / NS055165; United States / NINDS NIH HHS / NS / NS37556; United States / NICHD NIH HHS / HD / T32HD043730; United States / NHLBI NIH HHS / HL / HL70143; United States / NINDS NIH HHS / NS / NS46384; United States / NINDS NIH HHS / NS / R01 NS037556; United States / NINDS NIH HHS / NS / R01 NS055165; United States / NINDS NIH HHS / NS / R21 NS046384
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tubulin
  • [Other-IDs] NLM/ NIHMS686089; NLM/ PMC4425277
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86. Lavon I, Refael M, Zelikovitch B, Shalom E, Siegal T: Serum DNA can define tumor-specific genetic and epigenetic markers in gliomas of various grades. Neuro Oncol; 2010 Feb;12(2):173-80
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  • [Title] Serum DNA can define tumor-specific genetic and epigenetic markers in gliomas of various grades.
  • We evaluated whether cell-free circulating DNA can be used as a noninvasive approach for detection of genetic/epigenetic alterations in brain tumors during the course of the disease.
  • Paired tumor-serum samples from 70 patients with either high-grade astrocytomas (n = 41) or oligodendrogliomas of various grades were analyzed.
  • DNA was extracted from whole blood, serum, and paraffin-embedded tumor sections.
  • LOH and/or methylation that could identify DNA as tumor-specific was found in 80.5% of astrocytic tumors and in all oligodendrogliomas.
  • Statistically significant tumor-serum concordance was found for MGMT methylation in both astrocytic tumors (83%; P < .001) and oligodendroglial tumors (72%; P < .003) and for LOH of 10q (79%; P < .002) and 1p (62%; P < .03) in oligodendrogliomas.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. DNA / blood. Glioma / genetics
  • [MeSH-minor] Adult. Aged. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Epigenesis, Genetic. Female. Humans. Loss of Heterozygosity. Male. Microsatellite Repeats. Middle Aged. PTEN Phosphohydrolase / genetics. Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Suppressor Proteins / genetics. Young Adult

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  • (PMID = 20150384.001).
  • [ISSN] 1523-5866
  • [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 / Tumor Suppressor Proteins; 9007-49-2 / DNA; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ PMC2940579
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87. Kumar AJ, Leeds NE, Kumar VA, Fuller GN, Lang FF, Milas Z, Weinberg JS, Ater JL, Sawaya R: Magnetic resonance imaging features of pilocytic astrocytoma of the brain mimicking high-grade gliomas. J Comput Assist Tomogr; 2010 Jul;34(4):601-11
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  • [Title] Magnetic resonance imaging features of pilocytic astrocytoma of the brain mimicking high-grade gliomas.
  • OBJECTIVE: The typical magnetic resonance/computed tomographic imaging appearance of pilocytic astrocytoma (PA) is that of a cyst with an intensely enhancing mural nodule.
  • METHODS: One hundred patients referred to the cancer center with brain tumors histologically proven to be PA were retrospectively reviewed (95 by magnetic resonance imaging and 5 by computed tomographic imaging) and analyzed.
  • Tumor locations consisted of the following: optic chiasm (22), lateral ventricle (3), thalamus (12), basal ganglia (1), cerebral hemisphere (10), corpus callosum (2), brain stem (26), fourth ventricle (1), and cerebellum (23).
  • CONCLUSIONS: It is important to recognize the aggressive imaging appearance of PA (grade 1 astrocytoma) because it can be mistaken for high-grade gliomas and may thus lead to inappropriate therapy.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Glioma / diagnosis. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Brain / pathology. Brain / radiography. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies. Tomography, X-Ray Computed / methods. Young Adult

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  • (PMID = 20657231.001).
  • [ISSN] 1532-3145
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Stevenson L, Matesanz N, Colhoun L, Edgar K, Devine A, Gardiner TA, McDonald DM: Reduced nitro-oxidative stress and neural cell death suggests a protective role for microglial cells in TNFalpha-/- mice in ischemic retinopathy. Invest Ophthalmol Vis Sci; 2010 Jun;51(6):3291-9
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  • The reduction coincided with enhanced astrocytic survival and an increase in microglial cells actively engaged in phagocytosing apoptotic debris that displayed low ROS, RNS, and NO production and high arginase activity.

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  • (PMID = 20107169.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Nitrogen Species; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; EC 3.5.3.1 / Arginase; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2891480
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89. Weber RG, Hoischen A, Ehrler M, Zipper P, Kaulich K, Blaschke B, Becker AJ, Weber-Mangal S, Jauch A, Radlwimmer B, Schramm J, Wiestler OD, Lichter P, Reifenberger G: Frequent loss of chromosome 9, homozygous CDKN2A/p14(ARF)/CDKN2B deletion and low TSC1 mRNA expression in pleomorphic xanthoastrocytomas. Oncogene; 2007 Feb 15;26(7):1088-97
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  • The molecular pathogenesis of pleomorphic xanthoastrocytoma (PXA), a rare astrocytic brain tumor with a relatively favorable prognosis, is still poorly understood.
  • Interphase fluorescence in situ hybridization to tissue sections confirmed the presence of tumor cells with homozygous 9p21.3 deletions.
  • [MeSH-major] Astrocytoma / genetics. Chromosome Deletion. Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Deletion. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Proteins / deficiency

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  • (PMID = 16909113.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein
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90. Amos S, Redpath GT, Dipierro CG, Carpenter JE, Hussaini IM: Epidermal growth factor receptor-mediated regulation of urokinase plasminogen activator expression and glioblastoma invasion via C-SRC/MAPK/AP-1 signaling pathways. J Neuropathol Exp Neurol; 2010 Jun;69(6):582-92
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  • One of the major pathophysiological features of malignant astrocytomas is their ability to infiltrate surrounding brain tissue.
  • The epidermal growth factor receptor (EGFR) and proteases are known to be overexpressed in glioblastomas (GBMs), but the interaction between the activation of the EGFR and urokinase plasminogen activator (uPA) in promoting astrocytic tumor invasion has not been fully elucidated.
  • Here, we characterized the signal transduction pathway(s) by which EGF regulates uPA expression and promotes astrocytoma invasion.


91. Jacobs JF, Grauer OM, Brasseur F, Hoogerbrugge PM, Wesseling P, Gidding CE, van de Rakt MW, Figdor CG, Coulie PG, de Vries IJ, Adema GJ: Selective cancer-germline gene expression in pediatric brain tumors. J Neurooncol; 2008 Jul;88(3):273-80
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  • [Title] Selective cancer-germline gene expression in pediatric brain tumors.
  • Cancer-germline genes (CGGs) code for immunogenic antigens that are present in various human tumors and can be targeted by immunotherapy.
  • We measured the expression of 12 CGGs in pediatric brain tumors, to identify targets for therapeutic cancer vaccines.
  • Real Time PCR was used to quantify the expression of genes MAGE-A1, MAGE-A2, MAGE-A3, MAGE-A4, MAGE-A6, MAGE-A10, MAGE-A12, MAGE-C2, NY-ESO-1 and GAGE-1,2,8 in 50 pediatric brain tumors of different histological subtypes.
  • Fifty-five percent of the medulloblastomas (n = 11), 86% of the ependymomas (n = 7), 40% of the choroid plexus tumors (n = 5) and 67% of astrocytic tumors (n = 27) expressed one or more CGGs.
  • With exception of a minority of tumors, the overall level of CGG expression in pediatric brain tumors was low.
  • CGG-encoded antigens are therefore suitable targets in a very selected group of pediatric patients with a brain tumor.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression. Genes, Neoplasm

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  • (PMID = 18398575.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2440921
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92. McGirt MJ, Chaichana KL, Gathinji M, Attenello FJ, Than K, Olivi A, Weingart JD, Brem H, Quiñones-Hinojosa AR: Independent association of extent of resection with survival in patients with malignant brain astrocytoma. J Neurosurg; 2009 Jan;110(1):156-62
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  • [Title] Independent association of extent of resection with survival in patients with malignant brain astrocytoma.
  • OBJECT: With recent advances in the adjuvant treatment of malignant brain astrocytomas, it is increasingly debated whether extent of resection affects survival.
  • METHODS: The authors retrospectively reviewed the cases of 1215 patients who underwent surgery for malignant brain astrocytomas (World Health Organization [WHO] Grade III or IV) at a single institution from 1996 to 2006.
  • Surgery consisted of primary resection in 549 patients (58%) and revision resection for tumor recurrence in 400 patients (42%).
  • Adjusting for factors associated with survival for WHO Grade III astrocytoma (age, KPS score, and revision resection), GTR versus STR (p < 0.05) was associated with improved survival.
  • CONCLUSIONS: In the authors' experience with both primary and secondary resection of malignant brain astrocytomas, increasing extent of resection was associated with improved survival independent of age, degree of disability, WHO grade, or subsequent treatment modalities used.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery

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  • (PMID = 18847342.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Decanoic Acids; 0 / Polyesters; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 90409-78-2 / decanedioic acid-4,4'-(1,3-propanediylbis(oxy))bis(benzoic acid) copolymer; U68WG3173Y / Carmustine
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93. Faria MH, Khayat AS, Burbano RR, Rabenhorst SH: c -MYC amplification and expression in astrocytic tumors. Acta Neuropathol; 2008 Jul;116(1):87-95
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  • [Title] c -MYC amplification and expression in astrocytic tumors.
  • The aim of this study was to evaluate the nuclear and cytoplasmic expression of c-MYC protein in human astrocytic tumors of different histopathological grades and to determine whether its expression correlates with c-MYC gene amplification.
  • An immunohistochemical study of c-MYC protein was performed in 140 paraffin-embedded astrocytic tumors of different grades.
  • The distribution of the positive cases according to the tumor grade increased in both nuclear and cytoplasmic staining with malignancy.
  • The median nuclear LI also increased with tumor grade, with highest c-MYC nuclear expression in grade III.
  • These results indicate that c-MYC expression in astrocytic tumors is strongly associated with increased c-MYC gene copy number and suggest that c-MYC plays a role in the early tumorigenesis of astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Genes, myc

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  • (PMID = 18369647.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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94. Huang L, Jiang T, Yuan F, Li GL, Cui Y, Liu EZ, Wang ZC: Correlation of chromosomes 1p and 19q status and expressions of O6-methylguanine DNA methyltransferase (MGMT), p53 and Ki-67 in diffuse gliomas of World Health Organization (WHO) grades II and III: a clinicopathological study. Neuropathol Appl Neurobiol; 2009 Aug;35(4):367-79
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  • RESULTS: Loss of heterozygosity (LOH) on 1p, combined LOH on 1p and 19q, low MGMT expression and high Ki-67 expression were associated with oligodendroglial tumours, whereas high p53 expression was associated with astrocytic and mixed tumours.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Glioma / genetics. Ki-67 Antigen / metabolism. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / genetics. Astrocytoma / metabolism. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Child. Female. Gene Expression. Humans. Loss of Heterozygosity. Male. Middle Aged. Neoplasm Staging. Oligodendroglioma / genetics. Oligodendroglioma / metabolism

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  • (PMID = 19019173.001).
  • [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 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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95. Tihan T, Vohra P, Berger MS, Keles GE: Definition and diagnostic implications of gemistocytic astrocytomas: a pathological perspective. J Neurooncol; 2006 Jan;76(2):175-83
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  • Gemistocytic astrocytoma still continues to be enigmatic; both in terms of definition and prognostic implications.
  • The currently accepted definition of gemistocytic astrocytoma requires 20% or more gemistocytes, and considers the neoplasm as a diffuse astrocytoma, which is a WHO grade II tumor.
  • Some suggest that gemistocytic morphology should be considered as evidence of a higher grade astrocytoma.
  • There is still a need for studies with sufficient numbers of well-matched gemistocytic and non-gemistocytic astrocytic neoplasms to decide whether upgrading a tumor with 'significant' number of gemistocytes is justifiable.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / pathology. Brain Neoplasms / diagnosis. Brain Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Terminology as Topic

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  • (PMID = 16132490.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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96. Xu YZ, Nygård M, Kristensson K, Bentivoglio M: Regulation of cytokine signaling and T-cell recruitment in the aging mouse brain in response to central inflammatory challenge. Brain Behav Immun; 2010 Jan;24(1):138-52
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  • [Title] Regulation of cytokine signaling and T-cell recruitment in the aging mouse brain in response to central inflammatory challenge.
  • Aging is often accompanied by increased levels of inflammatory molecules in the organism, but age-related changes in the brain response to inflammatory challenges still require clarification.
  • We first analyzed the expression of molecules involved in T-cell infiltration and cytokine signaling regulation in the septum and hippocampus of 2-3 months and 20- to 24-month-old mice at 4h after intracerebroventricular injections of tumor necrosis factor (TNF)-alpha or interferon-gammaversus saline injections.
  • Double immunofluorescence revealed ICAM-1 expression in microglia and astrocytic processes.
  • CD3(+), CD4(+) and CD8(+) T-cells exhibited progressive age-related increases in brain parenchyma and choroid plexus after cytokine exposure.
  • The findings indicate that the brain responses to inflammatory challenges are not only preserved with advancing age, but also include gradual amplification of ICAM-1 expression and T-cell recruitment.
  • The data highlight molecular and cellular correlates of age-related increase of brain sensitivity to inflammatory stimuli, which could be involved in altered brain vulnerability during aging.
  • [MeSH-major] Aging / physiology. Brain / growth & development. Brain / immunology. Cytokines / physiology. Inflammation / pathology. Signal Transduction / physiology. T-Lymphocytes / physiology
  • [MeSH-minor] Animals. Blotting, Western. Data Interpretation, Statistical. Immunohistochemistry. Injections, Intraventricular. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. Male. Mice. Mice, Inbred C57BL. RNA / biosynthesis. RNA / isolation & purification. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic / physiology. Tumor Necrosis Factor-alpha / administration & dosage. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 19765643.001).
  • [ISSN] 1090-2139
  • [Journal-full-title] Brain, behavior, and immunity
  • [ISO-abbreviation] Brain Behav. Immun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 63231-63-0 / RNA
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97. Dai C, Lyustikman Y, Shih A, Hu X, Fuller GN, Rosenblum M, Holland EC: The characteristics of astrocytomas and oligodendrogliomas are caused by two distinct and interchangeable signaling formats. Neoplasia; 2005 Apr;7(4):397-406
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  • Different histologies of these tumors imply that the pathways activated by these two oncogenic stimulations are different, and that the apparent lineage of the tumor cells may result from specific signaling activity.
  • Furthermore, forced Akt activity in the context of chronic PDGF stimulation results in cells with an astrocytic differentiation pattern both in culture and in vivo.
  • The ability of signaling activity to convert tumor cells from one lineage to another presents a mechanism for the development of tumors apparently comprised of cells from multiple lineages.

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  • (PMID = 15967117.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01CA894314-1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC1501153
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98. Balciūniene N, Tamasauskas A, Valanciūte A, Deltuva V, Vaitiekaitis G, Gudinaviciene I, Weis J, von Keyserlingk DG: Histology of human glioblastoma transplanted on chicken chorioallantoic membrane. Medicina (Kaunas); 2009;45(2):123-31
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  • Glioblastoma is the most malignant tumor in the range of cerebral astrocytic gliomas.
  • Invasion of vessels from the chicken into transplanted tumor is not observed.
  • Chicken erythrocytes did not appear within the transplants, and tumor cells invade chicken tissue at the minimum.
  • The features of original tumor-host reaction of the patient remained too.
  • [MeSH-major] Brain Neoplasms / pathology. Chorioallantoic Membrane. Glioblastoma / pathology
  • [MeSH-minor] Animals. Chick Embryo. Genes, p53. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Neoplasm Transplantation. Neoplasms, Experimental. Paraffin Embedding. Photography. Time Factors. Vimentin / metabolism

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  • (PMID = 19289902.001).
  • [ISSN] 1648-9144
  • [Journal-full-title] Medicina (Kaunas, Lithuania)
  • [ISO-abbreviation] Medicina (Kaunas)
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Lithuania
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
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99. Carson-Walter EB, Winans BN, Whiteman MC, Liu Y, Jarvela S, Haapasalo H, Tyler BM, Huso DL, Johnson MD, Walter KA: Characterization of TEM1/endosialin in human and murine brain tumors. BMC Cancer; 2009;9:417
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  • [Title] Characterization of TEM1/endosialin in human and murine brain tumors.
  • BACKGROUND: TEM1/endosialin is an emerging microvascular marker of tumor angiogenesis.
  • We characterized the expression pattern of TEM1/endosialin in astrocytic and metastatic brain tumors and investigated its role as a therapeutic target in human endothelial cells and mouse xenograft models.
  • METHODS: In situ hybridization (ISH), immunohistochemistry (IH) and immunofluorescence (IF) were used to localize TEM1/endosialin expression in grade II-IV astrocytomas and metastatic brain tumors on tissue microarrays.
  • Intracranial U87MG glioblastoma (GBM) xenografts were analyzed in nude TEM1/endosialin knockout (KO) and wildtype (WT) mice.
  • RESULTS: TEM1/endosialin was upregulated in primary and metastatic human brain tumors, where it localized primarily to the tumor vasculature and a subset of tumor stromal cells.
  • Vascular Tem1/endosialin was induced in intracranial U87MG GBM xenografts grown in mice.
  • Tem1/endosialin KO vs WT mice demonstrated equivalent survival and tumor growth when implanted with intracranial GBM xenografts, although Tem1/endosialin KO tumors were significantly more vascular than the WT counterparts.
  • CONCLUSION: TEM1/endosialin was induced in the vasculature of high-grade brain tumors where its expression was inversely correlated with patient age.
  • Although lack of TEM1/endosialin did not suppress growth of intracranial GBM xenografts, it did increase tumor vascularity.
  • The cellular localization of TEM1/endosialin and its expression profile in primary and metastatic brain tumors support efforts to therapeutically target this protein, potentially via antibody mediated drug delivery strategies.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD / genetics. Antigens, Neoplasm / biosynthesis. Antigens, Neoplasm / genetics. Brain Neoplasms / genetics. Brain Neoplasms / metabolism

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  • (PMID = 19948061.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS046461; United States / NINDS NIH HHS / NS / K08 NS046461; United States / NIEHS NIH HHS / ES / T32 ES007026
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD248 protein, human
  • [Other-IDs] NLM/ PMC2793264
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100. Rose SR, Danish RK, Kearney NS, Schreiber RE, Lustig RH, Burghen GA, Hudson MM: ACTH deficiency in childhood cancer survivors. Pediatr Blood Cancer; 2005 Nov;45(6):808-13
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  • [Title] ACTH deficiency in childhood cancer survivors.
  • We assessed the prevalence of ACTHD in survivors of childhood cancer according to tumor diagnosis/therapy.
  • PROCEDURE: Chart review of endocrine/oncology history was performed in 310 childhood cancer survivors.
  • Of the 56 with ACTHD, 53 (95%) had received cranial irradiation (mean 45.5 Gy, range 14-70 Gy); three had not: one each with craniopharyngioma, hypothalamic astrocytoma, and brain stem glioma.
  • CONCLUSIONS: Childhood cancer survivors with greatest risk for ACTHD had craniopharyngioma, other suprasellar tumor, or medulloblastoma or > or =24 Gy cranial irradiation.
  • We recommend annual testing for ACTHD for 10-15 years and continued lifelong surveillance after CNS tumor or cranial irradiation, in patients with other hypothalamic-pituitary deficiencies or symptoms of ACTHD.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15700255.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R25 CA023944
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 9002-60-2 / Adrenocorticotropic Hormone
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