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1. Ichimura K, Mungall AJ, Fiegler H, Pearson DM, Dunham I, Carter NP, Collins VP: Small regions of overlapping deletions on 6q26 in human astrocytic tumours identified using chromosome 6 tile path array-CGH. Oncogene; 2006 Feb 23;25(8):1261-71
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  • [Title] Small regions of overlapping deletions on 6q26 in human astrocytic tumours identified using chromosome 6 tile path array-CGH.
  • Deletions of chromosome 6 are a common abnormality in diverse human malignancies including astrocytic tumours, suggesting the presence of tumour suppressor genes (TSG).
  • A total of 104 adult astrocytic tumours (10 diffuse astrocytomas, 30 anaplastic astrocytomas (AA), 64 glioblastomas (GB)) were analysed using this array.
  • [MeSH-minor] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosomes, Artificial, Bacterial. DNA, Neoplasm / analysis. Gene Dosage. Humans. Microsatellite Repeats. Telomere / genetics

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  • [Copyright] Oncogene (2006) 25, 1261-1271. doi:10.1038/sj.onc.1209156; published online 3 October 2005.
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  • (PMID = 16205629.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Other-IDs] NLM/ PMC2760128; NLM/ UKMS2686
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2. Jacques TS, Swales A, Brzozowski MJ, Henriquez NV, Linehan JM, Mirzadeh Z, O' Malley C, Naumann H, Alvarez-Buylla A, Brandner S: Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes. EMBO J; 2010 Jan 6;29(1):222-35
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  • [Title] Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes.
  • It has been suggested that intrinsic brain tumours originate from a neural stem/progenitor cell population in the subventricular zone of the post-natal brain.
  • However, the influence of the initial genetic mutation on the phenotype as well as the contribution of mature astrocytes to the formation of brain tumours is still not understood.
  • We deleted Rb/p53, Rb/p53/PTEN or PTEN/p53 in adult subventricular stem cells; in ectopically neurografted stem cells; in mature parenchymal astrocytes and in transplanted astrocytes.
  • We found that only stem cells, but not astrocytes, gave rise to brain tumours, independent of their location.
  • This suggests a cell autonomous mechanism that enables stem cells to generate brain tumours, whereas mature astrocytes do not form brain tumours in adults.
  • Our study underlines an important role of stem cells and the relevance of initial genetic mutations in the pathogenesis and phenotype of brain tumours.

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  • (PMID = 19927122.001).
  • [ISSN] 1460-2075
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD032116; United States / NICHD NIH HHS / HD / R37 HD032116; United States / NICHD NIH HHS / HD / HD-32116
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / glial fibrillary astrocytic protein, mouse; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2808375
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3. Suzuki T, Izumoto S, Fujimoto Y, Maruno M, Ito Y, Yoshimine T: Clinicopathological study of cellular proliferation and invasion in gliomatosis cerebri: important role of neural cell adhesion molecule L1 in tumour invasion. J Clin Pathol; 2005 Feb;58(2):166-71
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  • [Title] Clinicopathological study of cellular proliferation and invasion in gliomatosis cerebri: important role of neural cell adhesion molecule L1 in tumour invasion.
  • BACKGROUND/AIMS: In patients with gliomatosis cerebri (GC), glial fibrillary acidic protein (GFAP) positive cells invade the entire brain, particularly the white matter.
  • METHODS: An immunohistochemical analysis of neoplastic cells from four patients with GC and 20 with astrocytic tumours using antibodies against Ki-67, GFAP, and L1, the last of which is a neural cell adhesion molecule putatively related to glioma invasion.
  • RESULTS: GC tumour cells can be divided into two types, those mainly composed of strongly GFAP and L1 positive gemistocytic cells, the other composed of small, GFAP and L1 negative spindle shaped cells.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasms, Neuroepithelial / pathology. Neural Cell Adhesion Molecule L1 / analysis
  • [MeSH-minor] Adult. Aged. Antibodies, Neoplasm / analysis. Astrocytoma / chemistry. Astrocytoma / pathology. Brain Chemistry. Cell Division / physiology. Female. Glial Fibrillary Acidic Protein / analysis. Glioblastoma / chemistry. Glioblastoma / pathology. Humans. Immunohistochemistry / methods. Ki-67 Antigen / immunology. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness

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  • (PMID = 15677537.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Neural Cell Adhesion Molecule L1
  • [Other-IDs] NLM/ PMC1770574
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4. Qu M, Olofsson T, Sigurdardottir S, You C, Kalimo H, Nistér M, Smits A, Ren ZP: Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas. Acta Neuropathol; 2007 Feb;113(2):129-36
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  • [Title] Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas.
  • Oligoastrocytomas are glial tumours consisting of a mixture of neoplastic astrocytic and oligodendroglial cells.
  • To investigate whether these neoplastic cell types in oligoastrocytomas have different genetic profiles, we examined the two different components of oligoastrocytomas in comparison with the histological diagnosis of the specific tumour area for LOH 1p/19q and TP53 mutations by using microdissection technique.
  • We found a variety of lost markers for 1p and 19q, and the presence of two different TP53 mutations in the tumour samples.
  • In the majority of cases (9/11), the oligodendroglial and astrocytic components of an individual oligoastrocytoma displayed the same genotype.
  • We present two cases of biphasic oligoastrocytomas with aberrant findings, suggesting the coexistence of genetically and morphologically distinct tumour cell clones in these tumours.
  • In one case, the oligodendroglial part of the tumour showed LOH19q, whereas the astrocytic part showed TP53 mutation (codon 273).
  • In another case, we found LOH 1p/19q in the oligodendroglial component, but two retained areas on chromosome 1p in the astrocytic component of the tumour.
  • No evidence was found for the coexistence of tumour cells with the two genotypical changes within the same morphological region of one individual tumour.
  • The two cases of biphasic oligoastrocytomas in our sample that display a different genotype in the astrocytic and oligodendroglial part of the tumour show that different components of an oligoastrocytoma may be derived from different cell clones during neoplastic transformation.
  • [MeSH-major] Astrocytoma / classification. Astrocytoma / genetics. Brain Neoplasms / classification. Brain Neoplasms / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17031656.001).
  • [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
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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5. 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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  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • 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-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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6. Masi A, Becchetti A, Restano-Cassulini R, Polvani S, Hofmann G, Buccoliero AM, Paglierani M, Pollo B, Taddei GL, Gallina P, Di Lorenzo N, Franceschetti S, Wanke E, Arcangeli A: hERG1 channels are overexpressed in glioblastoma multiforme and modulate VEGF secretion in glioblastoma cell lines. Br J Cancer; 2005 Oct 3;93(7):781-92
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  • The expression pattern of these two channels was compared to that of the classical inward rectifying K(+) channels, IRK, that are widely expressed in astrocytic cells and classically considered a marker of astrocytic differentiation.
  • Our data provide important confirmation for studies proposing the hERG1 channel as a molecular marker of tumour progression and a possible target for novel anticancer therapies.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Potassium Channels, Voltage-Gated / metabolism. Vascular Endothelial Growth Factor A / secretion
  • [MeSH-minor] Adult. Aged. Base Sequence. Cell Line, Tumor. Child. DNA Primers. Ether-A-Go-Go Potassium Channels. Female. Humans. Immunohistochemistry. Male. Middle Aged. Patch-Clamp Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16175187.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / ERG1 potassium channel; 0 / Ether-A-Go-Go Potassium Channels; 0 / Potassium Channels, Voltage-Gated; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC2361632
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7. Bäcklund LM, Nilsson BR, Liu L, Ichimura K, Collins VP: Mutations in Rb1 pathway-related genes are associated with poor prognosis in anaplastic astrocytomas. Br J Cancer; 2005 Jul 11;93(1):124-30
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  • Anaplastic astrocytoma (AA, WHO grade III) is, second to Glioblastoma, the most common and most malignant type of adult CNS tumour.
  • The survival data on 37 carefully sampled AA was correlated with the results of a detailed analysis of the status of nine genes known to be involved in the development of astrocytic tumours.
  • We found that loss of both wild-type copies of any of the three tumour suppressor genes CDKN2A, CDKN2B and RB1 or gene amplification of CDK4, disrupting the Rb1 pathway, were associated with shorter survival (P=0.009).
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Genes, Retinoblastoma. Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Humans. Male. Middle Aged. Prognosis


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

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  • (PMID = 18362893.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 19920
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / FGF5 protein, human; 0 / Mutant Proteins; 0 / Recombinant Proteins; 129653-64-1 / Fibroblast Growth Factor 5
  • [Other-IDs] NLM/ PMC2879862; NLM/ UKMS30927
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9. Capper D, Mittelbronn M, Goeppert B, Meyermann R, Schittenhelm J: Secreted protein, acidic and rich in cysteine (SPARC) expression in astrocytic tumour cells negatively correlates with proliferation, while vascular SPARC expression is associated with patient survival. Neuropathol Appl Neurobiol; 2010 Apr;36(3):183-97
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  • [Title] Secreted protein, acidic and rich in cysteine (SPARC) expression in astrocytic tumour cells negatively correlates with proliferation, while vascular SPARC expression is associated with patient survival.
  • AIMS: Secreted protein, acidic and rich in cysteine (SPARC) is a regulator of cell-matrix interaction and has been associated with tumour stage and patient survival in various malignancies.
  • As no large-scale study has yet been undertaken, we investigated human brain and astrocytomas for SPARC expression and associations with tumour grade, proliferation, vascular density and patient survival.
  • METHODS: A spectrum of 188 WHO grade I-IV astrocytic tumours and 24 autopsy cases were studied by immunohistochemistry for SPARC, MIB-1 proliferation index and CD31-positive vessels.
  • RESULTS: In normal brain, SPARC is expressed in cortical marginal glia, cerebellar Bergmann glia and focally in white matter but is absent in neurones or vessels.
  • High SPARC expression levels in the cytoplasm of astrocytic tumour cells decreased with the grade of malignancy but showed an increase with grade of malignancy in tumour vessels.
  • SPARC negatively correlated with tumour proliferation but not with vascular density.
  • CONCLUSIONS: SPARC is highly expressed in astrocytomas and decreases with tumour progression.
  • While there is no association between the level of SPARC in the tumour cells and patient survival, increased tumour vascular SPARC expression is associated with decreased patient survival.
  • [MeSH-major] Astrocytoma / metabolism. Blood Vessels / metabolism. Brain / metabolism. Brain Neoplasms / metabolism. Cell Proliferation. Osteonectin / metabolism
  • [MeSH-minor] Adult. Cell Movement. Cytoplasm / metabolism. Cytoplasm / pathology. Female. Glioblastoma / blood supply. Glioblastoma / metabolism. Glioblastoma / mortality. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neovascularization, Pathologic. Nerve Fibers, Myelinated / metabolism. Nerve Fibers, Myelinated / pathology. Neuroglia / metabolism. Neuroglia / pathology. Neurons / metabolism. Neurons / pathology. RNA, Messenger / metabolism. Young Adult

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  • (PMID = 20132490.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Osteonectin; 0 / RNA, Messenger
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10. Li X, Wang Y, Wang Y, Zhen H, Yang H, Fei Z, Zhang J, Liu W, Wang Y, Zhang X: Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis. Tumour Biol; 2007;28(3):165-72
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  • [Title] Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis.
  • A high expression of EphA2 has been detected in many non-central nervous system tumors; however, the EphA2 expression in brain astrocytic tumors remains unclear.
  • In this study, we investigated the expression of EphA2 mRNA and protein in 90 cases of human astrocytic tumors by reverse transcription polymerase chain reaction and immunohistochemistry, respectively.
  • The proliferative index (PI) of tumor cells was evaluated by Ki-67 immunohistochemistry, and the apoptotic index (AI) was determined by TdT-mediated dUTP nick end labeling assay.
  • The correlation between EphA2 expression, pathologic grade, proliferation and apoptosis of astrocytic tumors was further analyzed.
  • Therefore, EphA2 may be a new biomarker for astrocytic tumors.
  • It may also affect the proliferation and apoptosis of tumor cells and be an attractive therapy target for astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Receptor, EphA2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Cell Division. Child. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / genetics

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17519535.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, EphA2
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11. Plotkin M, Amthauer H, Eisenacher J, Wurm R, Michel R, Wust P, Stockhammer F, Röttgen R, Gutberlet M, Ruf J, Felix R: Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours. Neuroradiology; 2005 Jan;47(1):18-26
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  • [Title] Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours.
  • In the current study we investigated whether IMT-SPECT could also be useful in the follow-up of brain metastases and other intracranial tumours of non-astrocytic origin.
  • The study included 22 patients with suspected recurrent intracranial tumours of non-astrocytic origin (12 brain metastases, one supratentorial primitive neuroendocrine tumour (PNET), one rhabdoid tumour, two clivus chordomas, three ependymomas, two pituitary tumours, one anaplastic meningioma) who had previously been treated by surgery and/or radio/chemotherapy.
  • We concluded that the IMT-SPECT is a promising complementary imaging tool for the detection of recurrences of non-astrocytic intracranial tumours and their distinguishing from treatment-induced changes.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Iodine Radioisotopes. Methyltyrosines. Neoplasm Recurrence, Local / diagnostic imaging. Radiopharmaceuticals. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Chordoma / diagnostic imaging. Ependymoma / diagnostic imaging. False Negative Reactions. False Positive Reactions. Female. Follow-Up Studies. Glioma / diagnostic imaging. Humans. Magnetic Resonance Imaging. Male. Meningioma / diagnostic imaging. Middle Aged. Neuroendocrine Tumors / diagnostic imaging. Pituitary Neoplasms / diagnostic imaging. Retrospective Studies. Rhabdoid Tumor / diagnostic imaging. Sensitivity and Specificity. Supratentorial Neoplasms / diagnostic imaging

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  • (PMID = 15630586.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Methyltyrosines; 0 / Radiopharmaceuticals; A77N8J5H5T / 3-iodo-alpha-methyltyrosine
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12. Landriscina M, Schinzari G, Di Leonardo G, Quirino M, Cassano A, D'Argento E, Lauriola L, Scerrati M, Prudovsky I, Barone C: S100A13, a new marker of angiogenesis in human astrocytic gliomas. J Neurooncol; 2006 Dec;80(3):251-9
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  • [Title] S100A13, a new marker of angiogenesis in human astrocytic gliomas.
  • We investigated the expression of S100A13 in human astrocytic gliomas in relation to tumour grading and vascularization.
  • A series of 26 astrocytic gliomas was studied to evaluate microvessel density and to assess FGF1, S100A13 and VEGF-A expression.
  • Moreover, both S100A13 and VEGF-A expression significantly correlated with microvessel density and tumour grading.
  • These data suggest that the up-regulation of S100A13 and VEGF-A expression correlates with the activation of angiogenesis in high-grade human astrocytic gliomas.
  • [MeSH-major] Astrocytoma / blood supply. Biomarkers, Tumor / metabolism. Brain Neoplasms / blood supply. Neovascularization, Pathologic / metabolism. S100 Proteins / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Adult. Aged. Female. Fibroblast Growth Factors / metabolism. Humans. Male. Middle Aged. Severity of Illness Index. Statistics, Nonparametric. Up-Regulation

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  • (PMID = 16773219.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL32348; United States / NHLBI NIH HHS / HL / HL35627; United States / NCRR NIH HHS / RR / RR1555
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / S100 Proteins; 0 / S100A13 protein, human; 0 / Vascular Endothelial Growth Factor A; 62031-54-3 / Fibroblast Growth Factors
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13. Bini A, Sodi A, Passerini I, Menchini U, Torricelli F: Retinal astrocytic hamartoma and Stargardt's disease: unusual association in a patient with ABCR mutation without phacomatosis. Clin Exp Ophthalmol; 2007 Nov;35(8):777-9
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  • [Title] Retinal astrocytic hamartoma and Stargardt's disease: unusual association in a patient with ABCR mutation without phacomatosis.
  • We report the unusual association of a retinal astrocytic hamartoma and Stargardt's disease in a patient with ABCR mutation.
  • The clinical findings were consistent with the diagnosis of retinal astrocytic hamartoma.
  • The connection between Stargardt's disease and this tumour has never been previously reported.
  • The astrocytic hamartoma of our patient showed unusual clinical features.
  • [MeSH-minor] Adult. Electroretinography. Fluorescein Angiography. Humans. Male. Tomography, Optical Coherence

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  • (PMID = 17997789.001).
  • [ISSN] 1442-6404
  • [Journal-full-title] Clinical & experimental ophthalmology
  • [ISO-abbreviation] Clin. Experiment. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / ABCA4 protein, human
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14. Tan G, Sun SQ, Yuan DL: Expression of the water channel protein aquaporin-9 in human astrocytic tumours: correlation with pathological grade. J Int Med Res; 2008 Jul-Aug;36(4):777-82
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  • [Title] Expression of the water channel protein aquaporin-9 in human astrocytic tumours: correlation with pathological grade.
  • This study investigated the expression of the water channel protein aquaporin-9 (AQP9) in 100 cases of human astrocytic tumour compared with normal brain tissue.
  • The expression of both AQP9 mRNA and protein in astrocytic tumours was significantly greater than in normal brain tissue and was positively correlated with pathological grade.
  • No significant correlations were found between the level of AQP9 mRNA or protein expression and gender, age, tumour size or tumour site.
  • This study indicates that AQP9 may play an important role in the malignant progression of brain astrocytic tumours and may, therefore, be useful as a biomarker in its diagnosis and as a new target for gene therapy.
  • The molecular mechanisms by which AQP9 affects the proliferation and apoptosis of astrocytic tumours need to be studied further.
  • [MeSH-major] Aquaporins / metabolism. Astrocytoma. Brain Neoplasms
  • [MeSH-minor] Adolescent. Adult. Aged. Brain / cytology. Brain / metabolism. Child. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18652774.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AQP9 protein, human; 0 / Aquaporins
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15. Shapiro WR, Carpenter SP, Roberts K, Shan JS: (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma. Expert Opin Biol Ther; 2006 May;6(5):539-45
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  • [Title] (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma.
  • Most malignant gliomas cannot be completely resected or irradiated due to their ability to infiltrate diffusely into normal brain tissue.
  • Brain tissue is protected from the systemic circulation via the blood-brain barrier (BBB), which impedes entry of water-soluble chemotherapeutic agents into the tumour at therapeutic concentrations. (131)I-chTNT-1/B mAb (Cotara) employs an innovative strategy to treat the invasive portion of the tumour and the core lesion. (131)I-chTNT-1/B mAb is a genetically engineered, radiolabelled, chimeric monoclonal antibody specific for a universal intracellular antigen (i.e., DNA/histone H1 complex) exposed in the necrotic core of malignant gliomas.
  • Once localised to necrotic regions of the tumour, (131)I-chTNT-1/B mAb delivers a cytotoxic dose of (131)I radiation to the core lesion. (131)I-chTNT-1/B mAb is delivered via convection-enhanced delivery in order to maximise coverage to the tumour and the invasive front of the glial tumour.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Astrocytoma / radiotherapy. Iodine Radioisotopes / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Clinical Trials as Topic. DNA / immunology. DNA / metabolism. Female. Histones / immunology. Histones / metabolism. Humans. Male. Middle Aged. Radioimmunotherapy / methods

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  • (PMID = 16610983.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Histones; 0 / Iodine Radioisotopes; 9007-49-2 / DNA
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16. Birlik B, Canda S, Ozer E: Tumour vascularity is of prognostic significance in adult, but not paediatric astrocytomas. Neuropathol Appl Neurobiol; 2006 Oct;32(5):532-8
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  • [Title] Tumour vascularity is of prognostic significance in adult, but not paediatric astrocytomas.
  • Astrocytomas are the commonest type of brain tumours in adults and children.
  • Although the most reliable prognostic indicators have been shown consistently to be patient age and tumour histological grade, biological progression in these tumours is inevitable and the overall prognosis has remained poor.
  • Due to the evidence that vascular changes are important histological features of astrocytomas, the aim of this study was to investigate prognostic significance of tumour vascularity in paediatric and adult astrocytomas.
  • Study population consisted of 70 patients (45 adult and 25 children) with histologically proven diagnosis of astrocytoma with no history of previous therapy.
  • Histological quantification of tumour vascularity was performed using three different methods: microvessel density, vascular grading and Chalkley counting.
  • In contrast to the results in paediatric astrocytomas, tumour vascularity in adult tumours correlated significantly with postoperative survival by univariate analysis (P < 0.05).
  • Patient age and tumour histological grade were also correlated with survival.
  • We conclude that histological quantification of tumour vascularity is a significant prognosticator in adult astrocytomas, but not in children.
  • Our data do not support the validity of applications of antiangiogenic agents in paediatric astrocytic tumours, particularly pilocytic astrocytomas.
  • [MeSH-major] Aging / pathology. Astrocytoma / blood supply. Astrocytoma / pathology. Brain Neoplasms / blood supply. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Angiogenesis Inhibitors / therapeutic use. Antigens, CD31 / metabolism. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Prognosis. Regional Blood Flow / physiology. Retrospective Studies. Survival

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  • (PMID = 16972887.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31
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17. Moenninghoff C, Maderwald S, Theysohn JM, Kraff O, Ladd ME, El Hindy N, van de Nes J, Forsting M, Wanke I: Imaging of adult astrocytic brain tumours with 7 T MRI: preliminary results. Eur Radiol; 2010 Mar;20(3):704-13
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  • [Title] Imaging of adult astrocytic brain tumours with 7 T MRI: preliminary results.
  • PURPOSE: In this study tumour vascularity and necrosis of intracranial astrocytomas were compared using 7 T and 1.5 T magnetic resonance imaging (MRI).
  • Histological findings and T2*-w MR images at both field strengths were compared for the presence of assumed tumour microvascularity and necrosis.
  • RESULTS: T2*-w images depicted susceptibility patterns representing presumed tumour microvascularity in 8 out of 15 (53%) gliomas at 7 T compared with 5 out of 15 (33%) gliomas at 1.5 T.
  • Compared with 1.5 T MRI three additional necrotic tumour areas were depicted only on 7 T T2- and T2*-w images of one glioblastoma.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Imaging / methods. Neovascularization, Pathologic / pathology
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Pilot Projects. Reproducibility of Results. Sensitivity and Specificity

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  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
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  • (PMID = 19763581.001).
  • [ISSN] 1432-1084
  • [Journal-full-title] European radiology
  • [ISO-abbreviation] Eur Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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18. Beetz C, Bergner S, Brodoehl S, Brodhun M, Ewald C, Kalff R, Krüger J, Patt S, Kiehntopf M, Deufel T: Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology. Int J Oncol; 2006 Nov;29(5):1183-91
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  • [Title] Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology.
  • Astrocytomas are intracranial malignancies for which invasive growth and high motility of tumour cells preclude total resection; the tumours usually recur in a more aggressive and, eventually, lethal form.
  • In order to identify novel molecular markers for prognosis we obtained expression profiles of: i) tumours associated with particularly long recurrence-free intervals, ii) tumours which led to rapid patient death, and iii) tumour-free control brain.
  • Our finding of cell-specificity for some of these outcome-determining genes relates global expression data to the presence of morphological correlates of tumour behaviour and, thus, provides a link between morphology-based and molecular pathology.
  • [MeSH-major] Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / mortality. Gene Expression Profiling. Genes, Neoplasm / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17016650.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Neoplasm
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19. Kim YJ, Cho YE, Kim YW, Kim JY, Lee S, Park JH: Suppression of putative tumour suppressor gene GLTSCR2 expression in human glioblastomas. J Pathol; 2008 Oct;216(2):218-24
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  • [Title] Suppression of putative tumour suppressor gene GLTSCR2 expression in human glioblastomas.
  • Glioma tumour-suppressor candidate region gene 2 (GLTSCR2/PICT-1) is localized within the well-known 1.4 Mb tumour-suppressive region of chromosome 19q, which is frequently altered in various human tumours, including diffuse gliomas.
  • Aside from its chromosomal localization, several lines of evidence, including PTEN-phosphorylating and cell-killing activities, suggests that GLTSCR2 participates in the suppression of tumour growth and development.
  • However, little is known about the biological functions and molecular mechanisms of GLTSCR2 as a tumour suppressor gene.
  • We investigated the pathological significance of GLTSCR2 expression in association with the development and progression of glioblastomas, the most common malignant brain tumour.
  • We used real-time PCR and western blot analysis to examine the expression levels of GLTSCR2 mRNA and protein in glioblastomas, normal brain tissue and in non-glial tumour tissue of different origin, and found that GLTSCR2 expression is down-regulated in glioblastomas.
  • Finally, our immunohistochemical study demonstrates that GLTSCR2 is sequentially down-regulated according to the histological malignant progression of the astrocytic glial tumour.
  • Taken together, our results suggest that GLTSCR2 is involved in astrocytic glioma progression.
  • [MeSH-major] Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / pathology. Cell Line, Tumor. Chi-Square Distribution. Female. Gene Deletion. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18729076.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLTSCR2 protein, human; 0 / Tumor Suppressor Proteins
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20. Kitai R, Horita R, Sato K, Yoshida K, Arishima H, Higashino Y, Hashimoto N, Takeuchi H, Kubota T, Kikuta K: Nestin expression in astrocytic tumors delineates tumor infiltration. Brain Tumor Pathol; 2010 Apr;27(1):17-21
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  • [Title] Nestin expression in astrocytic tumors delineates tumor infiltration.
  • Nestin is an intermediate filament protein expressed in undifferentiated cells during central nervous system development, and glioma is known to be a highly infiltrative tumor.
  • We determined whether nestin was expressed in astrocytic tumors and could identify infiltrating tumor cells.
  • We screened 65 archival, paraffin-embedded adult astrocytic tumors using immunohistochemical staining and computerized overlaid photographs.
  • Normal biopsied brains and metastatic brain tumors were also examined.
  • The intensity of nestin expression corresponded to the tumor grade.
  • Overlaid images showed that nestin immunostaining delineated tumor invasion into adjacent gray and white matter.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Intermediate Filament Proteins / metabolism. Intermediate Filament Proteins / physiology. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Child. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Nestin. Young Adult

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  • (PMID = 20425043.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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21. Elgamal EA, Coakham HB: Hemifacial spasm caused by pontine glioma: case report and review of the literature. Neurosurg Rev; 2005 Oct;28(4):330-2
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  • Hemifacial spasm (HFS) is an involuntary paroxysmal contractions of the facial musculature, caused generally by vascular compression of the seventh cranial nerve at its root exit zone from the brain stem.
  • The case of an adult man harbouring brain stem glioma (BSG) whose only neurological signs were left HFS and mild facial weakness is reported.
  • No responsible vessel could be identified during surgery, but the causative lesion was found to be an astrocytic tumour encasing the facial nerve at its root exit zone from the brain stem.
  • [MeSH-major] Astrocytoma / complications. Brain Stem Neoplasms / complications. Hemifacial Spasm / etiology

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  • (PMID = 16001287.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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22. Felsberg J, Yan PS, Huang TH, Milde U, Schramm J, Wiestler OD, Reifenberger G, Pietsch T, Waha A: DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours. Neuropathol Appl Neurobiol; 2006 Oct;32(5):517-24
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  • Using differential methylation hybridization as a genome-wide screening approach to determine DNA methylation patterns in gliomas, we recently identified two DNA fragments in 14q23.1 (CGI-clone musical sharp396) and 14q32.12 (CGI-clone musical sharp519) that were differentially methylated between astrocytic gliomas and mixed oligoastrocytomas.
  • To validate this observation, we examined these 14q32.12 locus for methylation in an extended series of 43 astrocytic and oligodendroglial gliomas.
  • Microsatellite analysis showed LOH in seven of 28 (25%) oligodendroglial tumours and three of 15 (20%) astrocytic tumours.
  • Taken together, our data lend further support for the location of one or more yet to be identified glioma-associated tumour suppressor gene(s) on 14q.
  • [MeSH-major] Brain Neoplasms / pathology. Chromosomes, Human, Pair 14 / genetics. DNA Methylation. Oligodendroglia / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Alleles. Child. Child, Preschool. DNA, Neoplasm / drug effects. Female. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Sulfites / pharmacology

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  • (PMID = 16972885.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Sulfites; TZX5469Z6I / sodium bisulfite
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23. Takaya S, Hashikawa K, Turkheimer FE, Mottram N, Deprez M, Ishizu K, Kawashima H, Akiyama H, Fukuyama H, Banati RB, Roncaroli F: The lack of expression of the peripheral benzodiazepine receptor characterises microglial response in anaplastic astrocytomas. J Neurooncol; 2007 Oct;85(1):95-103
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  • We examined two anaplastic astrocytomas showing minimal contrast-enhancement and therefore little damage of the blood brain barrier to minimise the presence of blood borne macrophages within tumour tissue.
  • The two lesions were studied in vivo using positron emission tomography (PET) with the specific PBR ligand [(11)C](R)-PK11195 and the corresponding tumour tissue was investigated with an anti-PBR antibody.
  • Our results demonstrated PBR suppression in glioma-infiltrating microglia and suggested that PBR may have a relevant role in modulating the anti-tumour inflammatory response in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Microglia / metabolism. Microglia / pathology. Receptors, GABA-A / biosynthesis
  • [MeSH-minor] Adult. Antibodies, Monoclonal. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Isoquinolines. Magnetic Resonance Imaging. Male. Middle Aged. Multiple Sclerosis / pathology. Oligonucleotide Array Sequence Analysis. Parkinson Disease / pathology. Peripheral Nerves / metabolism. Positron-Emission Tomography. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Radiopharmaceuticals

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  • (PMID = 17520179.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U120085814
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Isoquinolines; 0 / RNA, Messenger; 0 / Radiopharmaceuticals; 0 / Receptors, GABA-A; YNF83VN1RL / PK 11195
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24. Schittenhelm J, Beschorner R, Simon P, Tabatabai G, Herrmann C, Schlaszus H, Capper D, Weller M, Meyermann R, Mittelbronn M: Diagnostic value of WT1 in neuroepithelial tumours. Neuropathol Appl Neurobiol; 2009 Feb;35(1):69-81
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  • AIMS: Currently, clinical trials using WT1 (Wilms tumour gene) peptide vaccines are conducted in haematopoietic malignancies and solid cancers.
  • Single reports showed that the Wilms tumour gene product WT1 is also expressed in astrocytic neoplasms.
  • Controlling for WHO grade, the comparison of oligodendrogliomas with ependymal and astrocytic tumours showed higher expression values for the latter.
  • These results suggest an important role of WT1 in tumourigenesis and progression in human brain tumours.
  • [MeSH-major] Brain Neoplasms / diagnosis. Neoplasms, Neuroepithelial / diagnosis. WT1 Proteins / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Brain / metabolism. Child. Endothelial Cells / metabolism. Female. Humans. Immunohistochemistry. Logistic Models. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis. Young Adult

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  • (PMID = 18466223.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / WT1 Proteins
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25. El Ayachi I, Baeza N, Fernandez C, Colin C, Scavarda D, Pesheva P, Figarella-Branger D: KIAA0510, the 3'-untranslated region of the tenascin-R gene, and tenascin-R are overexpressed in pilocytic astrocytomas. Neuropathol Appl Neurobiol; 2010 Aug;36(5):399-410

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We took advantage of our previous study focused on genes that were critical in tumour invasion to further study here an unknown sequence, referred to as KIAA0510, the chromosomal location of which was 1q25, described as a 5596-bp long mRNA and that we found to be significantly overexpressed in pilocytic astrocytomas compared with glioblastomas.
  • We also analysed a large series of various brain tumours and found that in the group of astrocytic tumours, tenascin-R expression decreased with malignancy, whereas oligodendrogliomas sometimes retained a high level of tenascin-R even in high-grade tumours.
  • In normal brain, tenascin-R was exclusively expressed by normal oligodendrocytes and subsets of neurones during post-natal development and in adulthood, where it could differentially affect cellular adhesiveness and/or differentiation.
  • Whether tenascin-R overexpression negatively influences brain invasion remains to be determined.
  • [MeSH-minor] 3' Untranslated Regions / genetics. Adolescent. Adult. Aged. Child. Child, Preschool. Ependymoma / genetics. Ependymoma / physiopathology. Ganglioglioma / genetics. Ganglioglioma / physiopathology. Humans. Infant. Meningeal Neoplasms / genetics. Meningeal Neoplasms / physiopathology. Meningioma / genetics. Meningioma / physiopathology. Middle Aged. Supratentorial Neoplasms / genetics. Supratentorial Neoplasms / physiopathology. Young Adult

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  • (PMID = 20202125.001).
  • [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 / 3' Untranslated Regions; 0 / Tenascin; 147604-77-1 / tenascin R
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26. Weckesser M, Langen KJ, Rickert CH, Kloska S, Straeter R, Hamacher K, Kurlemann G, Wassmann H, Coenen HH, Schober O: O-(2-[18F]fluorethyl)-L-tyrosine PET in the clinical evaluation of primary brain tumours. Eur J Nucl Med Mol Imaging; 2005 Apr;32(4):422-9
Hazardous Substances Data Bank. L-TYROSINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] O-(2-[18F]fluorethyl)-L-tyrosine PET in the clinical evaluation of primary brain tumours.
  • PURPOSE: The aim of this study was to evaluate the differential uptake of O-(2-[18F]fluorethyl)-L-tyrosine (FET) in suspected primary brain tumours.
  • METHODS: Positron emission tomography (PET) was performed in 44 patients referred for the evaluation of a suspected brain tumour.
  • Tumour uptake was calculated as the ratio of maximal tumour intensity to mean activity within a reference region (FETmax).
  • No uptake was observed in nine lesions (one inflammatory lesion, one dysembryoplastic neuroepithelial tumour, one mature teratoma, six lesions without histological confirmation).
  • Similar results were obtained when the analysis was applied only to astrocytic tumours (2.0 vs 3.1 in the first frame; 2.4 vs 2.6 in the fourth frame).
  • CONCLUSION: These initial results indicate that FET PET is a useful method to identify malignant brain lesions.
  • It appears that high- and low-grade brain tumours exhibit a different uptake kinetics of FET.
  • A kinetic analysis of FET PET may provide additional information in the differentiation of suspected brain lesions.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Brain Neoplasms / metabolism. Fluorine Radioisotopes / pharmacokinetics. Positron-Emission Tomography / methods. Tyrosine / analogs & derivatives. Tyrosine / pharmacokinetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Radiopharmaceuticals / pharmacokinetics. Reproducibility of Results. Sensitivity and Specificity

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  • (PMID = 15650870.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / O-(2-fluoroethyl)tyrosine; 0 / Radiopharmaceuticals; 42HK56048U / Tyrosine
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27. Strojnik T, Kavalar R, Zajc I, Diamandis EP, Oikonomopoulou K, Lah TT: Prognostic impact of CD68 and kallikrein 6 in human glioma. Anticancer Res; 2009 Aug;29(8):3269-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIMS: To evaluate the expression of CD68 and kallikrein 6 in human gliomas, and investigate their prognostic significance for survival of brain cancer patients in comparison to some known prognostic markers.
  • PATIENTS AND METHODS: Histological sections of 51 primary astrocytic tumours (11 benign, 40 malignant) were immunohistochemically stained for CD68, cathepsin B, kallikrein 6 and Ki-67.
  • CD68 and kallikrein 6 expressions were also analyzed by real-time PCR in nine brain tumour biopsies.
  • RESULTS: Both microglia and tumour cells expressed CD68.
  • A CD68 staining score of tumour cells higher than 3 was a significant predictor of shorter overall survival (p<0.01) in all patients and of borderline significance in the malignant group (p=0.057).
  • [MeSH-major] Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. Kallikreins / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19661345.001).
  • [ISSN] 1791-7530
  • [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 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / RNA, Messenger; EC 3.4.21.- / KLK6 protein, human; EC 3.4.21.- / Kallikreins
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28. Joensuu H, Puputti M, Sihto H, Tynninen O, Nupponen NN: Amplification of genes encoding KIT, PDGFRalpha and VEGFR2 receptor tyrosine kinases is frequent in glioblastoma multiforme. J Pathol; 2005 Oct;207(2):224-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The frequency of KIT and VEGFR2 amplification in glioblastomas is not known, and few data are available in any other human tumour type.
  • The four secondary glioblastomas arising from pre-existing lower grade astrocytic tumours investigated had KIT amplification but none had EGFR amplification.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Vascular Endothelial Growth Factor Receptor-2 / genetics
  • [MeSH-minor] Adult. Aged. Endothelial Cells / pathology. Exons / genetics. Female. Gene Amplification / genetics. Genes, erbB-1 / genetics. Humans. Immunohistochemistry / methods. In Situ Hybridization, Fluorescence / methods. Male. Middle Aged. Mutation. Phosphorylation. Survival Analysis

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16021678.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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