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1. Adamek D, Radwańska E, Gajda M: Expression of RCAS1 protein in microglia/macrophages accompanying brain tumours. An immunofluorescence study. Folia Neuropathol; 2009;47(3):240-6
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  • The expression of protein RCAS1 (receptor-binding cancer antigen expressed on SiSo cells), possibly involved in the mechanisms of evasion of immune surveillance by tumours, has been studied in brain astrocytomas grade III and IV and in metastatic carcinomas to the brain by means of double immunofluorescence with antibodies against RCAS1 and respectively anti-GFAP (astroglia) or CD68 or CD74 (macrophages/microglia).

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  • (PMID = 19813143.001).
  • [ISSN] 1641-4640
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / EBAG9 protein, human
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2. Figarella-Branger D, Bouvier C: [Histological classification of human gliomas: state of art and controversies]. Bull Cancer; 2005 Apr;92(4):301-9
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  • The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.
  • According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).
  • Circumscribed gliomas mainly corresponds to pilocytic astrocytomas (grade I).
  • Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.
  • According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).
  • [MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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  • (PMID = 15888386.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
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3. Hussein MR, El-Ghorori RM, El-Rahman YG: Alterations of p53, BCL-2, and hMSH2 protein expression in the normal brain tissues, gliosis, and gliomas. Int J Exp Pathol; 2006 Aug;87(4):297-306
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  • Tumorigenesis involves alterations in the tumor suppressor genes (p53), protooncogenes (BCL-2), and housekeeping genes (human MutS homologue-2 (hMSH2).
  • To test our hypothesis and to examine these issues, we immunostained 60 specimens entailing normal brain tissues, gliosis, and gliomas (Grade I, II, III, IV) for p53, BCL-2, and hMSH2 protein expression.
  • As compared with the normal brain and gliosis, examination of the average weighted scores in gliomas (Grade I, II, III, IV, respectively) showed significant up-regulation of: (i) p53 protein (0.0 +/- 0.0; 0.0 +/- 0.0; 0.9 +/- 0.5; 1.6 +/- 0.8; 1.7 +/- 0.5; and 4.1 +/- 0.8, P < 0.0001) (ii) hMSH2 (1.3 +/- 0.3; 1.5 +/- 0.7; 1.9 +/- 1.1; 2.2 +/- 0.5; 4.1 +/- 1.5; and 4.7 +/- 1.1, P < 0.0006), and (iii) BCL-2 (0.8 +/- 0.5; 1.9 +/- 0.5; 1.9 +/- 0.6; 2.0 +/- 0.6; 4.4 +/- 1.2; and 4.6 +/- 0.8, P < 0.001).
  • The expression values (p53, BCL-2, and hMSH2) were statistically significantly higher (P < 0.05) in astrocytomas (Grade III) than in other gliomas.
  • [MeSH-major] Brain Neoplasms / chemistry. Gene Expression Regulation, Neoplastic. Glioma / chemistry. MutS Homolog 2 Protein / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Astrocytoma / chemistry. Brain Chemistry. Case-Control Studies. Gliosis / metabolism. Humans. Immunohistochemistry / methods

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  • (PMID = 16875495.001).
  • [ISSN] 0959-9673
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
  • [Other-IDs] NLM/ PMC2517375
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4. Matusan-Ilijas K, Behrem S, Jonjic N, Zarkovic K, Lucin K: Osteopontin expression correlates with angiogenesis and survival in malignant astrocytoma. Pathol Oncol Res; 2008 Sep;14(3):293-8
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  • [Title] Osteopontin expression correlates with angiogenesis and survival in malignant astrocytoma.
  • The aim of the study was to analyze the expression of OPN in human astrocytomas and to correlate it with angiogenesis and patients' outcome.
  • Seventy-six human astrocytomas including eight pilocytic astrocytomas (grade I), 10 diffuse astrocytomas (grade II), 8 anaplastic astrocytomas (grade III) and 50 glioblastomas (grade IV) were immunohistochemically stained for OPN protein.
  • Astrocytomas were heterogeneous regarding the OPN expression.
  • Our results indicate the overexpression of OPN protein in astrocytoma cells and suggest the role of OPN in astrocytoma progression and angiogenesis.
  • [MeSH-major] Astrocytoma / blood supply. Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / blood supply. Brain Neoplasms / metabolism. Neovascularization, Pathologic / metabolism. Osteopontin / metabolism

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  • (PMID = 18493866.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 106441-73-0 / Osteopontin
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5. Nafe R, Schlote W, Schneider B: Histomorphometry of tumour cell nuclei in astrocytomas using shape analysis, densitometry and topometric analysis. Neuropathol Appl Neurobiol; 2005 Feb;31(1):34-44
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  • [Title] Histomorphometry of tumour cell nuclei in astrocytomas using shape analysis, densitometry and topometric analysis.
  • Although tumour cell nuclei are important histological structures for grading of astrocytomas according to the WHO-classification of brain tumours, there is no reported morphometric study of astrocytomas which describes quantitatively the four main morphologic criteria of tumour cell nuclei: size, shape, texture (densitometric characteristics) and spatial relationships between the nuclei (topometric analysis).
  • Using a set of morphometric parameters describing these criteria as well as the Ki67-proliferation index, 74 astrocytomas from 74 patients were studied by means of a digital image analysis system.
  • The objective of the study was to test, if these morphometric parameters were sufficient for statistical discrimination between pilocytic astrocytomas WHO-grade I, astrocytomas grade II and anaplastic astrocytomas grade III.
  • Our results showed a correct reclassification of 97.3% (72/74) of the cases with respect to the tumour grade by means of cross-validated discriminant analysis.
  • In conclusion, the present morphometric procedure provided good discrimination between the tumour grades, supporting the view that histomorphometry of tumour cell nuclei could be a valuable tool for grading of astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / ultrastructure. Brain Neoplasms / pathology. Brain Neoplasms / ultrastructure. Cell Nucleus / pathology. Cell Nucleus / ultrastructure

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  • (PMID = 15634229.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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6. Marsh J, Mukherjee P, Seyfried TN: Drug/diet synergy for managing malignant astrocytoma in mice: 2-deoxy-D-glucose and the restricted ketogenic diet. Nutr Metab (Lond); 2008 Nov 25;5:33
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  • [Title] Drug/diet synergy for managing malignant astrocytoma in mice: 2-deoxy-D-glucose and the restricted ketogenic diet.
  • BACKGROUND: Astrocytomas are largely dependent on glycolysis to satisfy their bioenergetic requirements for growth and survival.
  • Therapies that target glycolysis can potentially manage astrocytoma growth and progression.
  • Dietary restriction of the high fat/low carbohydrate ketogenic diet (KD-R) reduces glycolysis and is effective in managing experimental mouse and human astrocytomas.
  • The goal here was to determine if low doses of 2-DG could act synergistically with the KD-R to better manage growth of the CT-2A malignant mouse astrocytoma.
  • METHODS: The therapeutic effect of a KD-R supplemented with a low dose of 2-DG (25 mg/kg) was examined in adult C57BL/6J mice bearing the syngeneic CT-2A malignant astrocytoma grown orthotopically.
  • Mice were fed the standard unrestricted diet for the first 3 days after tumor implantation prior to their separation into one of four diet groups fed either a standard rodent diet in unrestricted amounts (SD-UR) or a KD-R with or without 2-DG for 10 days.
  • 2-DG was initiated 6 days after tumor implantation and was continued for 7 days.
  • RESULTS: Energy intake, body weights, and CT-2A tumor weights were similar in the SD-UR and the SD-UR+2-2DG mouse groups over the dietary treatment period (days 3-13).
  • Tumor weights were about 48% and 80% lower in the KD-R and in the KD-R+2-DG groups, respectively, than in the SD-UR group.
  • CONCLUSION: Astrocytoma growth was reduced more in the KD-R mouse group supplemented with 2-DG than in the mouse groups receiving either dietary restriction or 2-DG alone, indicating a synergistic interaction between the drug and the diet.
  • The results suggest that management of malignant astrocytoma with restricted ketogenic diets could be enhanced when combined with drugs that inhibit glycolysis.

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  • (PMID = 19032781.001).
  • [ISSN] 1743-7075
  • [Journal-full-title] Nutrition & metabolism
  • [ISO-abbreviation] Nutr Metab (Lond)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102135; United States / NINDS NIH HHS / NS / R01 NS055195; United States / NINDS NIH HHS / NS / R56 NS055195
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2607273
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7. Rao SA, Santosh V, Somasundaram K: Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma. Mod Pathol; 2010 Oct;23(10):1404-17
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  • [Title] Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma.
  • Malignant astrocytoma includes anaplastic astrocytoma (grade III) and glioblastoma (grade IV).
  • Among them, glioblastoma is the most common primary brain tumor with dismal responses to all therapeutic modalities.
  • We performed a large-scale, genome-wide microRNA (miRNA) (n=756) expression profiling of 26 glioblastoma, 13 anaplastic astrocytoma and 7 normal brain samples with an aim to find deregulated miRNA in malignant astrocytoma.
  • More importantly, we identified a most discriminatory 23-miRNA expression signature, by using PAM, which precisely distinguished glioblastoma from anaplastic astrocytoma with an accuracy of 95%.
  • The differential expression pattern of nine miRNAs was further validated by real-time RT-PCR on an independent set of malignant astrocytomas (n=72) and normal samples (n=7).
  • Thus we have identified the miRNA expression signature for malignant astrocytoma, in particular glioblastoma, and showed the miRNA involvement and their importance in astrocytoma development.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. MicroRNAs / genetics

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  • (PMID = 20711171.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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8. Khwaja FW, Duke-Cohan JS, Brat DJ, Van Meir EG: Attractin is elevated in the cerebrospinal fluid of patients with malignant astrocytoma and mediates glioma cell migration. Clin Cancer Res; 2006 Nov 1;12(21):6331-6
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  • [Title] Attractin is elevated in the cerebrospinal fluid of patients with malignant astrocytoma and mediates glioma cell migration.
  • The goal of our study was to find reliable markers that could be used for disease monitoring as well as to identify new targets for the therapeutic intervention for malignant astrocytoma (WHO grades 3 and 4).
  • EXPERIMENTAL DESIGN: We employed proteomic techniques to identify secreted proteins in the cerebrospinal fluid that were specific to patients with malignant astrocytoma.
  • RESULTS: Among 60 cerebrospinal fluid samples of patients with various central nervous system diseases, attractin was consistently found to be elevated in the samples of patients with malignant astrocytoma.
  • To independently validate these results, we examined attractin expression in a new set of 108 normal and tumoral brain tissue specimens and found elevated expression in 97% of malignant astrocytomas, with the highest levels in grade 4 tumors.
  • Using immunohistochemistry, we further showed that attractin is produced and secreted by the tumor cells.
  • Finally, we showed that cerebrospinal fluid from brain tumor patients induces glioma cell migration and that attractin is largely responsible for this promigratory activity.
  • CONCLUSIONS: Our results find attractin to be a reliable secreted marker for high-grade gliomas.
  • Additionally, our migration studies suggest that it may be an important mediator of tumor invasiveness, and thus, a potential target in future therapies.
  • [MeSH-major] Astrocytoma / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Cell Movement / physiology. Glioma / cerebrospinal fluid. Membrane Proteins / cerebrospinal fluid
  • [MeSH-minor] Blotting, Western. Electrophoresis, Gel, Two-Dimensional. Humans. Immunohistochemistry. Neoplasm Invasiveness

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  • (PMID = 17085642.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 86335
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATRN protein, human; 0 / Membrane Proteins
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9. Yamamoto Y, Nishiyama Y, Kimura N, Kameyama R, Kawai N, Hatakeyama T, Kaji M, Ohkawa M: 11C-acetate PET in the evaluation of brain glioma: comparison with 11C-methionine and 18F-FDG-PET. Mol Imaging Biol; 2008 Sep;10(5):281-7
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  • Five patients had low-grade gliomas (grade II), three had anaplastic astrocytomas (grade III), and seven had glioblastomas (grade IV).
  • For semiquantitative analysis, the standardized uptake value (SUV) and tumor to contralateral normal gray matter (T/N) ratio were calculated.
  • The sensitivity for detection of high-grade gliomas was calculated using visual analysis.
  • ACE and FDG SUV in high-grade gliomas were significantly higher than that in low-grade gliomas.
  • CONCLUSIONS: ACE PET is a potentially useful radiotracer for detecting brain gliomas and differentiating high-grade gliomas.

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  • [CommentIn] Mol Imaging Biol. 2009 Jul-Aug;11(4):223 [19326176.001]
  • (PMID = 18543041.001).
  • [ISSN] 1536-1632
  • [Journal-full-title] Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging
  • [ISO-abbreviation] Mol Imaging Biol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetates; 0 / Carbon Isotopes; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AE28F7PNPL / Methionine
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10. Lapointe M, Lanthier J, Moumdjian R, Régina A, Desrosiers RR: Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors. Brain Res Mol Brain Res; 2005 Apr 27;135(1-2):93-103
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  • [Title] Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors.
  • Here we investigated PIMT regulation in astrocytic tumors, which are the most common human brain tumors.
  • PIMT expression and enzyme activity were significantly decreased in all grades of human astrocytic tumors.
  • More precisely, PIMT levels were significantly lower by 76% in pilocytic astrocytomas (grade I), 46% in astrocytomas (grade II), 69% in anaplastic astrocytomas (grade III), and a marked 80% in glioblastomas (grade IV) as compared to normal brains.
  • RT-PCR analysis showed that levels of type I PIMT mRNA were up-regulated while those of type II PIMT mRNA were down-regulated in glioblastomas.
  • Furthermore, the reduced PIMT levels correlated closely with a decrease in the number of neuron cells in astrocytic tumors as assessed by measuring the neuron-specific enolase level.
  • Many proteins with abnormal aspartyl residues accumulated in brain tumors and some were specific to individual grades of astrocytic tumors.
  • Similar results were obtained, either by measuring the reduction in PIMT activity and expression or by measuring the formation of abnormal proteins, in an orthotopic rat brain tumor model implanted with invasive CNS-1 glioma cells.
  • The novelty of these findings was to provide the first evidence for a marked reduction of PIMT expression and activity during stage progression of astrocytic tumors in humans.
  • [MeSH-minor] Animals. Blotting, Northern. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry / methods. Male. Methylation. Neoplasm Transplantation / methods. Phosphopyruvate Hydratase / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred Lew. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 15857672.001).
  • [ISSN] 0169-328X
  • [Journal-full-title] Brain research. Molecular brain research
  • [ISO-abbreviation] Brain Res. Mol. Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / RNA, Messenger; EC 2.1.1.77 / Protein D-Aspartate-L-Isoaspartate Methyltransferase; EC 4.2.1.11 / Phosphopyruvate Hydratase
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11. Ren ZP, Olofsson T, Qu M, Hesselager G, Soussi T, Kalimo H, Smits A, Nistér M: Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors. J Neuropathol Exp Neurol; 2007 Oct;66(10):944-54
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  • [Title] Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors.
  • We investigated genetic heterogeneity of astrocytic gliomas using p53 gene mutations as a marker.
  • Different parts of morphologically heterogeneous astrocytic gliomas were microdissected, and direct DNA sequencing of p53 gene exons 5 through 8 was performed.
  • Thirty-five glioma samples and tumor-adjacent normal-appearing brain tissue from 11 patients were analyzed.
  • The mutations were present in grade II, III, and IV astrocytic glioma areas.
  • Both severe functionally dead mutants and mutants with remaining transcriptional activity could be observed in the same tumor.
  • Coexistence of p53 gene mutations and the locus of heterozygosity was common, at least in astrocytomas grade III and in glioblastomas, and also occurred in astrocytoma grade II areas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, p53 / genetics
  • [MeSH-minor] Adult. Aged. DNA Primers. DNA, Neoplasm / genetics. Female. Gene Frequency. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Microdissection. Middle Aged. Mutation / genetics. Mutation / physiology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17917588.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm
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12. Ohnishi M, Matsumoto T, Nagashio R, Kageyama T, Utsuki S, Oka H, Okayasu I, Sato Y: Proteomics of tumor-specific proteins in cerebrospinal fluid of patients with astrocytoma: usefulness of gelsolin protein. Pathol Int; 2009 Nov;59(11):797-803
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  • [Title] Proteomics of tumor-specific proteins in cerebrospinal fluid of patients with astrocytoma: usefulness of gelsolin protein.
  • Changes in cerebrospinal fluid (CSF) composition have been shown to accurately reflect pathological processes in the CNS, and are potential indicators of abnormal CNS states, such as tumor growth.
  • To detect biomarkers in high-grade astrocytomas, the differential expression of proteins in the cerebrospinal fluid was analyzed from two cases each of diffuse astrocytoma (grade II), and glioblastoma (grade IV) using agarose 2-D gel electrophoresis (2-DE).
  • It was found that the expression of gelsolin protein decreased with histological grade.
  • To examine whether gelsolin is a useful indicator of tumor aggressiveness or patient outcome, its expression was further studied on immunohistochemistry in 41 formalin-fixed and paraffin-embedded astrocytomas.
  • The positive cell rate of gelsolin in tumors was 59.4% in grade II, 30.0% in grade III and 29.4% in grade IV, respectively.
  • Gelsolin expression was significantly lower in high-grade astrocytomas (grade III or IV) than in low-grade astrocytomas (grade II; P < 0.05).
  • Moreover, in astrocytomas the overall survival of patients in the low-expression group was significantly poorer than in the high expression group (P < 0.05).
  • These data suggest that gelsolin is a prognostic factor in astrocytoma.
  • [MeSH-major] Astrocytoma / cerebrospinal fluid. Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Gelsolin / cerebrospinal fluid

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  • (PMID = 19883430.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Gelsolin
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13. Faria MH, Gonçalves BP, do Patrocínio RM, de Moraes-Filho MO, Rabenhorst SH: Expression of Ki-67, topoisomerase IIalpha and c-MYC in astrocytic tumors: correlation with the histopathological grade and proliferative status. Neuropathology; 2006 Dec;26(6):519-27
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  • [Title] Expression of Ki-67, topoisomerase IIalpha and c-MYC in astrocytic tumors: correlation with the histopathological grade and proliferative status.
  • Astrocytomas represent the most frequent primary tumors of the central nervous system.
  • Recently, the determination of the proliferative index of astrocytic tumors by different methods has been proposed as a valuable tool for tumor grading and also as a prognostic marker.
  • The aim of the present study was to evaluate the expression of cell proliferation-related proteins in human astrocytic tumors of different histopathological grades (WHO).
  • An immunohistochemical study of the Ki-67, Topoisomerase IIalpha (Topo IIalpha) and c-MYC proteins using the avidin-biotin-peroxidase method was performed in 55 astrocytomas (13 grade I, 14 grade II, 7 grade III and 21 grade IV) and five samples of non-tumor brain tissue (control group).
  • Ki-67, Topo IIalpha and c-MYC positive indices tended to increase according to malignant progression, were absent in non-tumor brain tissue and showed maximum values in high-grade astrocytomas (III and IV).
  • Ki-67 antigen detection in more than 8.0% of the tumor cells distinguished astrocytoma grade IV, while a labeling index between 1.5 and 8.0% characterized astrocytomas grade III and values below 1.5% discriminated low-grade tumors (I and II).
  • These results indicate that Topo IIalpha and c-MYC expression is associated with cell proliferation in astrocytomas, although not in an exclusive way.
  • Moreover, Ki-67 antigen was found to be the best marker of cellular proliferation, and its expression predicts the grade of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, Neoplasm / metabolism. Cell Division. Child. Child, Preschool. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. Female. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. Infant. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins c-myc / metabolism

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  • (PMID = 17203587.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-myc; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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14. Karrasch M, Gillespie GY, Braz E, Liechty PG, Nabors LB, Lakeman AD, Palmer CA, Parker JN, Whitley RJ, Markert JM: Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results. J Clin Oncol; 2009 May 20;27(15_suppl):2042

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

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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas.
  • : e13037 Background: Anaplastic astrocytoma (AA), oligodendroglioma (AOD), and oligoastrocytoma (AOA) are rare tumors showing variable outcome due to their histological heterogeneity and different chemo- and radio-sensitivity.
  • Currently, the addition of chemotherapy to radiotherapy (RT) for newly diagnosed anaplastic gliomas is not sustained by available data.
  • We evaluated the addition of temozolomide (TMZ) to radiotherapy for newly diagnosed anaplastic gliomas in terms of tolerability, progression-free survival (PFS), and overall survival (OS).
  • METHODS: Since September 2004, following initial surgery, patients (pts) with histologically confirmed anaplastic glioma, Karnofsky Performance Status (KPS) ≥40, adequate organ function, no prior chemotherapy, were treated with RT to limited fields once daily at 2 Gy per fraction, 5 days a week, for a total of 60 Gy with concomitant TMZ (75 mg/m<sup>2</sup> for 7 days a week) followed by 6 cycles of maintenance TMZ at 200 mg/m<sup>2</sup> on days 1-5 every 28 days.
  • Nine pts (32%) underwent tumor complete resection, 10 partial resection (36%), and 9 (32%) tumor biopsy.
  • Frequent mild toxicities were grade 1-2 nausea/vomiting (17 pts-63%), and grade 1-2 asthenia (8 pts-30%).
  • CONCLUSIONS: The addition of temozolomide to radiation therapy for newly diagnosed anaplastic gliomas is well tolerated and seems active; efficacy needs confirmation in a randomized clinical trial.

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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma.
  • : e13018 Background: The study was aimed to evaluate the efficacy of TMZ on a protracted dose-dense schedule after standard 5-day TMZ regimen in patients with progressive high-grade glioma.
  • METHODS: In this phase II prospective study, patients who had progression on standard 5-day TMZ for recurrence (group 1) or recurrence after concurrent radiotherapy+TMZ and ≥ 2 cycles of adjuvant TMZ (group 2) for high-grade glioma received TMZ 100 mg/m2× 21 q28 days until progression according to MacDonald's criteria.
  • The histopathology was glioblastoma in 18 and grade 3 glioma (anaplastic astrocytoma, anaplastic oligoastrocytoma or anaplastic oligodendroglioma) in 7.
  • Out of 80 cycles received there was no anemia; 5 (6%) grade 1, 8 (10%) grade 2, 2 (3%) grade 3 leucopenia; 1 (1%) grade 1, 2 (3%) grade 2, 1 (1%) grade 3, 1 (1%) grade 4 thrombocytopenia; 9 (11%) grade 1, 7 (9%) grade 2, 32 (40%) grade 3, and 11 (14%) grade 4 lymphopenia.
  • Study was terminated in 2 patients (one with grade 4 thrombocytopenia and the other with grade 4 hepatic toxicity).

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  • (PMID = 27962826.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Herndon J 2nd, Vredenburgh J, Reardon D, Desjardins A, Peters K, Gururangan S, Norfleet J, Friedman A, Bigner D, Friedman HS: Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13016

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  • [Title] Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas.
  • : e13016 Background: Recurrent malignant gliomas have a poor prognosis, with a median survival of 6-15 months, with grade 4 glioblastomas more aggressive than grade 3 anaplastic astrocytomas or oligodendrogliomas.
  • We report a phase I trial of vandetanib in combination with oral etoposide for recurrent malignant glioma.
  • METHODS: Patients with histologically documented recurrent grade 3 or grade 4 malignant glioma were eligible.
  • There was more hematologic toxicity than expected, with 3/6 of the patients enrolled at dose level 1 developing grade 4 neutropenia.

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  • (PMID = 27962830.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Potthast L, Chowdhary S, Pan E, Yu D, Zhu W, Brem S: The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab.
  • Histologies included glioblastoma (GB), anaplastic astrocytomas (AA), anaplastic oligodendrogliomas (AO), anaplastic oligoastrocytomas (AOA), and low-grade astrocytomas.
  • It is unclear why the disparity among this subset of patients occurs, however, we hypothesize that this may once again highlight the distinct tumor biology among young glioma patients.

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  • (PMID = 27964663.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Desjardins A, Reardon DA, Gururangan S, Peters K, Threatt S, Friedman A, Friedman H, Vredenburgh J: Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG). J Clin Oncol; 2009 May 20;27(15_suppl):e13004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG).
  • METHODS: Eligibility included: adult patients with stable or recurrent MG (GBM, anaplastic astrocytoma [AA], anaplastic oligodendroglioma [AO]) previously treated with radiation therapy (RT) and with or without chemotherapy; interval of at least two weeks between prior RT, or four weeks between prior chemotherapy; Karnofsky ≥ 60%; and adequate hematologic, renal and liver function.
  • Dose-limiting toxicities were: deep venous thrombosis (1 grade 3); nausea and vomiting (1 grade 3); diarrhea (1 grade 3); elevated ALT (1 grade 3); elevated creatinine (1 grade 3); and fatigue (1 grade 3).

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  • (PMID = 27962751.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Franceschi E, Tosoni A, Ermani M, Spagnolli F, La Torre L, Galzio RJ, Pozzati E, Talacchi A, Benevento F, Brandes AA: Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13003

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

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  • (PMID = 27962754.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Tosoni A, Franceschi E, Ermani M, Bacci A, Volpin L, Lombardo L, Ravenna G, Pinna G, Poggi R, Brandes AA: MGMT methylation status as a prognostic factor in anaplastic astrocytomas. J Clin Oncol; 2009 May 20;27(15_suppl):2052

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  • [Title] MGMT methylation status as a prognostic factor in anaplastic astrocytomas.
  • However, further data on the epigenetic feature are needed before its role in rare diseases such as anaplastic astrocytomas (AA) can be established.

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  • (PMID = 27964674.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Hlobilkova A, Ehrmann J, Sedlakova E, Krejci V, Knizetova P, Fiuraskova M, Kala M, Kalita O, Kolar Z: Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression? Neoplasma; 2007;54(4):334-41
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  • [Title] Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression?
  • The most frequent alterations found in astrocytomas are two major groups of signaling proteins: the cell cycle and the growth factor-regulated signaling pathways.
  • The aim of our study was to detect changes in expression of the following proteins: the tumor suppressors PTEN, p53, and p21Waf1/Cip1, glial fibrillary acidic protein (GFAP, as a marker of astroglial differentiation), the phosphorylated form of protein kinase B/Akt (PKB/Akt), which is downstream to the epidermal growth factor receptor (EGFR), and MDM2, which degrades p53.
  • Paraffin-embedded astrocytoma tissue samples from 89 patients were divided into low grade (grade I-II; 42 samples) and high grade astrocytomas (grade III-IV; 47 samples).
  • EGFR protein was detected in 29 % of low grade and in 60 % of high grade astrocytomas.
  • The expression of phosphorylated PKB/Akt was found in roughly the same proportions: in 86% of low grade and in 79% of high grade astrocytomas.
  • PTEN was not found in most of astrocytomas, 64% of low grade and 74% of high grade tumors showed no PTEN staining.
  • Overexpression of the mutated form of p53 or loss of p53 expression, however, was found in about 63% in both groups of astrocytomas with no differences between them.
  • GFAP expression was decreased in tumor astrocytes compared to normal astrocytes and this decreased with grading.
  • GFAP positive tumor cells were detected in only 50% of low grade, and 32% of high grade astrocytomas.
  • Loss of p21Waf1/Cip1 expression was shown in 20% of low and in 45% of high grade tumors.
  • In the subgroup of high grade tumors with wild type p53, 86% showed p21Waf1/Cip1 expression, whereas in the subgroup of high grade tumors with altered p53, only 35% displayed p21Waf1/Cip1.
  • We conclude that EGFR expression increases with astrocytoma grading.
  • PTEN defects may also participate in aggressive tumor behaviour through activation of the PKB/Akt pathway.
  • The alteration of p53 supports the finding that the cell cycle regulation is also disrupted during development of astrocytomas.
  • EGFR is one of the factors, which drives the progression of astrocytomas from low to high grade stage.
  • [MeSH-major] Astrocytoma / metabolism. Cell Cycle. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Mutation / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / pathology. PTEN Phosphohydrolase / metabolism. Phosphorylation. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17822324.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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23. Rudnick JD, Phuphanich S, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Black KL, Wheeler C, Yu J: A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma.
  • : 2033 Background: Our prior immunotherapy trials demonstrated efficacy in generating a tumor specific immune response in malignant glioma and the potential for high tumor-specific toxicity and sustained tumoricidal activity.
  • METHODS: We exploited this synergistic effect to maintain a cytotoxic environment around the tumor milieu.
  • Patients with high-grade glioma were eligible after maximal resection with biodegradable carmustine (BCNU) wafer placement.
  • Screening leukapheresis is used to isolate mononuclear cells which are differentiated into dendritic cells, pulsed with tumor lysate, and then 3 intradermal vaccines are administered at 2-week intervals.
  • The histology included 3 newly diagnosed glioblastoma multiforme (GBM), 8 recurrent GBM, 2 newly diagnosed anaplastic astrocytoma (AA), and 2 recurrent AA.
  • Our preliminary data on 15 patients and 39 courses of Dendritic Cell vaccines demonstrate one grade 3 toxicity of fever/chest pain.
  • CONCLUSIONS: This phase I study demonstrates the safety, feasibility of dendritic cell vaccination with biodegradable carmustine (BCNU) wafers with one grade 3 AE.

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  • (PMID = 27964627.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Khalatbari M, Borghei-Razavi H, Shayanfar N, Behzadi AH, Sepehrnia A: Collision tumor of meningioma and malignant astrocytoma. Pediatr Neurosurg; 2010;46(5):357-61
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  • [Title] Collision tumor of meningioma and malignant astrocytoma.
  • The pathology of tumors reported collision tumors composed of meningioma and malignant astrocytoma.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Meningeal Neoplasms / surgery. Meningioma / surgery

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  • [Copyright] Copyright © 2011 S. Karger AG, Basel.
  • (PMID = 21389747.001).
  • [ISSN] 1423-0305
  • [Journal-full-title] Pediatric neurosurgery
  • [ISO-abbreviation] Pediatr Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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25. Momota H, Narita Y, Matsushita Y, Miyakita Y, Shibui S: p53 abnormality and tumor invasion in patients with malignant astrocytoma. Brain Tumor Pathol; 2010 Oct;27(2):95-101
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  • [Title] p53 abnormality and tumor invasion in patients with malignant astrocytoma.
  • Malignant astrocytomas are characterized by diffusely infiltrating nature, and the abnormality of p53 is a cytogenetic hallmark of astrocytic tumors.
  • To elucidate the relationship between p53 abnormality and invasiveness of the tumors, we studied mutation and protein expression of p53 in 48 consecutive patients with malignant astrocytoma (14 anaplastic astrocytomas and 34 glioblastoma multiformes).
  • The tumors were classified into three categories according to the features of magnetic resonance imaging, and 5, 7, and 36 tumors were classified into diffuse, multiple, and single type, respectively.
  • We then examined how these tumor types correlate with MIB-1 staining index, TP53 gene mutation, and p53 protein expression.
  • Furthermore, diffuse- and multiple-type tumors were significantly correlated with poor progression-free survival, whereas only multiple-type tumors were significantly correlated with poor overall survival.
  • As diffuse and multiple features on imaging modalities represent invasive characteristics of the tumors, p53 abnormalities may affect the invasive and aggressive nature of malignant astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Genes, p53 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. DNA, Neoplasm / genetics. Female. Glial Fibrillary Acidic Protein / genetics. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Mitotic Index. Mutation / genetics. Mutation / physiology. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Survival Analysis. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / metabolism. Young Adult

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  • (PMID = 21046311.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A
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26. Ryu HH, Jung S, Sun HS, Jung TY, Jin SG, Jin YH, Kim IY, Jeong YI, Kang SS: Screening for motility-associated genes in malignant astrocytoma cell lines. J Neurooncol; 2007 Apr;82(2):125-31
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  • [Title] Screening for motility-associated genes in malignant astrocytoma cell lines.
  • The most characteristic feature of a malignant astrocytoma is its early and extensive infiltration into adjacent parenchymal structures.
  • We focused on detecting the possible expression changes as the determining factors for malignant astrocytoma's motile ability.
  • These findings suggest that the genes identified may be important for determining high motility in astrocytoma cell lines.
  • These findings may help us understand the molecular invasion mechanism in astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Cell Movement. Gene Expression Profiling
  • [MeSH-minor] Humans. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17048098.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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27. Walker DG, Laherty R, Tomlinson FH, Chuah T, Schmidt C: Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy. J Clin Neurosci; 2008 Feb;15(2):114-21
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  • [Title] Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy.
  • Dendritic cell vaccination has been applied to the treatment of a variety of cancers, including malignant astrocytoma.
  • We have treated 13 patients with malignant astrocytoma using dendritic cell vaccination and have shown that this treatment is safe and is likely to be effective in combination with standard adjuvant therapy.
  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Chemotherapy, Adjuvant / methods. Dendritic Cells / immunology. Immunotherapy, Active / methods

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  • (PMID = 18083572.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD8; 0 / Cancer Vaccines; EC 3.1.3.48 / Antigens, CD45
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28. Parafiniuk D, Jezewski D, Nowacki P: [Malignant astrocytoma as a recurrance of astrocytoma II WHO after 13 years. Case report and literature review]. Ann Acad Med Stetin; 2010;56(2):45-50
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  • [Title] [Malignant astrocytoma as a recurrance of astrocytoma II WHO after 13 years. Case report and literature review].
  • Astrocytomas--neroepithelial originated tumors that belong to the big, differential group of tumors, which derive from astrocytic glial.
  • They include slow growing tumors such as fibillary astrocytoma or very malignant glioblastoma multiforme.
  • The case which is being presented is of a forty nine year old woman operated in July 1997 because of a protoplasmic astrocytoma II WHO in the left frontal lobe.
  • Due to this adverse event MRI was ordered and suspicion of tumor recurrence was put forward.
  • Histopathology identified anaplastic astrocytoma III WHO.
  • According to literature, the factors regarding remission time, tumor malignancy and therapeutic aim were analyzed.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / diagnosis
  • [MeSH-minor] Adult. Astrocytoma. Female. Frontal Lobe. Humans. Reoperation. Seizures / etiology

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  • (PMID = 21473001.001).
  • [ISSN] 1427-440X
  • [Journal-full-title] Annales Academiae Medicae Stetinensis
  • [ISO-abbreviation] Ann Acad Med Stetin
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Poland
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29. Combs SE, Gutwein S, Thilmann C, Debus J, Schulz-Ertner D: Reirradiation of recurrent WHO grade III astrocytomas using fractionated stereotactic radiotherapy (FSRT). Strahlenther Onkol; 2005 Dec;181(12):768-73
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  • [Title] Reirradiation of recurrent WHO grade III astrocytomas using fractionated stereotactic radiotherapy (FSRT).
  • PURPOSE: To assess the effect of reirradiation in recurrent WHO grade III astrocytomas.
  • PATIENTS AND METHODS: From January 1995 to July 2003, 40 patients with grade III gliomas were treated with fractionated stereotactic reirradiation at the time point of recurrence.
  • No toxicities > CTC grade 2 developed.
  • CONCLUSION: Fractionated stereotactic radiotherapy is well tolerated and effective in patients with recurrent grade III astrocytomas.
  • [MeSH-major] Astrocytoma / mortality. Astrocytoma / surgery. Brain Neoplasms / mortality. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / surgery. Radiosurgery / statistics & numerical data

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  • (PMID = 16362786.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
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30. Nano R, Capelli E, Facoetti A, Benericetti E: Immunobiological and experimental aspects of malignant astrocytoma. Anticancer Res; 2009 Jul;29(7):2461-5
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  • [Title] Immunobiological and experimental aspects of malignant astrocytoma.
  • Starting from 1992, the goal of our studies was to obtain new biological data on malignant astrocytomas to better understand the basic biology of the tumour and these are reviewed here.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology

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  • (PMID = 19596914.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interleukin-2
  • [Number-of-references] 51
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31. Jayawardena S, Sooriabalan D, Indulkar S, Kim HH, Matin A, Maini A: Regression of grade III astrocytoma during the treatment of CML with imatinib mesylate. Am J Ther; 2006 Sep-Oct;13(5):458-9
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  • [Title] Regression of grade III astrocytoma during the treatment of CML with imatinib mesylate.
  • Astrocytomas are central nervous system neoplasms, which are derived predominately from astrocytes.
  • On the basis of the histopathologic characteristics astrocytomas are graded from I to IV.
  • The cells that demonstrate the greatest degree of anaplasia are used to determine the histologic grade of the tumor.
  • The mean age of survival are approximately 10 years from the time of diagnosis for pilocystic astrocytomas (World Health Organization grade I), more than 5 years for patients with low-grade diffuse astrocytomas (WHO grade II), 2 to 5 years for those with anaplastic astrocytomas (WHO grade III), and less than 1 year for patients with glioblastoma (WHO grade IV).
  • The treatment is a combination of surgery, radiation, and chemotherapy depending of the grade of astrocytoma.
  • We present a case of 31-year-old man with grade III astrocytoma with subsequent chronic myelogenous leukemia treated with imatinib mesylate as part of his chronic myelogenous leukemia treatment failing to show recurrence of the astrocytoma 10 years after standard treatment for astrocytoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 16988542.001).
  • [ISSN] 1075-2765
  • [Journal-full-title] American journal of therapeutics
  • [ISO-abbreviation] Am J Ther
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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32. Jang SY, Kong MH, Song KY, Frazee JG: Intracranial Metastases of Cervical Intramedullary Low-Grade Astrocytoma without Malignant Transformation in Adult. J Korean Neurosurg Soc; 2009 Jun;45(6):381-5

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  • [Title] Intracranial Metastases of Cervical Intramedullary Low-Grade Astrocytoma without Malignant Transformation in Adult.
  • The first case of intracranial metastases of a cervical intramedullary low-grade astrocytoma without malignant transformation in adult is presented in this report.
  • Seven years ago, a 45 year-old male patient underwent biopsy to confirm pathologic characteristics and received craniocervical radiation and chemotherapy for a grade II astrocytoma in the cervical spinal cord.
  • The tumor at the cervical and brain lesions was classified as an astrocytoma (WHO grade II).
  • When a patient with low-grade astrocytoma in the spinal cord has new cranial symptoms after surgery, radiaton, and chemotherapy, the possibility of its metastasis should be suspected because it can spread to the intracranial cavity even without malignant transformation as shown in this case.

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  • (PMID = 19609424.001).
  • [ISSN] 2005-3711
  • [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/ PMC2711238
  • [Keywords] NOTNLM ; Astrocytoma / Cranial metastases / Intramedullary / Spinal cord tumor
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33. Guan X, Lai S, Lackey J, Shi J, Techavipoo U, Moulding HD, Flanders AE, Andrews DW: Revisiting anaplastic astrocytomas II: further characterization of an expansive growth pattern with visually enhanced diffusion tensor imaging. J Magn Reson Imaging; 2008 Dec;28(6):1322-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Revisiting anaplastic astrocytomas II: further characterization of an expansive growth pattern with visually enhanced diffusion tensor imaging.
  • PURPOSE: To seek to distinguish and visualize the different magnetic resonance imaging (MRI) growth patterns among malignant gliomas utilizing visually enhanced diffusion tensor imaging (DTI).
  • MATERIALS AND METHODS: Nineteen consecutive patients undergoing image-guided resection of a newly diagnosed malignant glioma underwent add-on acquisition of DTI data based on an Institutional Review Board (IRB)-approved imaging protocol during preoperative MRI scans for routine intraoperative image guidance.
  • Tumor growth patterns were assigned to expansive or mixed/infiltrative classes as described in the companion article (24).
  • Infiltrating tumors were WHO Grade IV astrocytomas and all expansive tumors were either WHO Grade III astrocytomas or WHO Grade II astrocytomas.
  • DTI-based white matter tractography was conducted and the DTI data were fused with anatomical images using an in-house software package we developed to enhance the visualization of the tumor/fiber interface.
  • RESULTS: Out of the 19 tumor patients studied, 11 had infiltrative tumors and the other 8 had expansive tumors.
  • While less clear with 2D axial diffusion color maps, visually enhanced 3D reconstructions of the tumor/fiber interface successfully corroborated distinctive growth patterns.
  • This was particularly evident when viewed in 3D video loops of each tumor/fiber interface.
  • CONCLUSION: We have successfully developed software that visually enhances the anatomic details of the tumor/fiber interface in patients with anaplastic astrocytomas.
  • These data support the existence of a subgroup of patients within the WHO Grade III classification with expansive tumors and a significantly better prognosis.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods. Image Enhancement / methods. Image Processing, Computer-Assisted
  • [MeSH-minor] Adult. Aged. Female. Humans. Imaging, Three-Dimensional. Magnetic Resonance Imaging, Interventional. Male. Middle Aged. Neoplasm Staging

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 19025901.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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34. Maiti AK, Ghosh K, Chatterjee U, Chakrobarti S, Chatterjee S, Basu S: Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas. Neurol India; 2008 Oct-Dec;56(4):456-62
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  • [Title] Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas.
  • AIMS: The involvement of various growth factors, growth factor receptors and proliferative markers in the molecular pathogenesis of astrocytic neoplasms are being studied extensively.
  • Since EGFR and proliferating cell nuclear antigen (PCNA) are involved in mitogenic signal transduction and cellular proliferation pathway, we have studied the correlation between the expression of EGFR and PCNA labeling index in astrocytic tumors.
  • MATERIALS AND METHODS: We investigated the immunohistochemical expression of EGFR and PCNA using the appropriate monoclonal antibodies in 40 cases of astrocytic tumors of which 21 cases were glioblastoma, eight cases were Grade III or anaplastic astrocytomas and six cases were Grade II or diffuse astrocytomas and five cases were Grade I or pilocytic astrocytomas.
  • RESULTS: Both the EGFR expression and PCNA labeling index increase with increasing grades of astrocytomas with a significantly high percentage of cells showing positive staining for both EGFR and PCNA in GBM and Grade III astrocytomas compared to Grade II astrocytomas.
  • The expression levels of both EGFR and PCNA were low in Grade I or pilocytic astrocytomas.
  • CONCLUSIONS: A significant correlation was found between EGFR overexpression and PCNA labeling index in Grade III and Grade II astrocytomas and glioblastoma.
  • These suggest that the tumor proliferation, at least in higher grades of astrocytomas is dependent in some measure on EGF and EGFR-related signaling pathways.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 19127042.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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35. Reardon DA, Rich JN, Friedman HS, Bigner DD: Recent advances in the treatment of malignant astrocytoma. J Clin Oncol; 2006 Mar 10;24(8):1253-65
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  • [Title] Recent advances in the treatment of malignant astrocytoma.
  • Malignant gliomas, including the most common subtype, glioblastoma multiforme (GBM), are among the most devastating of neoplasms.
  • Limited delivery and tumor heterogeneity are two fundamental factors that have critically hindered therapeutic progress.
  • The simultaneous development of multiple advanced therapies based on specific tumor biology may finally offer glioma patients improved survival.
  • [MeSH-major] Astrocytoma / therapy. Central Nervous System Neoplasms / therapy

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  • (PMID = 16525180.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 P20 CA096890; United States / NCI NIH HHS / CA / CA11898; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NINDS NIH HHS / NS / NS20023
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Number-of-references] 209
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36. Kojadinovic Z, Papic V, Cigic T, Vulekovic P, Popovic Lj, Jajic Dj: A new scoring system for malignant astrocytomas. Zentralbl Neurochir; 2008 May;69(2):65-70

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  • [Title] A new scoring system for malignant astrocytomas.
  • BACKGROUND: Currently there are a few scoring systems for malignant astrocytoma, but they are not widely accepted.
  • The aim of this study was to create a scoring system for supratentorial malignant astrocytoma, which could be used in both developed and developing societies.
  • METHODS: This study was performed in 128 patients who had supratentorial malignant astrocytoma (grade III or IV).
  • By using the most appropriate four parameters (age, KPS, initial seizure and histopathological grade) we created a scoring system - MAS (Malignant Astrocytoma Score).
  • CONCLUSIONS: We are of the opinion that MAS represents a useful scoring system to determine the severity of the illness and make a prognosis for both individuals and groups of patients with malignant supratentorial astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Kaplan-Meier Estimate. Karnofsky Performance Status. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Neurosurgical Procedures / mortality. Prognosis. Proportional Hazards Models. ROC Curve. Survival Analysis. Tomography, X-Ray Computed

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  • (PMID = 18444219.001).
  • [ISSN] 0044-4251
  • [Journal-full-title] Zentralblatt für Neurochirurgie
  • [ISO-abbreviation] Zentralbl. Neurochir.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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37. Sathornsumetee S, Cao Y, Marcello JE, Herndon JE 2nd, McLendon RE, Desjardins A, Friedman HS, Dewhirst MW, Vredenburgh JJ, Rich JN: Tumor angiogenic and hypoxic profiles predict radiographic response and survival in malignant astrocytoma patients treated with bevacizumab and irinotecan. J Clin Oncol; 2008 Jan 10;26(2):271-8
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  • [Title] Tumor angiogenic and hypoxic profiles predict radiographic response and survival in malignant astrocytoma patients treated with bevacizumab and irinotecan.
  • PURPOSE: The combination of a vascular endothelial growth factor (VEGF) -neutralizing antibody, bevacizumab, and irinotecan is associated with high radiographic response rates and improved survival outcomes in patients with recurrent malignant gliomas.
  • The aim of these retrospective studies was to evaluate tumor vascularity and expression of components of the VEGF pathway and hypoxic responses as predictive markers for radiographic response and survival benefit from the bevacizumab and irinotecan therapy.
  • PATIENTS AND METHODS: In a phase II trial, 60 patients with recurrent malignant astrocytomas were treated with bevacizumab and irinotecan.
  • Tumor specimens collected at the time of diagnosis were available for further pathologic studies in 45 patients (75%).
  • RESULTS: Of 45 patients, 27 patients had glioblastoma multiforme, and 18 patients had anaplastic astrocytoma.
  • CONCLUSION: In this patient cohort, tumor expression levels of VEGF, the molecular target of bevacizumab, were associated with radiographic response, and the upstream promoter of angiogenesis, hypoxia, determined survival outcome, as measured from treatment initiation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Biomarkers, Tumor / analysis. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Female. Humans. Hypoxia. Male. Middle Aged. Neovascularization, Pathologic. Proportional Hazards Models. Radiography. Retrospective Studies. Survival Analysis. Treatment Outcome. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 18182667.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS054276; United States / NCI NIH HHS / CA / R01 CA116659; United States / NCI NIH HHS / CA / CA116659; United States / NINDS NIH HHS / NS / K02 NS047409; United States / NINDS NIH HHS / NS / NS047409; United States / NINDS NIH HHS / NS / R01 NS054276
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; 0H43101T0J / irinotecan; 2S9ZZM9Q9V / Bevacizumab; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ NIHMS508913; NLM/ PMC3930173
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38. Raco A, Piccirilli M, Landi A, Lenzi J, Delfini R, Cantore G: High-grade intramedullary astrocytomas: 30 years' experience at the Neurosurgery Department of the University of Rome "Sapienza". J Neurosurg Spine; 2010 Feb;12(2):144-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-grade intramedullary astrocytomas: 30 years' experience at the Neurosurgery Department of the University of Rome "Sapienza".
  • OBJECT: The goal in this study was to review a series of patients who underwent surgical removal of intramedullary high-grade gliomas, focusing on the functional outcome, recurrence rates, and technical problems continually debated in neurosurgical practice.
  • METHODS: Between December 1976 and December 2006, 22 patients underwent removal of intramedullary high-grade gliomas.
  • RESULTS: Histological examinations showed 10 Grade III astrocytomas and 12 glioblastomas.
  • Only 2 of the 22 high-grade astrocytomas could be completely removed.
  • In this series, multimodality treatment of intramedullary high-grade astrocytomas has been shown to increase length of survival without improving the neurological status.
  • [MeSH-major] Astrocytoma / surgery. Spinal Cord Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Cervical Vertebrae. Child. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Neurosurgical Procedures / methods. Neurosurgical Procedures / mortality. Rome. Spinal Cord / pathology. Spinal Cord / surgery. Thoracic Vertebrae. Time Factors. Treatment Outcome. Young Adult

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  • [CommentIn] J Neurosurg Spine. 2010 Feb;12(2):141-2; discussion 142-3 [20121347.001]
  • (PMID = 20121348.001).
  • [ISSN] 1547-5646
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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39. Llaguno SA, Chen J, Kwon CH, Parada LF: Neural and cancer stem cells in tumor suppressor mouse models of malignant astrocytoma. Cold Spring Harb Symp Quant Biol; 2008;73:421-6
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  • [Title] Neural and cancer stem cells in tumor suppressor mouse models of malignant astrocytoma.
  • Malignant astrocytomas are highly invasive brain tumors that portend poor prognosis and dismal survival.
  • We previously reported tumor suppressor mouse models based on conditional inactivation of human astrocytoma-relevant genes p53, Nf1, and Pten.
  • These mice develop, with full penetrance, varying grades of astrocytic malignancy that recapitulate the human condition histologically and molecularly.
  • Our studies indicate a central role for neural stem cells and stem-cell-like cancer cells in tumor initiation and progression.
  • These mouse models thus represent powerful tools for investigating various aspects of tumor development that otherwise cannot be explored in humans.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology. Neurons / pathology
  • [MeSH-minor] Animals. Disease Models, Animal. Genes, Tumor Suppressor. Humans. Mice. Models, Neurological. Mutation

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  • (PMID = 19022744.001).
  • [ISSN] 1943-4456
  • [Journal-full-title] Cold Spring Harbor symposia on quantitative biology
  • [ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / P50NS05260602
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 43
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40. Grujicic M, Vuckovic N, Vulekovic P, Novakovic B: The basic morphological characteristics of astrocytomas in Vojvodina in the period 2001-2006. J BUON; 2009 Oct-Dec;14(4):625-8
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  • [Title] The basic morphological characteristics of astrocytomas in Vojvodina in the period 2001-2006.
  • PURPOSE: Astrocytomas are the most common primary intracranial neoplasms.
  • The aim of this investigation was to register the age, sex, tumor localization, frequency and histological types of patients with astrocytomas.
  • Tumor histological studies were carried out in the Laboratory of the Centre for Pathology and Histology of the Clinical Centre of Vojvodina.
  • Out of 490 patients with diagnosed intracranial tumors, 139 (28.4%) had astrocytomas.
  • RESULTS: Astrocytomas were more frequent in males (63.3%) and were most common in the 50-59-year age group (39.5%).
  • In regard to other histological types of intracranial tumors, astrocytomas were more frequent in males (34.8%).
  • Grade III astrocytomas were most common (55.4%).
  • The frequency of hemorrhage and thrombosis showed a positive correlation with the histological grade of astrocytomas.
  • CONCLUSION: The typical patient with astrocytoma is a male of 50-59 years.
  • The tumor is grade III located in the right frontal region.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology
  • [MeSH-minor] Adult. Age Factors. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Sex Factors. Yugoslavia

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  • (PMID = 20148453.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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41. Arslantas A, Artan S, Oner U, Müslümanoglu MH, Ozdemir M, Durmaz R, Arslantas D, Vural M, Cosan E, Atasoy MA: Genomic alterations in low-grade, anaplastic astrocytomas and glioblastomas. Pathol Oncol Res; 2007;13(1):39-46
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  • [Title] Genomic alterations in low-grade, anaplastic astrocytomas and glioblastomas.
  • To extend our understanding of potential stepwise genetic alterations that may underlie tumor progression from low-grade astrocytomas to glioblastomas, histopathologic and comparative genomic hybridization analyses were performed on tumor specimens from 68 primary lesions, including 40 glioblastomas, 10 anaplastic and 18 low-grade astrocytomas.
  • The number of aberrations per case increased towards the higher grade tumors (grade II: 1.66+/-1.49; grade III: 2.80+/-1.68; grade IV: 3.02+/-1.07; F=6.955, p=0.002).
  • A gain of 7/7q was common and the most frequently seen aberration in low-grade astrocytomas, whereas loss of 10q was the most frequently seen anomaly in anaplastic astrocytomas and glioblastomas.
  • Chromosome 10/10q deletion and combination of 1p, 19q and 17p deletions were specific to high-grade astrocytic tumors.
  • The genomic copy deletions of chromosomes 1p and 19q might provide an alternative mechanism in the genesis of astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Aberrations. Chromosome Deletion. Glioblastoma / genetics

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  • (PMID = 17387387.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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42. Gimenez M, Souza VC, Izumi C, Barbieri MR, Chammas R, Oba-Shinjo SM, Uno M, Marie SK, Rosa JC: Proteomic analysis of low- to high-grade astrocytomas reveals an alteration of the expression level of raf kinase inhibitor protein and nucleophosmin. Proteomics; 2010 Aug;10(15):2812-21
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  • [Title] Proteomic analysis of low- to high-grade astrocytomas reveals an alteration of the expression level of raf kinase inhibitor protein and nucleophosmin.
  • The aim of this study was to identify differentially expressed proteins in diffuse astrocytoma grade II, anaplastic astrocytoma grade III and glioblastoma multiforme grade IV in human tumor samples and in non-neoplastic brain tissue as control using 2-DE and MS.
  • Tumor and control brain tissue dissection was guided by histological hematoxylin/eosin tissue sections to provide more than 90% of tumor cells and astrocytes.
  • Six proteins were detected as up-regulated in higher grade astrocytomas and the most important finding was nucleophosmin (NPM) (p<0.05), whereas four proteins were down-regulated, among them raf kinase inhibitor protein (RKIP) (p<0.05).
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics. Phosphatidylethanolamine Binding Protein / genetics. Proteomics


43. Nafe R, Van de Nes J, Yan B, Schlote W: Distribution of nuclear size and internuclear distance are important criteria for grading astrocytomas. Clin Neuropathol; 2006 Jan-Feb;25(1):48-56
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  • [Title] Distribution of nuclear size and internuclear distance are important criteria for grading astrocytomas.
  • AIM: The differentiation between low-grade astrocytomas and anaplastic astrocytomas is susceptible to considerable inter-observer variability.
  • In order to contribute to a better standardization of astrocytoma-grading based on quantitative data, the present study focuses on two important aspects not being considered in previous morphometric studies: elaboration of a decision flow chart for tumor grading based on morphometric parameters and appropriate cut-off-values, easily performed using low-cost equipment such as measuring oculars; investigation of the distribution (histograms) of parameters describing nuclear size and internuclear distance, which had been represented in previous studies by their mean and standard deviation only.
  • MATERIAL AND METHODS: At least 300 tumor cell nuclei per case were investigated in paraffin sections from surgical specimen of 75 patients with astrocytomas WHO grade II (n = 23) and anaplastic astrocytomas WHO grade III (n = 52) by means of a digital image analysis system.
  • According to multivariate analysis, the best contribution to tumor grading was achieved by means of parameters concerning the distribution of values for nuclear diameters and internuclear distances.
  • A decision tree was constructed using a knowledge based algorithm, which provided astrocytoma grading based on the distribution of values for nuclear diameter, as well as the numerical nuclear density and proliferation index.
  • CONCLUSION: The study demonstrates that a morphometric examination of tumor cell nuclei in paraffin sections supports the clinically important differential diagnosis between low-grade and high-grade astrocytomas.
  • The method for classification and the data published in the present study constitute a good basis for a standardized and reproducible grading procedure for astrocytomas, which can be performed in any histologic laboratory even without a digital image analysis system.
  • [MeSH-major] Astrocytoma / classification. Astrocytoma / pathology. Brain Neoplasms / classification. Brain Neoplasms / pathology. Cell Nucleus / ultrastructure

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  • (PMID = 16465775.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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44. Watanabe Y, Yamasaki F, Kajiwara Y, Saito T, Nishimoto T, Bartholomeusz C, Ueno NT, Sugiyama K, Kurisu K: Expression of phosphoprotein enriched in astrocytes 15 kDa (PEA-15) in astrocytic tumors: a novel approach of correlating malignancy grade and prognosis. J Neurooncol; 2010 Dec;100(3):449-57
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  • [Title] Expression of phosphoprotein enriched in astrocytes 15 kDa (PEA-15) in astrocytic tumors: a novel approach of correlating malignancy grade and prognosis.
  • Despite its many important roles, the clinical significance of PEA-15 expression levels in astrocytic tumors has yet to be properly defined.
  • We studied the PEA-15 expression pattern of 65 patients [diagnosed according to World Health Organization (WHO) criteria] with diffuse astrocytoma (WHO grade II), anaplastic astrocytoma (grade III), and glioblastoma (grade IV).
  • In grade II astrocytoma (diffuse astrocytoma) and grade III astrocytoma (anaplastic astrocytoma), 100% and 88.9% of patients expressed high PEA-15 levels, respectively, while a smaller number (50%) of patients with grade IV astrocytoma (glioblastoma) expressed high PEA-15 levels.
  • PEA-15 expression level was inversely associated with WHO grade (P = 0.0006).
  • Next, we evaluated prognosis and PEA-15 expression levels in 43 patients with high-grade astrocytomas based on the following parameters: age, gender, WHO grade, surgical resection extent, MIB-1 labeling index (LI), and PEA-15 expression level.
  • Multivariable analyses revealed that high PEA-15 expression level displayed a significant correlation with longer overall survival (OS) in high-grade astrocytomas (P = 0.0024).
  • In conclusion, PEA-15 expression level was inversely associated with WHO grade and may serve as an important prognostic factor for high-grade astrocytomas.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / metabolism. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Phosphoproteins / metabolism. Statistics as Topic

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  • (PMID = 20455002.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Ki-67 Antigen; 0 / PEA15 protein, human; 0 / Phosphoproteins
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45. Fujita A, Sato JR, Festa F, Gomes LR, Oba-Shinjo SM, Marie SK, Ferreira CE, Sogayar MC: Identification of COL6A1 as a differentially expressed gene in human astrocytomas. Genet Mol Res; 2008;7(2):371-8
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  • [Title] Identification of COL6A1 as a differentially expressed gene in human astrocytomas.
  • Gliomas are classified by the WHO according to their histopathological and clinical characteristics into four classes: grade I (pilocytic astrocytoma), grade II (diffuse astrocytoma), grade III (anaplastic astrocytoma), and grade IV (glioblastoma multiforme).
  • Several genes have already been correlated with astrocytomas, but many others are yet to be uncovered.
  • By analyzing the public SAGE data from 21 patients, comprising low malignant grade astrocytomas and glioblastomas, we found COL6A1 to be differentially expressed, confirming this finding by real time RT-PCR in 66 surgical samples.
  • The expression of this gene has significantly different means when normal glia is compared with low-grade astrocytomas (grades I and II) and high-grade astrocytomas (grades III and IV), with a tendency to be greater in higher grade samples, thus rendering it a powerful tumor marker.
  • [MeSH-major] Astrocytoma / genetics. Collagen Type VI / genetics. Gene Expression Profiling
  • [MeSH-minor] Gene Expression Regulation, Neoplastic. Humans. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18551403.001).
  • [ISSN] 1676-5680
  • [Journal-full-title] Genetics and molecular research : GMR
  • [ISO-abbreviation] Genet. Mol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Collagen Type VI; 0 / RNA, Neoplasm
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46. Compostella A, Tosoni A, Blatt V, Franceschi E, Brandes AA: Prognostic factors for anaplastic astrocytomas. J Neurooncol; 2007 Feb;81(3):295-303
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  • [Title] Prognostic factors for anaplastic astrocytomas.
  • Anaplastic astrocytomas (WHO grade III) constitute about 10% of all gliomas.
  • Definitive data on predictive and prognostic factors are lacking for these neoplasms that are considered the most enigmatic entity among the whole spectrum of astrocytic tumors because of their unclear biologic behavior and variable clinical outcome.
  • Currently, only few factors have been identified as useful for prognosis of anaplastic astrocytoma: age and Karnofsky Performance Status.
  • Potential prognostic biomarkers concern tumor suppressor genes on chromosome 9q that are involved in the RB1 pathway; PTEN, the PI3k/Akt/p70s6k cascade, survivin gene, Formylpeptide receptor, minichromosome maintenance protein 3 and genes on chromosome 7.
  • The state of the art pictured here underlie the recent interest on gene expression profile to identify aberrations useful to understand the biologic behavior of astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Brain Neoplasms / pathology


47. El-Habr EA, Tsiorva P, Theodorou M, Levidou G, Korkolopoulou P, Vretakos G, Petraki L, Michalopoulos NV, Patsouris E, Saetta AA: Analysis of PIK3CA and B-RAF gene mutations in human astrocytomas: association with activation of ERK and AKT. Clin Neuropathol; 2010 Jul-Aug;29(4):239-45
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  • [Title] Analysis of PIK3CA and B-RAF gene mutations in human astrocytomas: association with activation of ERK and AKT.
  • OBJECTIVE: The analysis of the presence of PIK3CA and B-RAF gene mutations in relation to ERK and AKT activation in diffusely infiltrating astrocytomas, in order to determine their potential role in tumor aggressiveness.
  • Neither low grade astrocytomas nor anaplastic astrocytomas revealed any mutations in these genes.
  • Moreover, pERK nuclear expression increased in parallel with tumor grade (II, III v/s IV, p = 0.0262).
  • pAKT cytoplasmic expression increased with increasing tumor grade (II,III v/s IV, p = 0.0930), although the latter relationship was of marginal significance. pAKT cytoplasmic expression was also positively correlated with pERK nuclear expression (p = 0.0156).
  • CONCLUSIONS: Our study reports the low frequency of PIK3CA and B-RAF mutations in astrocytomas, despite the presence of activated ERK and AKT proteins.
  • Moreover, the correlation of pERK nuclear and pAKT cytoplasmic expression with tumor grade suggests the possible crucial role of the activation of these proteins in human gliomagenesis.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. MAP Kinase Signaling System / physiology. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics. Proto-Oncogene Proteins B-raf / genetics

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  • (PMID = 20569675.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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48. Wiencke JK, Zheng S, Jelluma N, Tihan T, Vandenberg S, Tamgüney T, Baumber R, Parsons R, Lamborn KR, Berger MS, Wrensch MR, Haas-Kogan DA, Stokoe D: Methylation of the PTEN promoter defines low-grade gliomas and secondary glioblastoma. Neuro Oncol; 2007 Jul;9(3):271-9
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  • [Title] Methylation of the PTEN promoter defines low-grade gliomas and secondary glioblastoma.
  • Glioblastoma multiforme (GBM) can present as either de novo or secondary tumors arising from previously diagnosed low-grade gliomas.
  • Although these tumor types are phenotypically indistinguishable, de novo and secondary GBMs are associated with distinct genetic characteristics.
  • PTEN mutations, which result in activation of the phosphoinositide 3-kinase (PI3K) signal transduction pathway, are frequent in de novo but not in secondary GBMs or their antecedent low-grade tumors.
  • Results we present here show that grade II astrocytomas, oligodendrogliomas, and oligoastrocytomas commonly display methylation of the PTEN promoter, a finding that is absent in nontumor brain specimens and rare in de novo GBMs.
  • Our results also demonstrate frequent methylation of the PTEN promoter in grade III astrocytomas and secondary GBMs, consistent with the hypothesis that these tumors arise from lower grade precursors.
  • PTEN methylation is rare in de novo GBMs and is mutually exclusive with PTEN mutations.
  • We conclude that methylation of the PTEN promoter may represent an alternate mechanism by which PI3K signaling is increased in grade II and III gliomas as well as secondary GBMs, a finding that offers new therapeutic approaches in these patients.

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  • (PMID = 17504928.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA97257; United States / NCI NIH HHS / CA / R01 CA52689; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA082783-06; United States / NCI NIH HHS / CA / R01 CA082783; United States / NCI NIH HHS / CA / CA082783-06; United States / NCI NIH HHS / CA / R01 CA052689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC1907411
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49. Chamberlain MC, Chowdhary SA, Glantz MJ: Anaplastic astrocytomas: biology and treatment. Expert Rev Neurother; 2008 Apr;8(4):575-86
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  • [Title] Anaplastic astrocytomas: biology and treatment.
  • Anaplastic astrocytomas (AA), WHO grade III gliomas, comprise 10-15% of all glial neoplasms.
  • The most important predictor of response to therapy and survival in AA tumors is the presence or absence of the 1p19q co-deletion, a translocation that defines a subset of oligodendroglial tumors, and anaplastic oligodendrogliomas in particular.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / therapy. Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Clinical Trials as Topic

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  • (PMID = 18416660.001).
  • [ISSN] 1744-8360
  • [Journal-full-title] Expert review of neurotherapeutics
  • [ISO-abbreviation] Expert Rev Neurother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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50. MacDonald TJ, Pollack IF, Okada H, Bhattacharya S, Lyons-Weiler J: Progression-associated genes in astrocytoma identified by novel microarray gene expression data reanalysis. Methods Mol Biol; 2007;377:203-22
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  • [Title] Progression-associated genes in astrocytoma identified by novel microarray gene expression data reanalysis.
  • Astrocytoma is graded as pilocytic (WHO grade I), diffuse (WHO grade II), anaplastic (WHO grade III), and glioblastoma multiforme (WHO grade IV).
  • The progression from low- to high-grade astrocytoma is associated with distinct molecular changes that vary with patient age, yet the prognosis of high-grade tumors in children and adults is equally dismal.
  • Whether specific gene expression changes are consistently associated with all high-grade astrocytomas, independent of patient age, is not known.
  • To address this question, we reanalyzed the microarray datasets comprising astrocytomas from children and adults, respectively.
  • We identified nine genes consistently dysregulated in high-grade tumors, using four novel tests for identifying differentially expressed genes.
  • Four genes encoding ribosomal proteins (RPS2, RPS8, RPS18, RPL37A) were upregulated, and five genes (APOD, SORL1, SPOCK2, PRSS11, ID3) were downregulated in high-grade by all tests.
  • Expression results were validated using a third astrocytoma dataset.
  • APOD, the most differentially expressed gene, has been shown to inhibit tumor cell and vascular smooth muscle cell proliferation.
  • This suggests that dysregulation of APOD may be critical for malignant astrocytoma formation, and thus a possible novel universal target for therapeutic intervention.
  • Further investigation is needed to evaluate the role of APOD, as well as the other genes identified, in malignant astrocytoma development.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Gene Expression. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Adult. Child. Chromosomes, Human. Cluster Analysis. Data Interpretation, Statistical. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Models, Genetic. Neoplasm Recurrence, Local. Reproducibility of Results

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  • (PMID = 17634619.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 49
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51. Zhu Y, Guignard F, Zhao D, Liu L, Burns DK, Mason RP, Messing A, Parada LF: Early inactivation of p53 tumor suppressor gene cooperating with NF1 loss induces malignant astrocytoma. Cancer Cell; 2005 Aug;8(2):119-30
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  • [Title] Early inactivation of p53 tumor suppressor gene cooperating with NF1 loss induces malignant astrocytoma.
  • Malignant astrocytoma, the most prevalent primary brain tumor, is resistant to all known therapies and frequently harbors mutations that inactivate p53 and activate Ras signaling.
  • We have generated mouse strains that lack p53 and harbor a conditional allele of the NF1 tumor suppressor that negatively regulates Ras signaling.
  • The mice develop malignant astrocytomas with complete penetrance.
  • The majority of tumors display characteristics of glioblastoma multiforme with concomitant alteration of signaling pathways previously described in the human counterparts of this neoplasm.
  • We find that the sequence of tumor suppressor inactivation influences tumorigenicity and that earliest evidence of tumor formation localizes to regions of the brain that contain a multipotent stem cell population capable of in vivo differentiation into neurons and glia.

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  • (PMID = 16098465.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS034296-07; United States / NINDS NIH HHS / NS / NS034296-07; United States / NCI NIH HHS / CA / P20 CA086354; United States / NINDS NIH HHS / NS / R01 NS034296-06; United States / NINDS NIH HHS / NS / R01 NS034296; United States / NINDS NIH HHS / NS / NS034296-06; United States / NCI NIH HHS / CA / P20 CA86354
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS263629; NLM/ PMC3024718
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52. Malhan P, Husain N, Bhalla S, Gupta RK, Husain M: Proliferating cell nuclear antigen, p53 and micro vessel density: Grade II vs. Grade III astrocytoma. Indian J Pathol Microbiol; 2010 Jan-Mar;53(1):20-3
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  • [Title] Proliferating cell nuclear antigen, p53 and micro vessel density: Grade II vs. Grade III astrocytoma.
  • Histological classification and grading are prime procedures in the management of patients with astrocytoma, providing vital data for therapeutic decision making and prognostication.
  • However, it has limitations in assessing biological tumor behavior.
  • This study was carried out to compare proliferative indices using proliferating cell nuclear antigen (PCNA), extent of p53 expression and micro vessel morphometric parameters in patients with low grade and anaplastic astrocytoma.
  • Twenty-five patients, each of grade II and grade III astrocytoma were evaluated using monoclonal antibodies to PCNA, p53 protein and factor VIII related antigen.
  • Patients with grade III astrocytoma had higher PCNA and p53 labeling indices as compared with grade II astrocytoma (29.14 plus/minus 9.87% vs. 16.84 plus/minus 6.57%, p 0.001; 18.18 plus/minus 6.14% vs. 6.14 plus/minus 7.23%, p 0.001, respectively).
  • Micro vessel percentage area of patients with grade III astrocytoma was also (4.26 plus/minus 3.70 vs. 1.05 plus/minus 0.56, p 0.001), higher along with other micro vessel morphometric parameters.
  • Discordance between histology and one or more IHC parameters was seen in 5/25 (20%) of patients with grade III astrocytoma and 9/25 (36%) of patients with grade II disease.
  • Increased proliferative fraction, genetic alterations and neovascularization mark biological aggressiveness in astrocytoma.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / pathology. Neovascularization, Pathologic. Proliferating Cell Nuclear Antigen / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 20090216.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Proliferating Cell Nuclear Antigen; 0 / Tumor Suppressor Protein p53
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53. Nagai S, Kurimoto M, Washiyama K, Hirashima Y, Kumanishi T, Endo S: Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines. J Neurooncol; 2005 Sep;74(2):105-11
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  • [Title] Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines.
  • In malignant astrocytoma cells, it was reported that NF-kappaB was activated aberrantly and promoted their proliferation.
  • Thus, inhibition of NF-kappaB activity is considered to be a promising therapeutic strategy for malignant astrocytoma.
  • In this study, we investigated inhibitory effects of curcumin on NF-kappaB activity and cellular proliferation, and induction of apoptosis by curcumin in human malignant astrocytoma cell lines.
  • Alteration of NF-kappaB activity in NP-2 human malignant astrocytoma cell line after treatment with curcumin was examined using electrophoretic mobility shift assay.
  • Alterations of DNA synthesis and cellular growth in five human malignant astrocytoma cell lines after treatment with curcumin were examined using [(3)H]thymidine incorporation assay and the trypan blue dye exclusion method, respectively.
  • Induction of apoptosis by curcumin in NP-2 and NP-3 human malignant astrocytoma cell lines was examined by DNA-fragmentation analysis and morphological observation.
  • The DNA synthesis and the cellular growth were inhibited by curcumin in dose-dependent manner in all the five malignant astrocytoma cell lines.
  • These results indicate that curcumin inhibits the cellular proliferation and induces apoptosis in human malignant astrocytoma cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Astrocytoma / drug therapy. Cell Proliferation / drug effects. Curcumin / therapeutic use. NF-kappa B / drug effects
  • [MeSH-minor] Electrophoretic Mobility Shift Assay. Humans. Thymidine / metabolism. Tumor Cells, Cultured

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  • (PMID = 16193380.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; IT942ZTH98 / Curcumin; VC2W18DGKR / Thymidine
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54. Kanamori M, Kumabe T, Watanabe M, Tominaga T: Anaplastic astrocytoma and anaplastic oligodendroglioma occurring 6 years after subtotal resection of a central neurocytoma. Case report. J Neurosurg; 2007 Jul;107(1):185-9
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  • [Title] Anaplastic astrocytoma and anaplastic oligodendroglioma occurring 6 years after subtotal resection of a central neurocytoma. Case report.
  • The authors present the case of a 51-year-old man who presented with an anaplastic astrocytoma and anaplastic oligodendroglioma that developed 6 years after subtotal resection of a central neurocytoma in his right lateral ventricle.
  • Histological examination revealed anaplastic oligodendroglioma in the parietal lobe and anaplastic astrocytoma in the insula.
  • One year later, the anaplastic astrocytoma was found to have transformed into a glioblastoma multiforme.
  • Fluorescence in situ hybridization analysis and immunohistochemical examinations detected deletions of the lp36 and 19q13 loci, and nuclear accumulation of TP53 protein in the anaplastic oligodendroglioma but not in the glioblastoma multiforme.
  • These findings suggest that central neurocytoma or progenitor cells have the potential for oligodendrocytic and astrocytic transformation with different genetic aberrations.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplasm Recurrence, Local / pathology. Neurocytoma / surgery. Oligodendroglioma / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Neurosurgical Procedures. Time Factors


55. Wu-Chen WY, Jacobs DA, Volpe NJ, Dalmau JO, Moster ML: Intracranial malignancies occurring more than 20 years after radiation therapy for pituitary adenoma. J Neuroophthalmol; 2009 Dec;29(4):289-95
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  • Imaging disclosed a left parasellar mass and a midbrain/pontine signal abnormality.
  • Biopsy of the parasellar mass revealed a malignant sarcoma.
  • The brainstem abnormality was presumptively diagnosed as a malignant glioma.
  • A 63-year-old man developed a malignant astrocytoma of the left optic nerve and chiasm 23 years after partial excision and radiation of a nonsecreting pituitary adenoma.

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  • (PMID = 19952902.001).
  • [ISSN] 1536-5166
  • [Journal-full-title] Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
  • [ISO-abbreviation] J Neuroophthalmol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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56. Kawarabuki K, Ohta T, Hashimoto N, Wada K, Maruno M, Yamaki T, Ueda S: Cerebellar glioblastoma genetically defined as a secondary one. Clin Neuropathol; 2005 Mar-Apr;24(2):64-8
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  • In the present case, tumor lesions were observed in each cerebellar hemisphere.
  • The left-side lesion was diagnosed as glioblastoma, and the right-side lesion as malignant astrocytoma by histopathology.
  • Immunohistochemistry revealed that the tumor cells of the left-side lesion was positive for p53, whereas epidermal growth factor receptors (EGFR) were negative in tumor cells from both sides.
  • Genetic alterations were investigated using a genome DNA microarray (GenoSensor Array 300), which has led us to define this tumor as a secondary glioblastoma.

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  • (PMID = 15803805.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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57. Miura FK, Alves MJ, Rocha MC, da Silva R, Oba-Shinjo SM, Marie SK: Xenograft transplantation of human malignant astrocytoma cells into immunodeficient rats: an experimental model of glioblastoma. Clinics (Sao Paulo); 2010 Mar;65(3):305-9
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  • [Title] Xenograft transplantation of human malignant astrocytoma cells into immunodeficient rats: an experimental model of glioblastoma.
  • INTRODUCTION: Astrocytic gliomas are the most common intracranial central nervous system neoplasias, accounting for about 60% of all primary central nervous system tumors.
  • OBJECTIVE: To develop an experimental malignant astrocytoma model with the characteristics of the human tumor.
  • METHOD: Primary cells from subcutaneous xenograft tumors produced with malignant astrocytoma U87MG cells were inoculated intracerebrally by stereotaxis into immunosuppressed (athymic) Rowett rats.
  • CONCLUSION: A malignant astrocytoma intracerebral xenograft model with poorly invasive behavior was achieved in athymic Rowett rats.
  • Tumor invasiveness in an experimental animal model may depend on a combination of several factors, including the cell line used to induce tumor formation, the rat strains and the status of the animal's immune system.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Immunocompromised Host
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Female. Humans. Neoplasm Transplantation. Rats. Rats, Nude. Transplantation, Heterologous

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  • [Cites] Anticancer Res. 2006 Jul-Aug;26(4B):2887-900 [16886610.001]
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  • (PMID = 20360922.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC2845772
  • [Keywords] NOTNLM ; Athymic Rowett rats / Brain tumor / Experimental model / U87MG cells
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58. Roselli F, Pisciotta NM, Aniello MS, Niccoli-Asabella A, Defazio G, Livrea P, Rubini G: Brain F-18 Fluorocholine PET/CT for the assessment of optic pathway glioma in neurofibromatosis-1. Clin Nucl Med; 2010 Oct;35(10):838-9
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  • Magnetic resonance imaging, magnetic resonance spectroscopy (MRS), and F-18 fluorocholine revealed a splenial mass with imaging features compatible with malignant astrocytoma.

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  • (PMID = 20838306.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / fluorocholine; N91BDP6H0X / Choline
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59. Kikuchi T: [Novel immunotherapeutic approach]. Gan To Kagaku Ryoho; 2005 Apr;32(4):453-7
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  • Malignant astrocytoma is the most common primary brain tumor in adults.
  • The median survival time of patients with high-grade malignant astrocytoma is about 1 year, despite aggressive treatment with surgical resection, radiotherapy, and cytotoxic chemotherapy.
  • The author reviews immunotherapeutic approaches for malignant gliomas and the relevance of recent clinical trials and their outcomes.
  • DCs have been investigated in several clinical trials in patients with malignant tumors including malignant gliomas.
  • So far, seven papers concerning immunotherapy with DCs against malignant gliomas have been published.
  • These reports demonstrate that immunotherapy with DCs induces immune responses and clinically antitumor effects in some patients with malignant glioma.
  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Glioma / therapy. Immunotherapy

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  • (PMID = 15853209.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunotoxins; 0 / Interleukin-13; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 23
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60. Li B, Qi XQ, Chen X, Huang X, Liu GY, Chen HR, Huang CG, Luo C, Lu YC: Expression of targeting protein for Xenopus kinesin-like protein 2 is associated with progression of human malignant astrocytoma. Brain Res; 2010 Sep 17;1352:200-7
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  • [Title] Expression of targeting protein for Xenopus kinesin-like protein 2 is associated with progression of human malignant astrocytoma.
  • However, the contribution of TPX2 expression to astrocytoma progression is unclear.
  • The aim of this study was to investigate TPX2 expression in human astrocytoma samples and cell lines.
  • TPX2 protein expression was detected in the nucleus of astrocytoma tissues by immunohistochemistry and immunofluorescence staining.
  • Real-time PCR and Western blot analysis showed that the expression levels of TPX2 were higher in high-grade astrocytoma tissues and cell lines than that in low-grade astrocytoma tissues and normal cell lines.
  • Immunohistochemical analysis of tumor tissues from 52 patients with astrocytoma showed that TPX2 over-expression was significantly associated with decreased patient survival.
  • These data suggest that TPX2 expression is associated with the progression of malignant astrocytoma.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Cell Cycle Proteins / genetics. Microtubule-Associated Proteins / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Apoptosis. Aurora Kinases. Brain / metabolism. Cell Division. Cell Line, Tumor. Cyclin B1 / genetics. Cyclin D1 / genetics. Disease Progression. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Protein-Serine-Threonine Kinases / genetics. Proto-Oncogene Proteins c-myc / genetics. Survival Rate. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 20599806.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Microtubule-Associated Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / TPX2 protein, human; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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61. Wykosky J, Gibo DM, Stanton C, Debinski W: Interleukin-13 receptor alpha 2, EphA2, and Fos-related antigen 1 as molecular denominators of high-grade astrocytomas and specific targets for combinatorial therapy. Clin Cancer Res; 2008 Jan 1;14(1):199-208
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  • [Title] Interleukin-13 receptor alpha 2, EphA2, and Fos-related antigen 1 as molecular denominators of high-grade astrocytomas and specific targets for combinatorial therapy.
  • PURPOSE: We investigated the expression of interleukin-13 receptor alpha2 (IL-13R alpha 2), EphA2, and Fos-related antigen 1 (Fra-1) in astrocytomas and normal brain.
  • We sought to document whether the expression of the three factors changed with progression to higher grade malignancy and whether two or three targets in combination might be sufficient to target all patients with high-grade astrocytomas.
  • EXPERIMENTAL DESIGN: Immunohistochemistry was done for IL-13R alpha 2, EphA2, and Fra-1 using human brain tumor tissue microarrays containing 30 specimens of WHO grades II and III astrocytomas, 46 glioblastoma multiformes (GBM), and 9 normal brain samples.
  • Western blotting was done for all three markers using GBM tumor specimens and xenograft cell lines.
  • RESULTS: Expression of all three proteins was significantly higher in GBM compared with normal brain, low-grade, and anaplastic astrocytomas.
  • CONCLUSIONS: IL-13R alpha 2, EphA2, and Fra-1 are attractive therapeutic targets representing molecular denominators of high-grade astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Interleukin-13 Receptor alpha2 Subunit / biosynthesis. Proto-Oncogene Proteins c-fos / biosynthesis. Receptor, EphA2 / biosynthesis

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  • (PMID = 18172271.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 1F31 NS055533-01; United States / NCI NIH HHS / CA / R01 CA74145
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bacterial Toxins; 0 / Biomarkers, Tumor; 0 / Exotoxins; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / Proto-Oncogene Proteins c-fos; 0 / Virulence Factors; 0 / fos-related antigen 1; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa; EC 2.7.10.1 / Receptor, EphA2
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62. Bozinov O, Köhler S, Samans B, Benes L, Miller D, Ritter M, Sure U, Bertalanffy H: Candidate genes for the progression of malignant gliomas identified by microarray analysis. Neurosurg Rev; 2008 Jan;31(1):83-9; discussion 89-90
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  • [Title] Candidate genes for the progression of malignant gliomas identified by microarray analysis.
  • Malignant astrocytomas of World Health Organization (WHO) grade III or IV have a reduced median survival time, and possible pathways have been described for the progression of anaplastic astrocytomas and glioblastomas, but the molecular basis of malignant astrocytoma progression is still poorly understood.
  • We compared the transcriptional profile of 4,608 genes in tumours of 15 patients including 6 anaplastic astrocytomas (WHO grade III) and 9 glioblastomas (WHO grade IV) using microarray analysis.
  • We identified 166 gene alterations with a fold change of 2 and higher whose mRNA levels differed (absolute value of the t statistic of 1.96) between the two malignant glioma groups.
  • Further analyses confirmed same transcription directions for Olig2 and IL-13Ralpha2 in anaplastic astrocytomas as compared to glioblastomas.
  • IL-13Ralpha2 and Olig2 have been identified and confirmed to be interesting candidate genes whose differential expression likely plays a role in malignant progression of astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Gene Expression Profiling. Glioblastoma / genetics. Oligonucleotide Array Sequence Analysis

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  • [ErratumIn] Neurosurg Rev. 2008 Apr;31(2):247-8
  • (PMID = 17917751.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / Nerve Tissue Proteins; 0 / OLIG2 protein, human
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63. Yue WY, Chen ZP: Does vasculogenic mimicry exist in astrocytoma? J Histochem Cytochem; 2005 Aug;53(8):997-1002
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  • [Title] Does vasculogenic mimicry exist in astrocytoma?
  • Vasculogenic mimicry (VM) has been observed in melanoma and in some nonmelanoma tumor types.
  • It is unknown whether a similar VM phenomenon exists in astrocytoma.
  • The present study was to examine 45 astrocytomas (including World Health Organization grade II 15 cases, grade III 15 cases, and grade IV 15 cases) by CD34 endothelial marker periodic acid-Schiff (PAS) dual staining to see if VM existing in these tumors.
  • The results demonstrated that endothelium-lined vessels dominated the tumor microvasculature and stained positively for PAS, laminin, and endothelial marker.
  • PAS-positive pattern of VM was found in two grade IV astrocytomas.
  • Channels stained positively for PAS, laminin, and negatively for CD34 of the VM entrapped in the tumor tissue.
  • Furthermore, in astrocytoma, especially glioblastoma, focus of anaplastic tumor cells appeared with CD34 expression, whereas some tumor cells lost glial fibrillary acid protein expression.
  • It is assumed that genetically deregulated tumor cells in astrocytoma could lose the astrocyte-specific protein and express inappropriate markers not expected in cells of astrocyte lineage.
  • The present results suggest that VM phenomenon exists in some malignant astrocytoma.
  • [MeSH-major] Astrocytoma / blood supply. Brain Neoplasms / blood supply
  • [MeSH-minor] Antigens, CD34 / metabolism. Biomarkers / metabolism. Coloring Agents. Endothelium, Vascular / metabolism. Humans. Microcirculation. Neoplasm Staging. Periodic Acid. Schiff Bases

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  • (PMID = 15923371.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers; 0 / Coloring Agents; 0 / Schiff Bases; 10450-60-9 / Periodic Acid
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64. Ehling R, Sterlacci W, Maier H, Berger T: A 45-year old male with left-sided hemihypesthesia. Brain Pathol; 2010 Mar;20(2):515-8
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  • Extensive immunological and radiological investigations were not able to differentiate between an intrinsic brain tumor and a demyelinating disease.
  • Stereotactic biopsies of the brainstem were performed; the findings of abundant Rosenthal fibers, interjacent spindle-shaped and gemistocytic cells partially with dark and irregularly formed nuclei favored primarily the diagnosis of a malignant astrocytoma, although a demyelinating disease could not be definitely excluded.

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  • (PMID = 20438473.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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65. Mott RT, Turner KC, Bigner DD, McLendon RE: Utility of EGFR and PTEN numerical aberrations in the evaluation of diffusely infiltrating astrocytomas. Laboratory investigation. J Neurosurg; 2008 Feb;108(2):330-5
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  • [Title] Utility of EGFR and PTEN numerical aberrations in the evaluation of diffusely infiltrating astrocytomas. Laboratory investigation.
  • OBJECT: Diffusely infiltrating astrocytomas are the most common primary brain tumors.
  • As a group, they demonstrate an inherent tendency toward malignant progression.
  • Given the important roles for EGFR and PTEN in the malignant progression of astrocytomas, the authors hypothesized that the fraction of tumor cells with aberrations in these genetic loci would correlate with the histological grade.
  • METHODS: The authors evaluated 217 consecutive diffusely infiltrating astrocytomas that were graded using the WHO guidelines, including 16 diffuse astrocytomas (WHO Grade II), 72 anaplastic astrocytomas ([AAs] WHO Grade III), and 129 glioblastomas multiforme ([GBMs] WHO Grade IV).
  • RESULTS: The population of tumor cells with polysomy of chromosome 7 and the EGFR locus and monosomy of chromosome 10 and the PTEN locus correlated significantly with histological grade.
  • In particular, high-grade astrocytomas (that is, AAs and GBMs) had elevated fractions of tumor cells with polysomy of chromosome 7 and the EGFR locus and monosomy of chromosome 10 and the PTEN locus.
  • Using these findings, the authors generated a mathematical model capable of subcategorizing high-grade astrocytomas.
  • The successful model incorporated only the percentage of tumor cells with polysomy of EGFR and monosomy of PTEN, as well as patient age.
  • CONCLUSIONS: The findings presented in this study emphasize the utility of combining histological interpretation and molecular testing in the evaluation of infiltrating astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Aberrations. Genes, erbB-1 / genetics. PTEN Phosphohydrolase / genetics

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  • (PMID = 18240930.001).
  • [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] EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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66. Shuangshoti S, Thorner PS, Ruangvejvorachai P, Saha B, Groshen S, Taylor CR, Malhotra S, Imam SA: J1-31 protein expression in astrocytes and astrocytomas. Neuropathology; 2009 Oct;29(5):521-7
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  • [Title] J1-31 protein expression in astrocytes and astrocytomas.
  • J1-31 is one of the astrocytic proteins, the expression of which has not been evaluated in astrocytomas.
  • In the present study, we studied the expression of J1-31 protein in astrocytes and astrocytomas in comparison with GFAP, p53 and Ki-67.
  • Materials consisted of formalin-fixed paraffin-embedded tissue specimens that included five cases of normal brain, 17 of gliosis, 15 of pilocytic astrocytoma (WHO grade I), 26 of low-grade diffuse astrocytoma (WHO grade II), four of anaplastic astrocytoma (WHO grade III), and eight of glioblastoma (WHO grade IV).
  • The antibody showed reactivity with tumor cells in 12/15 (80%) cases of pilocytic astrocytoma, although intensity of staining was generally weaker and more focal than observed in reactive gliosis.
  • J1-31-positive tumor cells were detected in only 9/26 (35%) cases of the low-grade diffuse astrocytoma and none of the cases of anaplastic astrocytoma and glioblastoma.
  • Increasing Ki-67 indices paralleled advancing tumor grades. p53 protein was expressed more commonly in infiltrating astrocytomas compared to pilocytic astrocytoma.
  • In conclusion, down-regulation of J1-31 expression correlates with advancing grade of astrocytomas.
  • The result suggests this protein plays some role in astrocytes that is progressively lost in malignant progression.
  • The anti-J1-31 antibody may help further our understanding of astrocytes in disease and may be useful as an aid in the pathologic diagnosis of astrocytic lesions.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Nerve Tissue Proteins / metabolism
  • [MeSH-minor] Cytoplasm / metabolism. Down-Regulation. Glial Fibrillary Acidic Protein / metabolism. Glioblastoma / metabolism. Gliosis / metabolism. Humans. Ki-67 Antigen / metabolism. Neoplasm Staging. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19019178.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / J1-31 protein, human; 0 / Ki-67 Antigen; 0 / Nerve Tissue Proteins; 0 / Tumor Suppressor Protein p53
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67. Moulding HD, Friedman DP, Curtis M, Kenyon L, Flanders AE, Paek SH, Andrews DW: Revisiting anaplastic astrocytomas I: an expansive growth pattern is associated with a better prognosis. J Magn Reson Imaging; 2008 Dec;28(6):1311-21
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  • [Title] Revisiting anaplastic astrocytomas I: an expansive growth pattern is associated with a better prognosis.
  • PURPOSE: To study whether anaplastic astrocytomas that are nonenhancing and/or well-circumscribed (expansive) are associated with a better prognosis.
  • MATERIALS AND METHODS: We retrospectively identified 59 patients with pathologically confirmed World Health Organizaiton (WHO) grade III anaplastic astrocytoma who underwent craniotomy at our institution from 1995 through 2006.
  • A multivariate (Cox proportional hazards) analysis showed that patient age and expansive tumor phenotype affected outcome, whereas RPA class, enhancement, and GTR did not.
  • CONCLUSION: Circumscribed growth in histologically proven anaplastic astrocytoma, which has not been emphasized in past studies, has a considerable survival advantage.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Chi-Square Distribution. Contrast Media. Craniotomy. Female. Gadolinium DTPA. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Proportional Hazards Models. Retrospective Studies. Statistics, Nonparametric. Survival Analysis. Treatment Outcome

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 19025897.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; K2I13DR72L / Gadolinium DTPA
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68. Knizetova P, Ehrmann J, Hlobilkova A, Vancova I, Kalita O, Kolar Z, Bartek J: Autocrine regulation of glioblastoma cell cycle progression, viability and radioresistance through the VEGF-VEGFR2 (KDR) interplay. Cell Cycle; 2008 Aug 15;7(16):2553-61
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  • Vascular endothelial growth factor (VEGF) plays a crucial role in angiogenesis and progression of malignant brain tumors.
  • Given the significance of tumor microenvironment in general, and the established role of paracrine VEGF signaling in glioblastoma (GBM) biology in particular, we explored the potential autocrine control of human astrocytoma behavior by VEGF.
  • Using a range of cell and molecular biology approaches to study a panel of astrocytoma (grade III and IV/GBM)-derived cell lines and a series of clinical specimens from low- and high-grade astrocytomas, we show that co-expression of VEGF and VEGF receptors (VEGFRs) occurs commonly in astrocytoma cells.
  • Blockade of VEGFR2 by the selective inhibitor (SU1498) abrogated the VEGF-mediated enhancement of astrocytoma cell growth and viability under unperturbed culture conditions.
  • In addition, such interference with VEGF-VEGFR2 signaling potentiated the ionizing radiation-induced tumor cell death.
  • In clinical specimens, both VEGFRs and VEGF were co-expressed in astroglial tumor cells, and higher VEGF expression correlated with tumor progression, thereby supporting the relevance of functional VEGF-VEGFR signaling in vivo.
  • Overall, our results are consistent with a potential autocrine role of the VEGF-VEGFR2 (KDR) interplay as a factor contributing to malignant astrocytoma growth and radioresistance, thereby supporting the candidacy of this signaling cascade as a therapeutic target, possibly in combination with radiotherapy.
  • [MeSH-minor] Autocrine Communication. Cell Cycle. Cell Line, Tumor. Humans. Radiation Tolerance. Signal Transduction

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  • (PMID = 18719373.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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69. Assimakopoulou M, Kondyli M, Gatzounis G, Maraziotis T, Varakis J: Neurotrophin receptors expression and JNK pathway activation in human astrocytomas. BMC Cancer; 2007;7:202
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  • [Title] Neurotrophin receptors expression and JNK pathway activation in human astrocytomas.
  • The aim of this exploratory study was to investigate the expression levels of neurotrophin receptors, Trks and p75NTR, and the activation of JNK pathway in human astrocytomas and in adjacent non-neoplastic brain tissue.
  • METHODS: Formalin-fixed paraffin-embedded serial sections from 33 supratentorial astrocytomas (5 diffuse fibrillary astrocytomas, WHO grade II; 6 anaplastic astrocytomas, WHO grade III; 22 glioblastomas multiforme, WHO grade IV) were immunostained following microwave pretreatment.
  • The labeling index (LI), defined as the percentage of positive (labeled) cells out of the total number of tumor cells counted, was determined.
  • RESULTS: Moderate to strong, granular cytoplasmic immunoreactivity for TrkA, TrkB and TrkC receptors was detected in greater than or equal to 10% of tumor cells in the majority of tumors independently of grade; on the contrary, p75NTR receptor expression was found in a small percentage of tumor cells (approximately 1%) in some tumors.
  • The endothelium of tumor capillaries showed conspicuous immunoreactivity for TrkB receptor.
  • Phosphorylated forms of JNK (pJNK) and c-Jun (pc-Jun) were significantly co-expressed in a tumor grade-dependent manner (p < 0.05).
  • CONCLUSION: In the context of astrocytomas, Trk receptors (TrkA, TrkB, TrkC) expression may promote tumor growth independently of grade.
  • Considering the fact that regional tumor heterogeneity may be a limiting factor for immunohistochemical studies, the significance of the reverse relationship between Trk receptors and pc-Jun/pJNK LIs with respect to biological behavior of human astrocytomas requires further evaluation.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. MAP Kinase Kinase 4 / metabolism. Nerve Tissue Proteins / biosynthesis. Nerve Tissue Proteins / genetics. Receptors, Nerve Growth Factor / biosynthesis. Receptors, Nerve Growth Factor / genetics
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cytoplasm / metabolism. Humans. Phosphorylation. Receptor, trkA / metabolism. Receptor, trkB / metabolism. Receptor, trkC / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17971243.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NGFR protein, human; 0 / Nerve Tissue Proteins; 0 / Receptors, Nerve Growth Factor; 0 / bcl-2-Associated X Protein; EC 2.7.10.1 / Receptor, trkA; EC 2.7.10.1 / Receptor, trkB; EC 2.7.10.1 / Receptor, trkC; EC 2.7.12.2 / MAP Kinase Kinase 4
  • [Other-IDs] NLM/ PMC2180182
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70. Comincini S, Ferrara V, Arias A, Malovini A, Azzalin A, Ferretti L, Benericetti E, Cardarelli M, Gerosa M, Passarin MG, Turazzi S, Bellazzi R: Diagnostic value of PRND gene expression profiles in astrocytomas: relationship to tumor grades of malignancy. Oncol Rep; 2007 May;17(5):989-96
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  • [Title] Diagnostic value of PRND gene expression profiles in astrocytomas: relationship to tumor grades of malignancy.
  • Recently, ectopic expression of doppel was found in two different tumor types, specifically in glial and haematological cancers.
  • In order to address clinical important issues, PRND mRNA expression was investigated in a panel of 111 astrocytoma tissue samples, histologically classified according to the World Health Organization (WHO) criteria (6 grade I pilocytic astrocytomas, 15 grade II low-grade astrocytomas, 26 grade III anaplastic astrocytomas and 64 grade IV glioblastoma multiforme).
  • Real-time PRND gene expression profiling, after normalisation with GAPDH, revealed large differences between low (WHO I and II) and high grade (III and IV) of malignancy (P<0.001).
  • Extensive differences in PRND gene expression were also found within each grade of malignancy, suggesting that PRND mRNA quantitation might be useful to distinguish astrocytoma subtypes, and important in disease stratification and in the assessment of specific treatment strategies.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Prions / biosynthesis

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  • (PMID = 17390034.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions
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71. Ido K, Nakagawa T, Sakuma T, Takeuchi H, Sato K, Kubota T: Expression of vascular endothelial growth factor-A and mRNA stability factor HuR in human astrocytic tumors. Neuropathology; 2008 Dec;28(6):604-11
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  • [Title] Expression of vascular endothelial growth factor-A and mRNA stability factor HuR in human astrocytic tumors.
  • High-grade astrocytic tumors, such as glioblastoma, possess rich vascular components, which are necessary for their growth.
  • VEGF-A is considered to be the major mediator of angiogenesis in malignant neoplasms including high-grade astrocytic tumors.
  • The upregulation of VEGF-A expression in tumor cells is induced by two mechanisms: the transcriptional activation and the post-transcriptional stabilization of VEGF-A mRNA.
  • While the former mechanism mediated by hypoxia inducible factor-1 alpha (HIF-1alpha) has been revealed, the latter mediated by mRNA stability factor HuR remains unclear in astrocytic tumors.
  • In the present study, we investigated the expression of VEGF-A and mRNA stability factor HuR in supratentorial astrocytic tumors of 27 adults using RT-PCR, ELISA, and immunohistochemistry.
  • Furthermore, we studied the involvement of HuR in the upregulation of VEGF-A expression using malignant astrocytoma cell lines.
  • In higher-grade astrocytic tumors, the level of VEGF-A and microvascular density were elevated, cytoplasmic expression of HuR, which potentially means the protection of VEGF-A mRNA from degradation by ribonucleases, appeared, and they were correlated positively.
  • In in vitro experiments, the inhibition of the cytoplasmic translocation of HuR protein by leptomycin B (LMB) reduced the upregulation of VEGF-A expression in malignant astrocytic tumor cells under hypoxic conditions.
  • These findings suggest that the expression of VEGF-A and cytoplasmic translocation of HuR relates to the histological grade, and that HuR is involved in the upregulation of VEGF-A expression, in human astrocytic tumors.
  • [MeSH-major] Antigens, Surface / metabolism. Astrocytoma / metabolism. RNA-Binding Proteins / metabolism. Supratentorial Neoplasms / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Angiogenesis Inducing Agents. Cytoplasm / metabolism. ELAV Proteins. ELAV-Like Protein 1. Enzyme-Linked Immunosorbent Assay. Fatty Acids, Unsaturated / pharmacology. Female. Glioblastoma / genetics. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. Male. Middle Aged. RNA Processing, Post-Transcriptional. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Up-Regulation. Young Adult

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  • (PMID = 18498284.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Antigens, Surface; 0 / ELAV Proteins; 0 / ELAV-Like Protein 1; 0 / ELAVL1 protein, human; 0 / Fatty Acids, Unsaturated; 0 / RNA-Binding Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 87081-35-4 / leptomycin B
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72. Zhu Y, Harada T, Liu L, Lush ME, Guignard F, Harada C, Burns DK, Bajenaru ML, Gutmann DH, Parada LF: Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation. Development; 2005 Dec;132(24):5577-88
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  • The gene responsible for neurofibromatosis type 1 (NF1) encodes a tumor suppressor that functions as a negative regulator of the Ras proto-oncogene.
  • Individuals with germline mutations in NF1 are predisposed to the development of benign and malignant tumors of the peripheral and central nervous system (CNS).
  • Children with this disease suffer a high incidence of optic gliomas, a benign but potentially debilitating tumor of the optic nerve; and an increased incidence of malignant astrocytoma, reactive astrogliosis and intellectual deficits.

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  • (PMID = 16314489.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS052606-01; United States / NINDS NIH HHS / NS / P50 NS052606; United States / NINDS NIH HHS / NS / P50 NS052606-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neurofibromin 1
  • [Other-IDs] NLM/ NIHMS149022; NLM/ PMC2760350
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73. Ward SJ, Karakoula K, Phipps KP, Harkness W, Hayward R, Thompson D, Jacques TS, Harding B, Darling JL, Thomas DG, Warr TJ: Cytogenetic analysis of paediatric astrocytoma using comparative genomic hybridisation and fluorescence in-situ hybridisation. J Neurooncol; 2010 Jul;98(3):305-18
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  • [Title] Cytogenetic analysis of paediatric astrocytoma using comparative genomic hybridisation and fluorescence in-situ hybridisation.
  • Little is known about the cytogenetic and molecular genetic events that lead to the formation of paediatric astrocytoma.
  • We have analysed 57 paediatric astrocytoma (WHO grades I-IV) using comparative genomic hybridisation in order to identify common regions of abnormality.
  • The presence of copy number alterations was significantly associated with increasing grade of malignancy, and gain of 12q and the presence of high-copy number amplification were associated with a poor outcome in patients with malignant astrocytoma (P = 0.0039 and 0.0085, respectively).
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Comparative Genomic Hybridization / methods. In Situ Hybridization, Fluorescence / methods


74. Widmer M, Hanemann CO, Zajicek J: High concentrations of cannabinoids activate apoptosis in human U373MG glioma cells. J Neurosci Res; 2008 Nov 1;86(14):3212-20
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  • Glioma cells (astrocyte-derived brain tumor cells) express cannabinoid receptors, and numerous in vitro and in vivo studies performed in rodents have concluded that apoptosis could be induced by cannabinoids in these cells.
  • Whether this also applies to human cells is controversial; we, therefore, assessed the effect of cannabinoids on human glioma cell viability with the human astrocytoma cell line U373MG.
  • Human U373MG glioma cells are sensitive only to very high, pharmacologically irrelevant concentrations of cannabinoids, so it seems unlikely that cannabinoids would constitute promising molecules for treating malignant astrocytoma; they do not induce glioma cell death at doses that could be applied safely to humans.
  • [MeSH-minor] Blotting, Western. Brain Neoplasms / metabolism. Cannabinoid Receptor Agonists. Cell Line, Tumor. Cell Proliferation / drug effects. Fluorescent Antibody Technique. Humans. Receptors, Cannabinoid / drug effects. Signal Transduction / drug effects. Signal Transduction / physiology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18615640.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cannabinoid Receptor Agonists; 0 / Receptors, Cannabinoid; 7J8897W37S / Dronabinol
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75. McGirt MJ, Chaichana KL, Gathinji M, Attenello F, Than K, Ruiz AJ, Olivi A, Quiñones-Hinojosa A: Persistent outpatient hyperglycemia is independently associated with decreased survival after primary resection of malignant brain astrocytomas. Neurosurgery; 2008 Aug;63(2):286-91; discussion 291
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  • [Title] Persistent outpatient hyperglycemia is independently associated with decreased survival after primary resection of malignant brain astrocytomas.
  • OBJECTIVE: Patients with malignant brain astrocytomas are at high risk for developing hyperglycemia secondary to frequent corticosteroid administration.
  • Furthermore, hyperglycemia augments in vitro astrocytoma growth, whereas hypoglycemia attenuates in vitro astrocytoma cell growth.
  • We hypothesized that persistent hyperglycemic states in the outpatient setting may serve as a prognostic marker of decreased survival in patients with malignant brain astrocytomas.
  • METHODS: We retrospectively reviewed 367 cases of craniotomy for malignant brain astrocytomas (World Health Organization Grade III or IV).
  • RESULTS: A total of 367 craniotomies (209 primary, 158 secondary) were performed for malignant brain astrocytomas (glioblastoma multiforme, 297; anaplastic astrocytomas, 70); 68 (19%) and 28 (8%) of the patients experienced isolated or persistent outpatient hyperglycemia, respectively.
  • Adjusting for intergroup differences and variables associated with survival in this model, age (P = 0.001), Karnofsky Performance Scale score (P = 0.001), tumor grade (P = 0.001), primary versus secondary resection (P = 0.008), temozolomide (P = 0.007), subsequent resection (P = 0.07), and continued outpatient dexamethasone therapy, persistent outpatient hyperglycemia (relative risk, 1.79; 95% confidence interval, 1.05-3.05, P = 0.03) remained independently associated with decreased survival.
  • CONCLUSION: In our experience, persistent outpatient hyperglycemia was associated with decreased survival in patients undergoing surgical resection for malignant astro- cytomas and was independent of the degree of disability, tumor grade, diabetes, prolonged dexamethasone use, or subsequent treatment modalities.
  • Increased glucose control is warranted in this patient population and may contribute to improved outcomes in the treatment of malignant brain astrocytomas.
  • [MeSH-major] Ambulatory Care / trends. Astrocytoma / mortality. Astrocytoma / surgery. Brain Neoplasms / mortality. Brain Neoplasms / surgery. Hyperglycemia / mortality

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  • (PMID = 18797358.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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76. Nagy M, Schulz-Ertner D, Bischof M, Welzel T, Hof H, Debus J, Combs SE: Long-term outcome of postoperative irradiation in patients with newly diagnosed WHO grade III anaplastic gliomas. Tumori; 2009 May-Jun;95(3):317-24
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  • [Title] Long-term outcome of postoperative irradiation in patients with newly diagnosed WHO grade III anaplastic gliomas.
  • PURPOSE: Patients with anaplastic gliomas have a more favorable overall survival than patients with glioblastomas.
  • In most analyses, WHO grade III and 1V tumors are not analyzed separately.
  • The present analysis reports outcome after postoperative radiotherapy in patients with WHO grade III gliomas.
  • PATIENTS AND METHODS: Between January 1988 and January 2007, 127 patients with WHO grade III tumors were treated with radiotherapy; the histological classification was pure astrocytoma in 104 patients, oligoastrocytoma in 12 and pure oligodendroglioma in 11 patients.
  • Median overall survival was 7 months for patients with anaplastic astrocytomas, 44 months for patients with mixed tumors, and 47 months for those with pure oligodendrogliomas.
  • CONCLUSION: Patients with WHO grade III anaplastic astrocytomas, oligodendrogliomas and oligoastrocytomas show favorable overall survival after postoperative radiotherapy compared with glioblastoma patients and should therefore be analyzed separately.
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / pathology. Astrocytoma / radiotherapy. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Oligodendroglioma / pathology. Oligodendroglioma / radiotherapy. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis. Time Factors. Treatment Outcome. Young Adult

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  • (PMID = 19688970.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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77. Hartmann C, Hentschel B, Wick W, Capper D, Felsberg J, Simon M, Westphal M, Schackert G, Meyermann R, Pietsch T, Reifenberger G, Weller M, Loeffler M, von Deimling A: Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas. Acta Neuropathol; 2010 Dec;120(6):707-18
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  • [Title] Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas.
  • WHO grading of human brain tumors extends beyond a strictly histological grading system by providing a basis predictive for the clinical behavior of the respective neoplasm.
  • For example, patients with glioblastoma WHO grade IV usually show a less favorable clinical course and receive more aggressive first-line treatment than patients with anaplastic astrocytoma WHO grade III.
  • Here we provide evidence that the IDH1 status is more prognostic for overall survival than standard histological criteria that differentiate high-grade astrocytomas.
  • We sequenced the isocitrate dehydrogenase 1 gene (IDH1) at codon 132 in 382 patients with anaplastic astrocytoma and glioblastoma from the NOA-04 trial and from a prospective translational cohort study of the German Glioma Network.
  • Patients with anaplastic astrocytomas carried IDH1 mutations in 60%, and patients with glioblastomas in 7.2%.
  • The sequence from more favorable to poorer outcome was (1) anaplastic astrocytoma with IDH1 mutation, (2) glioblastoma with IDH1 mutation, (3) anaplastic astrocytoma without IDH1 mutation and (4) glioblastoma without IDH1 mutation (p < 0.0001).
  • In this combined set of anaplastic astrocytomas and glioblastomas both, IDH1 mutation and IDH1 expression status were of greater prognostic relevance than histological diagnosis according to the current WHO classification system.
  • We propose to complement the current WHO classification and grading of high-grade astrocytic gliomas by the IDH1 mutation status and to use this combined histological and molecular classification in future clinical trials.
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Cohort Studies. Female. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Young Adult


78. 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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  • [Title] Mutations in Rb1 pathway-related genes are associated with poor prognosis in anaplastic astrocytomas.
  • 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


79. Laczko R, Szauter KM, Jansen MK, Hollosi P, Muranyi M, Molnar J, Fong KS, Hinek A, Csiszar K: Active lysyl oxidase (LOX) correlates with focal adhesion kinase (FAK)/paxillin activation and migration in invasive astrocytes. Neuropathol Appl Neurobiol; 2007 Dec;33(6):631-43
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  • We have recently reported the ECM enzyme, lysyl oxidase (LOX), in the central nervous system and observed up-regulation of LOX in anaplastic astrocytoma cells.
  • In this study, we tested the hypothesis that active LOX is expressed in anaplastic astrocytes and promotes FAK activation and invasive/migratory behaviour.
  • Results demonstrate that increased expression and activity of LOX positively correlated with invasive phenotype of malignant astrocytoma cell lines.
  • Immunohistochemistry detected increased LOX within tumour cells and ECM in grade I-IV astrocytic neoplasm compared with normal brain and coincidence of increased LOX with the loss of glial fibrillary acidic protein in higher-grade tumours.
  • These results demonstrate an important LOX-mediated mechanism that promotes migratory/invasive behaviour of malignant astrocytes.
  • [MeSH-minor] Astrocytoma / enzymology. Blotting, Western. Cell Line, Tumor. Cell Movement / physiology. Humans. Immunohistochemistry. Neoplasm Invasiveness. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17931358.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR47713; United States / NCRR NIH HHS / RR / G12RR003096
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Paxillin; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
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80. 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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  • [Title] 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.
  • AIMS: The objective of the present study was to verify the correlation of chromosomes 1p and 19q status and expressions of O(6)-methylguanine DNA methyltransferase (MGMT), p53 and Ki-67 in diffuse gliomas of World Health Organization grades II and III.
  • METHODS: A series of 146 diffuse gliomas, including 45 oligodendrogliomas, 42 oligoastrocytomas and 59 astrocytomas, were analysed by denaturing high-performance liquid chromatography for 1p and 19q status and by immunohistochemistry for MGMT, p53 and Ki-67 expression patterns.
  • 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.
  • LOH on 1p and low MGMT expression were associated with grade II oligodendroglial tumours, whereas high expressions of p53 and Ki-67 were associated with grade III oligodendroglial tumours.
  • In addition, high Ki-67 expression was associated with grade III astrocytomas.
  • CONCLUSIONS: The present study revealed significant interrelationships of the investigated molecular alterations and clinicopathological characteristics in diffuse gliomas of World Health Organization grades II and III, which support a promising role of molecular markers in the diagnostic assessment of these neoplasms.
  • [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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81. Marie SK, Okamoto OK, Uno M, Hasegawa AP, Oba-Shinjo SM, Cohen T, Camargo AA, Kosoy A, Carlotti CG Jr, Toledo S, Moreira-Filho CA, Zago MA, Simpson AJ, Caballero OL: Maternal embryonic leucine zipper kinase transcript abundance correlates with malignancy grade in human astrocytomas. Int J Cancer; 2008 Feb 15;122(4):807-15
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  • [Title] Maternal embryonic leucine zipper kinase transcript abundance correlates with malignancy grade in human astrocytomas.
  • We have performed cDNA microarray analyses to identify gene expression differences between highly invasive glioblastoma multiforme (GBM) and typically benign pilocytic astrocytomas (PA).
  • Despite the significant clinical and pathological differences between the 2 tumor types, only 63 genes were found to exhibit 2-fold or greater overexpression in GBM as compared to PA.
  • In the examination of more than 100 tumors of the central nervous system, we found progressively higher expression of MELK with astrocytoma grade and a noteworthy uniformity of high level expression in GBM.
  • We found neither gene promoter hypomethylation nor amplification to be a factor in MELK expression, but were able to demonstrate that MELK knockdown in malignant astrocytoma cell lines caused a reduction in proliferation and anchorage-independent growth in in vitro assays.
  • Among them, MELK correlated with malignancy grade in astrocytomas and represents a therapeutic target for the management of the most frequent brain tumors in adult and children.
  • [MeSH-major] Astrocytoma / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Adult. Apoptosis. Brain / metabolism. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Proliferation. Child. DNA Methylation. Gene Dosage. Humans. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17960622.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.1.- / MELK protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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82. Toy H, Yavas O, Eren O, Genc M, Yavas C: Correlation between osteopontin protein expression and histological grade of astrocytomas. Pathol Oncol Res; 2009 Jun;15(2):203-7
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  • [Title] Correlation between osteopontin protein expression and histological grade of astrocytomas.
  • The expression of osteopontin is reportedly increased in a number of transformed cell lines and tumor tissues.
  • The aim of the study is to demonstrate that expression of osteopontin in human astrocytomas correlates with histological tumor grade.
  • The expression of osteopontin in human astrocytomas was determined with immunohistochemistry.
  • Median osteopontin expression levels were 1%, 7.5%, 60%, and 50% in grade I, II, III, and IV tumors, respectively.
  • Osteopontin staining was significantly higher in high grade (grade III-IV) than low grade (grade I-II) tumors.
  • These findings indicate that osteopontin immunoreactivity in human astrocytomas may correlate with the grade of a tumor.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Osteopontin / metabolism
  • [MeSH-minor] Brain / metabolism. Brain / pathology. Humans. Immunoenzyme Techniques. Neoplasm Invasiveness. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 19048398.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 106441-73-0 / Osteopontin
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83. Gaiser T, Becker MR, Meyer J, Habel A, Siegelin MD: p53-mediated inhibition of angiogenesis in diffuse low-grade astrocytomas. Neurochem Int; 2009 Jun;54(7):458-63
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  • [Title] p53-mediated inhibition of angiogenesis in diffuse low-grade astrocytomas.
  • In this study we evaluated the associations of p53 status and vessel density (angiogenesis) in a set of diffuse low-grade astrocytomas.
  • Immunohistochemistry was performed on 23 diffuse low-grade astrocytomas for CD31 and p53.
  • We found that 9/23 (39%) of the astrocytomas stained positive for p53 in the immunohistochemistry.
  • We identified TP53 mutations in 11/23 (47%) of the astrocytomas.
  • However, the MVD was significantly increased in p53 mutated low-grade astrocytomas.
  • Furthermore, the absolute vessel number was significantly higher in p53 mutated than in p53 wild-type low-grade astrocytomas.
  • To analyse the molecular background for that epiphenomenon LN229 glioma cells which harbour a TP53 mutation were transfected with a plasmid encoding p53 wild-type and an angiogenesis protein array was performed.
  • We detected a significant increase for thrombospondin-1, coagulation factor III and serpin E1 and a significant decrease of MMP-9 in wild-type p53 transfected LN229 cells.
  • The higher microvessel density and the increased absolute vessel number in p53 mutated tumours supports the importance of p53 for tumour angiogenesis in diffuse low-grade astrocytomas.
  • Our results support the hypothesis that p53 regulates angiogenesis in low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neovascularization, Pathologic / pathology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Blotting, Western. Capillaries / pathology. Cell Line, Tumor. DNA Mutational Analysis. Humans. Immunohistochemistry. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinase 9 / genetics. Protein Array Analysis. Proteomics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19428789.001).
  • [ISSN] 1872-9754
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 3.4.24.35 / Matrix Metalloproteinase 9
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84. Winters BS, Shepard SR, Foty RA: Biophysical measurement of brain tumor cohesion. Int J Cancer; 2005 Apr 10;114(3):371-9
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  • [Title] Biophysical measurement of brain tumor cohesion.
  • An advantage of using 3D multicellular spheres to study tumor biology is that they better approximate the interactions encountered by cells in vivo.
  • This liquid-like behavior enables us to measure a key property influencing tumor behavior, namely, intercellular cohesion.
  • This study utilizes TST to measure the cohesivity of 3 widely used malignant astrocytoma cell lines of different in vitro invasive potentials.
  • We show that the cell lines exhibit liquid-like behavior since they form spheroids whose surface tension is both force- and volume-independent; that aggregates from each cell line have a distinct surface tension that correlates with their in vitro invasive capacity; that dexamethasone (Dex), a widely used therapeutic agent for the treatment of tumor-related cerebral edema, increases aggregate cohesivity and decreases invasiveness; that dexamethasone treatment decreases invasion in a dose-dependent manner but only when cells are in direct contact with one another; and that dex-mediated decreased invasiveness correlates with increased aggregate cohesivity as measured by TST but not with N-cadherin expression or function.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Adhesion. Models, Biological. Neoplasm Invasiveness / physiopathology. Spheroids, Cellular

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551307.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone
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85. Rorive S, Maris C, Debeir O, Sandras F, Vidaud M, Bièche I, Salmon I, Decaestecker C: Exploring the distinctive biological characteristics of pilocytic and low-grade diffuse astrocytomas using microarray gene expression profiles. J Neuropathol Exp Neurol; 2006 Aug;65(8):794-807
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  • [Title] Exploring the distinctive biological characteristics of pilocytic and low-grade diffuse astrocytomas using microarray gene expression profiles.
  • Although World Health Organization (WHO) grade I pilocytic astrocytomas and grade II diffuse astrocytomas have been classified for decades as different clinicopathologic entities, few, if any, data are available on the biologic features explaining these differences.
  • Although more than 50 microarray-related studies have been carried out to characterize the molecular profiles of astrocytic tumors, we have identified only 11 that provide sound data on low-grade astrocytomas.
  • We have incorporated these data into a comparative analysis for the purpose of identifying the most relevant molecular markers characterizing grade I pilocytic and grade II diffuse astrocytomas.
  • Our analysis has identified various interesting genes that are differentially expressed in either grade I or grade II astrocytomas when compared with normal tissue and/or high-grade (WHO grade III and IV) astrocytomas.
  • Interestingly, a group of 6 genes (TIMP4, C1NH, CHAD, THBS4, IGFBP2, and TLE2) constitute an expression profile characteristic of grade I astrocytomas as compared with all other categories of tissue (normal brain, grade II, and high-grade astrocytomas).
  • The end products (proteins) of these genes act as antimigratory compounds, a fact that could explain why pilocytic astrocytomas behave as compact (well-circumscribed) tumors as opposed to all the other astrocytic tumor types that diffusely invade the brain parenchyma.
  • Having validated these molecular markers by means of real-time reverse transcriptase-polymerase chain reaction, an integrated model was proposed illustrating how and why pilocytic astrocytomas constitute a distinct biologic and pathologic entity when compared with diffuse astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic / genetics. Genetic Predisposition to Disease / genetics
  • [MeSH-minor] Adult. Cell Adhesion / genetics. Cell Movement / genetics. Child. Extracellular Matrix Proteins / genetics. Extracellular Matrix Proteins / metabolism. Humans. Models, Neurological. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / physiopathology. Oligonucleotide Array Sequence Analysis / methods. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16896313.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins
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86. Ulrich TA, de Juan Pardo EM, Kumar S: The mechanical rigidity of the extracellular matrix regulates the structure, motility, and proliferation of glioma cells. Cancer Res; 2009 May 15;69(10):4167-74
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  • Glioblastoma multiforme (GBM) is a malignant astrocytoma of the central nervous system associated with a median survival time of 15 months, even with aggressive therapy.
  • This rapid progression is due in part to diffuse infiltration of single tumor cells into the brain parenchyma, which is thought to involve aberrant interactions between tumor cells and the extracellular matrix (ECM).
  • Here, we test the hypothesis that mechanical cues from the ECM contribute to key tumor cell properties relevant to invasion.
  • We cultured a series of glioma cell lines (U373-MG, U87-MG, U251-MG, SNB19, C6) on fibronectin-coated polymeric ECM substrates of defined mechanical rigidity and investigated the role of ECM rigidity in regulating tumor cell structure, migration, and proliferation.
  • On highly rigid ECMs, tumor cells spread extensively, form prominent stress fibers and mature focal adhesions, and migrate rapidly.
  • As ECM rigidity is lowered to values comparable with normal brain tissue, tumor cells appear rounded and fail to productively migrate.
  • Collectively, our results provide support for a novel model in which ECM rigidity provides a transformative, microenvironmental cue that acts through actomyosin contractility to regulate the invasive properties of GBM tumor cells.

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  • (PMID = 19435897.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / DP2 OD004213; United States / NIH HHS / OD / OD004213-01; United States / NIH HHS / OD / 1DP2OD004213; United States / NIH HHS / OD / DP2 OD004213-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibronectins; 9013-26-7 / Actomyosin
  • [Other-IDs] NLM/ NIHMS105478; NLM/ PMC2727355
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87. Nagatani M, Yamakawa S, Ando R, Edamoto H, Saito T, Tamura K: Highly invasive intracranial malignant schwannoma in a rat. J Toxicol Pathol; 2009 Jun;22(2):139-42

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Highly invasive intracranial malignant schwannoma in a rat.
  • A highly invasive intracranial malignant schwannoma containing several masses was detected in a 28-week-old male Crl:CD(SD) rat.
  • The tumor cells invaded not only the brain but also the parietal bone.
  • In the brain, the tumor cells infiltrated diffusely into the leptomeningeal and perivascular spaces and parenchyma, in which the tumor cell morphology and invasive pattern closely resembled those of malignant astrocytoma and malignant reticulosis.
  • Immunohistochemically, the tumor cells in the masses showed positive reactions for both S-100 protein and GFAP, while those in the cerebral invasion sites were negative for GFAP and less positive for S-100 protein.
  • Electron microscopically, a single basal lamina layer and short intricate cell processes were confirmed in the tumor cells.
  • From these results, the present tumor was diagnosed as a malignant schwannoma arising in the cranial cavity, probably originating from the trigeminal nerve.
  • The present tumor is considered to be a relatively unique malignant schwannoma based on its growth and invasion patterns.

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  • (PMID = 22271987.001).
  • [ISSN] 0914-9198
  • [Journal-full-title] Journal of toxicologic pathology
  • [ISO-abbreviation] J Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC3246059
  • [Keywords] NOTNLM ; cranial cavity / malignant schwannoma / rat / spontaneous
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88. Gopalakrishna-Pillai S, Iverson LE: Astrocytes derived from trisomic human embryonic stem cells express markers of astrocytic cancer cells and premalignant stem-like progenitors. BMC Med Genomics; 2010 Apr 27;3:12
SciCrunch. ArrayExpress: Data: Microarray .

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  • [Title] Astrocytes derived from trisomic human embryonic stem cells express markers of astrocytic cancer cells and premalignant stem-like progenitors.
  • Since most hESC-based therapies will utilize differentiated derivatives, it is imperative to investigate the potential of trisomic hESCs to undergo malignant transformation during differentiation prior to their use in the clinical setting.
  • METHODS: Diploid and trisomic hESCs were differentiated into astrocytic progenitors cells (APCs), RNA extracted and hybridized to human exon-specific microarrays.
  • Global gene expression profiles of diploid and trisomic APCs were compared to that of an astrocytoma cell line and glioblastoma samples, analyzed by others, using the same microarray platform.
  • RESULTS: Bioinformatic analysis of microarray data indicates that differentiated trisomic APCs exhibit global expression profiles with similarities to the malignant astrocytoma cell line.
  • An analogous trend is observed in comparison to glioblastoma samples indicating that trisomic APCs express markers of astrocytic cancer cells.
  • The analysis also allowed identification of transcripts predicted to be differentially expressed in brain tumor stem cells.
  • These data indicate that in vitro differentiation of trisomic hESCs along astrocytic pathways give rise to cells exhibiting properties of premalignant astrocytic stem/progenitor cells.
  • This in vitro culture system can be used to elucidate changes in gene expression occurring enroute to malignant transformation and to identify molecular markers of cancer stem/progenitor cells.

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  • (PMID = 20423517.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA033572
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2873256
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89. Bucci B, Misiti S, Cannizzaro A, Marchese R, Raza GH, Miceli R, Stigliano A, Amendola D, Monti O, Biancolella M, Amati F, Novelli G, Vecchione A, Brunetti E, De Paula U: Fractionated ionizing radiation exposure induces apoptosis through caspase-3 activation and reactive oxygen species generation. Anticancer Res; 2006 Nov-Dec;26(6B):4549-57
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • In particular, post-operative RT is considered the standard treatment adjuvant to surgery since its ability to prolong median survival of patients with malignant astrocytoma has been shown; nevertheless the ionizing radiation (IR) treatment fails in a considerable number of astrocytoma patients.
  • MATERIALS AND METHODS: Using an ADF human astrocytoma cell line the molecular mechanisms involved in the DNA damage induced by fractionated irradiation (FIR) and single IR treatment have been investigated.
  • RESULTS: FIR and single IR treatment inhibited the growth of the ADF human astrocytoma cell line.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Caspase 3 / metabolism. Radiation, Ionizing. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Apoptosis. Blotting, Western. Cell Line, Tumor. Dose Fractionation. Enzyme Activation. Humans. Oligonucleotide Array Sequence Analysis


90. Combs SE, Ellerbrock M, Haberer T, Habermehl D, Hoess A, Jäkel O, Jensen A, Klemm S, Münter M, Naumann J, Nikoghosyan A, Oertel S, Parodi K, Rieken S, Debus J: Heidelberg Ion Therapy Center (HIT): Initial clinical experience in the first 80 patients. Acta Oncol; 2010 Oct;49(7):1132-40
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  • Main treated indications consisted of skull base chordoma (n = 9) and chondrosarcoma (n = 18), malignant salivary gland tumors (n=29), chordomas of the sacrum (n = 5), low grade glioma (n=3), primary and recurrent malignant astrocytoma and glioblastoma (n=7) and well as osteosarcoma (n = 3).

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  • (PMID = 20831505.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ions; 0 / Protons; 7440-44-0 / Carbon
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91. Christensen K, Schrøder HD, Kristensen BW: CD133 identifies perivascular niches in grade II-IV astrocytomas. J Neurooncol; 2008 Nov;90(2):157-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD133 identifies perivascular niches in grade II-IV astrocytomas.
  • The aim of the present study was to investigate the localization and distribution of the putative brain tumour stem cell marker CD133 in formalin fixed paraffin embedded astrocytomas.
  • A retrospective analysis of 114 grade II, III and IV astrocytomas was undertaken.
  • There was no correlation between the mean volume fraction of CD133(+) niches and all CD133(+) tumour cells and tumour grade.
  • However, the volume fraction of CD133(+) blood vessels increased significantly from 0.4% in diffuse astrocytomas to 2.2% in glioblastomas.
  • In conclusion, a CD133(+) perivascular stem cell-like entity exists in astrocytomas.
  • [MeSH-major] Antigens, CD / metabolism. Astrocytoma / pathology. Brain Neoplasms / pathology. Endothelium, Vascular / metabolism. Glycoproteins / metabolism. Peptides / metabolism

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  • (PMID = 18612800.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Indoles; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Peptides; 47165-04-8 / DAPI; EC 6.3.2.19 / MIB1 ligase, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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92. Frenay MP, Fontaine D, Vandenbos F, Lebrun C: First-line nitrosourea-based chemotherapy in symptomatic non-resectable supratentorial pure low-grade astrocytomas. Eur J Neurol; 2005 Sep;12(9):685-90
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] First-line nitrosourea-based chemotherapy in symptomatic non-resectable supratentorial pure low-grade astrocytomas.
  • At the present time, there are no proven beneficial effects of chemotherapy (CT) for the treatment of pure low-grade astrocytomas.
  • Brain radiotherapy (RT) still remains the standard treatment in order to reduce or delay tumor progression or symptoms, despite possible long-term neurologic complications.
  • We report 10 patients, with histologically proven pure low-grade fibrillary astrocytomas, to which we administered a first-line nitrosourea-based CT.
  • CT was well tolerated; all patients developed myelosuppression with 40% of grade III/IV hematotoxicity.
  • These results demonstrate that some patients with symptomatic non-resectable fibrillary low-grade astrocytomas can be treated with up-front CT to improve their neurologic status.
  • [MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Drug Therapy / methods. Nitrosourea Compounds / therapeutic use

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  • (PMID = 16128869.001).
  • [ISSN] 1351-5101
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nitrosourea Compounds
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93. McGirt MJ, Mukherjee D, Chaichana KL, Than KD, Weingart JD, Quinones-Hinojosa A: Association of surgically acquired motor and language deficits on overall survival after resection of glioblastoma multiforme. Neurosurgery; 2009 Sep;65(3):463-9; discussion 469-70
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  • OBJECTIVE: Balancing the benefits of extensive tumor resection with the consequence of potential postoperative deficits remains a challenge in malignant astrocytoma surgery.


94. Serrano J, Rayo JI, Infante JR, Domínguez L, García-Bernardo L, Durán C, Fernández Portales I, Cabezudo JM: Radioguided surgery in brain tumors with thallium-201. Clin Nucl Med; 2008 Dec;33(12):838-40
MedlinePlus Health Information. consumer health - Brain Tumors.

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  • RATIONALE: Malignant astrocytomas show thallium uptake with a high target-to-background ratio, allowing the use of radioguided surgery.
  • METHOD: We report on 6 patients (3 men) diagnosed with malignant astrocytoma.
  • With the gamma probe we confirmed the tumor uptake, and a biopsy sample was taken.
  • After conventional tumor resection, we scanned the surgical bed with the gamma probe.
  • RESULTS: In all patients the biopsy confirmed a high-grade astrocytoma.
  • In all cases we found residual uptake in the surgical bed that was confirmed as residual tumor by pathologic examination.

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  • (PMID = 19033782.001).
  • [ISSN] 1536-0229
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Thallium Radioisotopes
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95. Sulman EP, Guerrero M, Aldape K: Beyond grade: molecular pathology of malignant gliomas. Semin Radiat Oncol; 2009 Jul;19(3):142-9
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  • [Title] Beyond grade: molecular pathology of malignant gliomas.
  • High-grade gliomas (HGGs) represent a heterogenous group of tumors and account for most primary brain tumors.
  • These tumors include the anaplastic (World Health Organization [WHO] grade III) histologies of astrocytomas, oligodendrogliomas, and ependymomas and the WHO grade IV glioblastoma multiforme (GBM).
  • Prognostication for patients with these tumors has relied principally on tumor grade and clinical factors (age, performance status, and so on) and has been inexact at best in identifying those with long-term survival potential.
  • An even greater challenge has been to identify predictive biomarkers of therapy in the hope of tailoring a patient's therapy based on their tumor's molecular characteristics.
  • This review discusses the molecular pathology of high-grade gliomas, with particular emphasis on anaplastic astrocytomas and GBMs because these represent the most common forms of malignant gliomas.
  • [MeSH-minor] Biomarkers, Tumor. Gene Expression Profiling. Humans. Prognosis

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  • (PMID = 19464628.001).
  • [ISSN] 1532-9461
  • [Journal-full-title] Seminars in radiation oncology
  • [ISO-abbreviation] Semin Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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96. Yang SH, Kim YH, Kim JW, Park CK, Park SH, Jung HW: Methylation Status of the O6-Methylguanine-Deoxyribonucleic Acid Methyltransferase Gene Promoter in World Health Organization Grade III Gliomas. J Korean Neurosurg Soc; 2009 Oct;46(4):385-8
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  • [Title] Methylation Status of the O6-Methylguanine-Deoxyribonucleic Acid Methyltransferase Gene Promoter in World Health Organization Grade III Gliomas.
  • OBJECTIVE: We analyzed the methylation status of the O6-methylguanine-DNA methyltransferase (MGMT) gene promoter in World Health Organization (WHO) grade III gliomas in association with other molecular markers to evaluate their prevalence.
  • METHODS: The samples of a total of 36 newly WHO grade III glioma patients including 19 anaplastic oligodendrogliomas (AO), 7 anaplastic oligoastrocytomas (AOA), and 10 anaplastic astrocytomas (AA) were analyzed.
  • CONCLUSION: There was extensive epigenetic silencing of MGMT gene in high grade gliomas with oligodendroglial component.
  • Together with frequent 1p/19q co-deletion in oligodendroglial tumors, this may add plausible explanations supporting the relative favorable prognosis in oligodendroglial tumors compared with pure astrocytic tumors.

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  • (PMID = 19893731.001).
  • [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/ PMC2773399
  • [Keywords] NOTNLM ; 1p/19q / MGMT gene promoter / Methylation / Methylation-specific PCR / Oligodendroglioma
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97. Attenello FJ, Mukherjee D, Datoo G, McGirt MJ, Bohan E, Weingart JD, Olivi A, Quinones-Hinojosa A, Brem H: Use of Gliadel (BCNU) wafer in the surgical treatment of malignant glioma: a 10-year institutional experience. Ann Surg Oncol; 2008 Oct;15(10):2887-93
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  • [Title] Use of Gliadel (BCNU) wafer in the surgical treatment of malignant glioma: a 10-year institutional experience.
  • BACKGROUND: Gliadel (polifeprosan 20 with carmustine [BCNU] implant) is commonly used for local delivery of BCNU to high-grade gliomas after resection and is associated with increased survival.
  • We set out to characterize Gliadel-associated morbidity in our 10-year experience with Gliadel wafers for treatment of malignant glioma.
  • METHODS: We retrospectively reviewed records of 1013 patients undergoing craniotomy for resection of malignant brain astrocytoma (World Health Organization grade III/IV disease).
  • RESULTS: A total of 1013 craniotomies were performed for malignant brain astrocytoma.
  • A total of 288 (28%) received Gliadel wafer (250 glioblastoma multiforme (GBM), 38 anaplastic astrocytoma/anaplastic oligodendroglioma (AA/AO), 166 primary resection, 122 revision resection).
  • Patients in Gliadel versus non-Gliadel cohorts had similar incidences of perioperative surgical site infection (2.8% vs. 1.8%, P = .33), cerebrospinal fluid leak (2.8% vs. 1.8%, P = .33), meninigitis (.3% vs. .3%, P = 1.00), incisional wound healing difficulty (.7% vs. .4%, P = .63), symptomatic malignant edema (2.1% vs. 2.3%, P = 1.00), 3-month seizure incidence (14.6% vs. 15.7%, P = .65), deep-vein thrombosis (6.3% vs. 5.2%, P = .53), and pulmonary embolism (PE) (4.9% vs. 3.7%, P = .41).
  • CONCLUSION: In our experience, use of Gliadel wafer was not associated with an increase in perioperative morbidity after surgical treatment of malignant astrocytoma.

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  • (PMID = 18636295.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biocompatible Materials; 0 / Decanoic Acids; 0 / Drug Carriers; 0 / Polyesters; 90409-78-2 / decanedioic acid-4,4'-(1,3-propanediylbis(oxy))bis(benzoic acid) copolymer; U68WG3173Y / Carmustine
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98. Samaras V, Piperi C, Levidou G, Zisakis A, Kavantzas N, Themistocleous MS, Boviatsis EI, Barbatis C, Lea RW, Kalofoutis A, Korkolopoulou P: Analysis of interleukin (IL)-8 expression in human astrocytomas: associations with IL-6, cyclooxygenase-2, vascular endothelial growth factor, and microvessel morphometry. Hum Immunol; 2009 Jun;70(6):391-7
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  • [Title] Analysis of interleukin (IL)-8 expression in human astrocytomas: associations with IL-6, cyclooxygenase-2, vascular endothelial growth factor, and microvessel morphometry.
  • Malignant astrocytomas are highly vascular neoplasms with potent angiogenic activity.
  • The present study aimed to investigate peripheral and local expression of interleukin (IL)-8 in astrocytomas with possible associations to IL-6, cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF) expression, and microvessel morphometry.
  • IL-6- and IL-8-secreting peripheral blood monocytes (PBMCs) were evaluated in 17 glioblastoma (WHO grade IV), 5 anaplastic astrocytoma (WHO grade III), and 6 diffuse astrocytoma patients (WHO grade II), in parallel with 23 healthy controls using enzyme-linked immunosorbent spot (ELISPOT) assay.
  • The IL-8 expression was assessed immunohistochemically in patients' tumor tissue sections and correlated with the expression of COX-2, VEGF, IL-6, and microvessel morphometry (assessed using CD34 antibody).
  • IL-8 immunoreactivity was detected in malignant cells or macrophages in perivascular areas and in pseudopalisading cells around necrosis and was positively correlated with histological grade (p = 0.0175) and tumor necrosis (p = 0.0793).
  • The coordinate expression and topographical relationship of IL-6, IL-8, COX-2, and VEGF in the same tumor areas (e.g., perinecrotic areas) attest to their intimate liaison in terms of cancer-induced angiogenesis, which is probably secondary to the induction of multiple interdependent molecular pathways.
  • Moreover, our study seems to be the first attempt to link IL-8 expression by tumor cells with histological grade, implicating its potent role in gliomagenesis.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Cyclooxygenase 2 / immunology. Microvessels / immunology. Vascular Endothelial Growth Factor A / immunology

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  • (PMID = 19332096.001).
  • [ISSN] 1879-1166
  • [Journal-full-title] Human immunology
  • [ISO-abbreviation] Hum. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Interleukin-6; 0 / Interleukin-8; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2
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99. Burim RV, Teixeira SA, Colli BO, Peria FM, Tirapelli LF, Marie SK, Malheiros SM, Oba-Shinjo SM, Gabbai AA, Lotufo PA, Carlotti-Júnior CG: ICAM-1 (Lys469Glu) and PECAM-1 (Leu125Val) polymorphisms in diffuse astrocytomas. Clin Exp Med; 2009 Jun;9(2):157-63
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  • [Title] ICAM-1 (Lys469Glu) and PECAM-1 (Leu125Val) polymorphisms in diffuse astrocytomas.
  • Single-nucleotide polymorphism in codon 469 of ICAM-1 and codon 125 of PECAM-1 were examined in 158 patients with astrocytomas and 162 controls using polymerase chain reaction and restriction enzyme analysis.
  • The distribution of PECAM-1 polymorphic genotypes in astrocytomas did not show any significant difference.
  • However, a specific ICAM-1 genotype (G/G, corresponding to Lys469Glu) exhibited higher frequency in grade II astrocytomas compared to controls, grade III, and grade IV astrocytomas; suggesting that this polymorphism could be involved in the development of grade II astrocytomas.
  • [MeSH-major] Antigens, CD31 / genetics. Astrocytoma / genetics. Intercellular Adhesion Molecule-1 / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 19306055.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD31; 126547-89-5 / Intercellular Adhesion Molecule-1
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100. Hara A, Saegusa M, Ichinoe M, Okayasu I: Diagnostic and prognostic significance of cyclin A expression in low-grade astrocytomas: comparison with astrogliosis and high-grade tumours. J Clin Pathol; 2008 Mar;61(3):287-92
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  • [Title] Diagnostic and prognostic significance of cyclin A expression in low-grade astrocytomas: comparison with astrogliosis and high-grade tumours.
  • AIM: Definitive distinction between low-grade astrocytoma and astrogliosis is a long-standing difficulty due to their similar histopathological characteristics.
  • To clarify differences in biological significance, this study focused on various components of the cell cycle machinery and proliferation as key parameters, comparing expression in astrogliosis, as well as low- and high-grade astrocytomas.
  • METHODS: The expression of p16, p21 and p27, and cyclin A, cyclin D1, cyclin E, Rb and Ki-67 was immunohistochemically examined in 40 cases of astrogliosis and 48 cases of low-grade astrocytomas (grade II), as well as 50 high-grade tumours (grades III and IV).
  • The results were also compared with survival data for the astrocytomas.
  • RESULTS: Cell proliferation determined by Ki-67 immunoreactivity did not differ between astrogliosis and low-grade tumours.
  • Average labelling indices (LIs) for p16, p21, Rb, cyclin A and cyclin E showed a stepwise increase from astrogliosis, through low- to high-grade astrocytomas, indicating the possibility that over 9%, 6% and 4% of LIs for p16, p21 and cyclin A, respectively, may be useful predictors in the case of the latter, in contrast to significant decrease in p27 LIs.
  • Significantly higher mean LI values for cyclin D1 were also evident in astrogliosis (12.42) as compared with astrocytomas (low grade, 2.26; high grade, 4.60).
  • Positive correlations between LIs for Rb and Ki-67 were observed with astrogliosis and low- but not high-grade tumours.
  • In addition, high cyclin A LI values were independently associated with poor outcome in low-grade tumours.
  • CONCLUSION: These findings provide evidence that expression of cell-cycle-related molecules may be a reliable parameter for differential diagnosis of low-grade astrocytomas and astrogliosis.
  • Moreover, detection of cyclin A appears to be useful for predicting behaviour of low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor. Cyclin A / genetics. Gene Expression Regulation, Neoplastic

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  • (PMID = 18156430.001).
  • [ISSN] 1472-4146
  • [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 / Biomarkers, Tumor; 0 / Cyclin A; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Ki-67 Antigen; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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