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1. Amos S, Mut M, diPierro CG, Carpenter JE, Xiao A, Kohutek ZA, Redpath GT, Zhao Y, Wang J, Shaffrey ME, Hussaini IM: Protein kinase C-alpha-mediated regulation of low-density lipoprotein receptor related protein and urokinase increases astrocytoma invasion. Cancer Res; 2007 Nov 1;67(21):10241-51
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  • [Title] Protein kinase C-alpha-mediated regulation of low-density lipoprotein receptor related protein and urokinase increases astrocytoma invasion.
  • Low-density lipoprotein receptor-related protein (LRP) is expressed by glioblastoma, but the role of this receptor in astrocytic tumor invasion remains poorly understood.
  • Pretreatment of tumor cells with PKC inhibitors, phosphoinositide 3-kinase (PI3K) inhibitor, PKC-alpha small interfering RNA (siRNA), and short hairpin RNA abrogated phorbol 12-myristate 13-acetate-induced down-regulation of LRP and inhibited astrocytic tumor invasion in vitro.
  • Taken together, our results strongly suggest the involvement of PKC-alpha/PI3K signaling pathways in the regulation of LRP-mediated astrocytoma invasion.

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  • (PMID = 17974965.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS035122; United States / NHLBI NIH HHS / HL / P01HL48807; United States / NCI NIH HHS / CA / CA090851; United States / NCI NIH HHS / CA / R01 CA090851; United States / NINDS NIH HHS / NS / R29 NS035122; United States / NINDS NIH HHS / NS / NS035122-10; United States / NINDS NIH HHS / NS / R01 NS035122-10; United States / NINDS NIH HHS / NS / NS035122; United States / NHLBI NIH HHS / HL / P01 HL048807
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Low Density Lipoprotein Receptor-Related Protein-1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.13 / Protein Kinase C-alpha; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ NIHMS48323; NLM/ PMC2386949
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2. Shen CF, Yuan XR, Qin ZQ: [Clinical significance of the expression of the RCAS1 mRNA and protein in astrocytic tumors]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2007 Oct;32(5):836-9
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  • [Title] [Clinical significance of the expression of the RCAS1 mRNA and protein in astrocytic tumors].
  • OBJECTIVE: To determine the mRNA and protein expressions of RCAS1 in human astrocytic tumors, and to explore the relation between their expression and the genesis and development of tumor.
  • METHODS: The RCAS1 mRNA expression in human astrocytic tumors was evaluated by RT-PCR, and the RCAS1 protein expression was studied by immunohistochemical staining.
  • RESULTS: The quantities of RCAS1 mRNA expression between diffusive astrocytoma(Grade II) and anaplastic astrocytoma(Grade III), anaplastic astrocytoma and glioblastoma(Grade IV) were significantly different(P<0.05), while the expression scores of RCAS1 protein were different only between the anaplastic astrocytoma and glioblastoma(P<0.01).
  • RCAS1 protein expression was positively correlated with the tumor grade (r=0.573,P<0.001).
  • CONCLUSION: The RCAS1 expression is related to the histological grade of astrocytic tumor.
  • In astrocytic tumors, the RCAS1 expression is regulated transcriptionally and posttranscriptionally.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism

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  • (PMID = 18007080.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / EBAG9 protein, human; 0 / RNA, Messenger
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3. Petalidis LP, Oulas A, Backlund M, Wayland MT, Liu L, Plant K, Happerfield L, Freeman TC, Poirazi P, Collins VP: Improved grading and survival prediction of human astrocytic brain tumors by artificial neural network analysis of gene expression microarray data. Mol Cancer Ther; 2008 May;7(5):1013-24
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  • [Title] Improved grading and survival prediction of human astrocytic brain tumors by artificial neural network analysis of gene expression microarray data.
  • Histopathologic grading of astrocytic tumors based on current WHO criteria offers a valuable but simplified representation of oncologic reality and is often insufficient to predict clinical outcome.
  • In this study, we report a new astrocytic tumor microarray gene expression data set (n = 65).
  • We have used a simple artificial neural network algorithm to address grading of human astrocytic tumors, derive specific transcriptional signatures from histopathologic subtypes of astrocytic tumors, and asses whether these molecular signatures define survival prognostic subclasses.
  • Fifty-nine classifier genes were identified and found to fall within three distinct functional classes, that is, angiogenesis, cell differentiation, and lower-grade astrocytic tumor discrimination.
  • These gene classes were found to characterize three molecular tumor subtypes denoted ANGIO, INTER, and LOWER.
  • The prognostic value of the three identified tumor subtypes was found to outperform histopathologic grading as well as tumor subtypes reported in other studies, indicating a high survival prognostic potential for the 59 gene classifiers.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / mortality. Brain Neoplasms / diagnosis. Brain Neoplasms / mortality. Gene Expression Profiling / methods. Neural Networks (Computer). Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Algorithms. Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Humans. Intracellular Signaling Peptides and Proteins / genetics. Phosphoproteins / genetics. Prognosis. Reproducibility of Results. Survival Rate

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  • (PMID = 18445660.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intracellular Signaling Peptides and Proteins; 0 / PEA15 protein, human; 0 / Phosphoproteins
  • [Other-IDs] NLM/ PMC2819720; NLM/ UKMS2687
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4. Sbalchiero E, Azzalin A, Palumbo S, Barbieri G, Arias A, Simonelli L, Ferretti L, Comincini S: Altered cellular distribution and sub-cellular sorting of doppel (Dpl) protein in human astrocytoma cell lines. Cell Oncol; 2008;30(4):337-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered cellular distribution and sub-cellular sorting of doppel (Dpl) protein in human astrocytoma cell lines.
  • Nevertheless, in astrocytomas, a particular kind of glial tumors, the doppel encoding gene (PRND) is over-expressed and the corresponding protein product (Dpl) is ectopically localized in the cytoplasm of the tumor cells.
  • In this study we have analysed the sub-cellular localization of Dpl using double-immunofluorescence staining and confocal microscopy examinations in two astrocytoma-derived human cell lines (IPDDC-A2 and D384-MG).
  • Our results confirmed that Dpl is localized in the cytoplasm of the astrocytoma cells and indicated that it is mostly associated with Lamp-1 and Limp-2 positive lysosomal vesicles and, marginally, to the Golgi apparatus and other cellular organelles.
  • Noticeably, none of the examined tumor cells showed a membrane-Dpl localization.
  • The membrane-associated Dpl expression was restored after the transfection of the astrocytoma cells with mutated Dpl-expression vectors in its glycosylation sites.
  • Altogether, these results indicated that in the astrocytic tumor cells Dpl has an altered biosynthetic trafficking, likely derived from abnormal post-translational processes: these modifications do not permit the localization of Dpl in correspondence of the plasma membrane and lead to its intracellular accumulation in the lysosomes.
  • In these proteolytic compartments, the astrocytic tumor cells might provide to the degradation of the excess of a potentially cytotoxic Dpl product.

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  • (PMID = 18607068.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Glycosylphosphatidylinositols; 0 / Mutant Proteins; 0 / PRND protein, human; 0 / Prions; 0 / Recombinant Proteins; 01Q9PC255D / Ammonium Chloride
  • [Other-IDs] NLM/ PMC4618817
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5. Uno M, Oba-Shinjo SM, Wakamatsu A, Huang N, Avancini Ferreira Alves V, Rosemberg S, Pires de Aguiar PH, Leite C, Miura F, Marino J R, Scaff M, Nagahashi-Marie SK: Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas. Int J Biol Markers; 2006 Jan - Mar;21(1):50-57

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

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  • (PMID = 28207094.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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6. Comincini S, Paolillo M, Barbieri G, Palumbo S, Sbalchiero E, Azzalin A, Russo MA, Schinelli S: Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens. J Biomed Biotechnol; 2009;2009:924565
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  • [Title] Gene expression analysis of an EGFR indirectly related pathway identified PTEN and MMP9 as reliable diagnostic markers for human glial tumor specimens.
  • To verify if this correlation was conserved in gliomas, PTEN and MMP9 expression was further investigated in an additional panel of 16 anaplastic astrocytoma specimens and, in parallel, in different human normal and astrocytic tumor cell lines.
  • In anaplastic astrocytomas PTEN expression was significantly higher than in glioblastoma multiforme, but no significant correlation was found between PTEN and MMP9 expression.
  • PTEN and MMP9 mRNA levels were also employed to identify subgroups of specimens within the different glioma malignancy grades and to define a gene expression-based diagnostic classification scheme.
  • In conclusion, this gene expression survey highlighted that the combined measurement of PTEN and MMP9 transcripts might represent a novel reliable tool for the differential diagnosis of high-grade gliomas, and it also suggested a functional link involving these genes in glial tumors.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Glioma / diagnosis. Glioma / enzymology. Matrix Metalloproteinase 9 / metabolism. PTEN Phosphohydrolase / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

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  • (PMID = 19657395.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2718324
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7. Sen S, Dong M, Kumar S: Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology. PLoS One; 2009 Dec 23;4(12):e8427
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  • [Title] Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology.
  • Glioblastoma Multiforme (GBM) is a malignant astrocytic tumor associated with low survival rates because of aggressive infiltration of tumor cells into the brain parenchyma.
  • To probe the cellular basis of this correlation, we have suppressed expression of the nonmuscle isoforms alpha-actinin-1 and alpha-actinin-4 and examined the contribution of each isoform to the structure, mechanics, and motility of human glioma tumor cells in culture.
  • Our results demonstrate that both alpha-actinin-1 and alpha-actinin-4 make critical and distinct contributions to cytoskeletal organization, rigidity-sensing, and motility of glioma cells, thereby yielding mechanistic insight into the observed correlation between alpha-actinin expression and GBM invasiveness in vivo.

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  • (PMID = 20037648.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / DP2 OD004213; United States / NIH HHS / OD / 1DP2OD004213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 11003-00-2 / Actinin; 125361-02-6 / Vinculin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2793025
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8. Naidoo V, Naidoo S, Mahabeer R, Raidoo DM: Localization of the endothelin system in human diffuse astrocytomas. Cancer; 2005 Sep 1;104(5):1049-57

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localization of the endothelin system in human diffuse astrocytomas.
  • Because only immunoreactive ET-1 has been observed within human astrocytic tumor cells, the authors investigated the localization of the entire ET-1 system (ET-1 mRNA, ET-1, ECE-1, ETA and ETB receptors) in surgical samples of human diffuse astrocytomas WHO Grade II (n = 6).
  • RESULTS: All ET components were detected in the six tumor samples.
  • Intense (3+) cytoplasmic ET-1 mRNA labeling was observed in more than 75% of cells in all 6 astrocytomas.
  • Up to 75% of tumor cells displayed intense ET-1 and ECE-1 immunolabeling distributed throughout their cytoplasm.
  • Immunoreactive ETA and ETB receptors, observed in 25% to 75% of astrocytic tumor cells, were of moderate intensity.
  • In addition, all components of the ET system were seen within endothelial cells of tumor blood vessels.
  • CONCLUSIONS: The presence of ET-1 mRNA, ECE-1, and ET-1 within tumor astrocytes suggests local ET synthesis and processing.
  • [MeSH-major] Aspartic Acid Endopeptidases / analysis. Astrocytoma / chemistry. Endothelin-1 / analysis. Metalloendopeptidases / analysis. Receptor, Endothelin A / analysis. Receptor, Endothelin B / analysis

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  • (PMID = 16007684.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endothelin-1; 0 / RNA, Messenger; 0 / Receptor, Endothelin A; 0 / Receptor, Endothelin B; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.71 / endothelin-converting enzyme
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9. Choi KC, Kwak SE, Kim JE, Sheen SH, Kang TC: Enhanced glial fibrillary acidic protein-delta expression in human astrocytic tumor. Neurosci Lett; 2009 Oct 9;463(3):182-7
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  • [Title] Enhanced glial fibrillary acidic protein-delta expression in human astrocytic tumor.
  • Astrocytic tumor is one of the most common primary tumors of the adult brain.
  • Although there are several biochemical markers for the categorization of astrocytic tumor, few markers are used for histopathological diagnosis.
  • In tissue samples from patients with low-grade astrocytic tumor (grades I and II), GFAP-delta(+) cells appeared stellate, polygonal or round shape.
  • In tissue samples from patients with high-grade astrocytic tumor (grades III and IV), GFAP-delta(+) cells showed round or spindle shape.
  • GFAP-delta immunoreactivities in grades III and IV astrocytic tumor cells were increased by 1.4- and 1.7-fold in comparison to grade I astrocytic tumor cells.
  • GFAP-delta immunoreactivity was also observed in cell bodies along the margins of astrocytic tumor showing normal histological findings, even though astroglia had normal morphology (showing strong GFAP and glutamine synthase immunoreactivities and a stellate shape with well-developed processes).
  • Furthermore, the malignancy of astrocytic tumor was directly correlated with the degree of GFAP-delta immunoreactivity.
  • These findings suggest that GFAP-delta may be a useful diagnostic marker for the evaluation of functional cataplasia or proliferation of astrocytic tumor.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Glial Fibrillary Acidic Protein / biosynthesis

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  • (PMID = 19647039.001).
  • [ISSN] 1872-7972
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; EC 6.3.1.2 / Glutamate-Ammonia Ligase
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10. Katoh N, Shirato H, Aoyama H, Onimaru R, Suzuki K, Hida K, Miyasaka K, Iwasaki Y: Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor. J Neurooncol; 2006 May;78(1):63-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.
  • PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord glioma with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumors.
  • MATERIALS AND METHODS: Forty-one patients with spinal cord glioma received post-operative radiotherapy between 1979 and 2003.
  • There were 12 low-grade astrocytic tumors, 11 high-grade astrocytic tumors, 16 low-grade ependymal tumors and 2 high-grade ependymal tumors.
  • Among 11 patients with high-grade astrocytic tumors, 5 with anaplastic astrocytoma and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation.
  • RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the astrocytic tumors and 84% for the ependymal tumors, respectively (P=0.009).
  • Among 11 patients with high-grade astrocytic tumors, the actuarial survival rate at 10 years was 35%.
  • DISCUSSION: The results for ependymal tumors and low-grade astrocytic tumors were comparable to those reported in the literature.
  • Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-grade astrocytic tumors.
  • [MeSH-major] Dose Fractionation. Glioma / radiotherapy. Spinal Cord Neoplasms / radiotherapy

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  • (PMID = 16314938.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Horger M, Fenchel M, Nägele T, Moehle R, Claussen CD, Beschorner R, Ernemann U: Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum. AJR Am J Roentgenol; 2009 Nov;193(5):1384-7
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  • [Title] Water diffusivity: comparison of primary CNS lymphoma and astrocytic tumor infiltrating the corpus callosum.
  • OBJECTIVE: The purpose of this study was to determine whether lymphoma and astrocytic tumor infiltrating the corpus callosum can be reliably differentiated with measurement of water diffusivity.
  • MATERIALS AND METHODS: Echo-planar diffusion-weighted MR images of 27 patients with glioblastoma multiforme, five patients with low-grade astrocytoma, five patients with gliomatosis cerebri, and nine patients with primary lymphoma infiltrating the corpus callosum were reviewed retrospectively.
  • Regions of interest were drawn on apparent diffusion coefficient (ADC) maps inside the callosal tumor.
  • ADCs were normalized by calculation of the ratio between the ADC of the tumor and the ADC of an uninvolved region of corpus callosum.
  • RESULTS: The mean ADC of glioblastoma multiforme was 1.13 +/- 0.31 (SD) x 10(-3) mm(2)/s, and the mean tumor to corpus callosum ADC ratio was 1.51 +/- 0.46; of low-grade astrocytoma, 1.14 +/- 0.23 x 10(-3) mm(2)/s and 1.54 +/- 0.28; gliomatosis cerebri, 1.01 +/- 0.20 x 10(-3) mm(2)/s and 1.31 +/- 0.36; and lymphoma, 0.71 +/- 0.13 x 10(-3) mm(2)/s and 0.93 +/- 0.19.
  • The difference between the mean tumor to corpus callosum ADC ratio of lymphoma and that of all grades of astrocytoma (1.48 +/- 0.43) was statistically significant (p < 0.001).
  • The optimal ADC threshold for discriminating astrocytic tumor and lymphoma was 0.90 x 10(-3) mm(2)/s (sensitivity, 84%; specificity, 89%).
  • The optimal threshold for tumor to corpus callosum ADC ratio was 1.22 (sensitivity, 73%; specificity, 100%).
  • CONCLUSION: The water diffusivity and the ADC ratio of the tumor to normal-appearing corpus callosum of astrocytic tumor differ significantly from those of lymphoma infiltrating the corpus callosum, allowing reliable differentiation of the two types of tumor.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Corpus Callosum / pathology. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / pathology. Lymphoma / pathology. Water / metabolism

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  • (PMID = 19843757.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 059QF0KO0R / Water
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12. Nagai S, Kurimoto M, Ishizawa S, Hayashi N, Hamada H, Kamiyama H, Endo S: A rare astrocytic tumor with rhabdoid features. Brain Tumor Pathol; 2009;26(1):19-24
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  • [Title] A rare astrocytic tumor with rhabdoid features.
  • We report an extremely rare tumor presenting with rhabdoid features in the left temporoparietal lobe near the trigone in an 18-year-old Japanese man.
  • This tumor mainly consisted of medium to large round cells that proliferated diffusely and incoherently with a scant extracellular matrix.
  • These tumor cells had an eccentric nucleus and an eosinophilic cytoplasm containing inclusion bodies and bundles of intermediate filaments.
  • This tumor had an area appearing to be diffuse astrocytoma peripherally and lacked a primitive neuroectodermal tumor component, a mesenchymal component, and epithelial differentiation.
  • INI expression, which is not observed in atypical teratoid/ rhabdoid tumor (AT/RT), was found in this tumor.
  • From these findings, we concluded that this tumor was not AT/RT but an astrocytic tumor with rhabdoid features.
  • We also concluded that the tumor cells exhibiting rhabdoid features had secondarily arisen from the peripheral area presenting an appearance of diffuse astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Rhabdoid Tumor / pathology

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  • (PMID = 19408093.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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13. Schittenhelm J, Mittelbronn M, Nguyen TD, Meyermann R, Beschorner R: WT1 expression distinguishes astrocytic tumor cells from normal and reactive astrocytes. Brain Pathol; 2008 Jul;18(3):344-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] WT1 expression distinguishes astrocytic tumor cells from normal and reactive astrocytes.
  • Particularly in small brain biopsies, it might be difficult to distinguish reactive astrogliosis from low-grade or infiltration zones of high-grade astrocytomas.
  • Recently, the over-expression of Wilms' tumor gene product WT1 was reported in astrocytic tumor cells.
  • Therefore, we investigated WT1 expression in paraffin-embedded brain sections from 28 controls, 48 cases with astrogliosis of various etiology and 219 astrocytomas [World Health Organization (WHO) grades I-IV] by immunohistochemistry.
  • In astrocytomas, WT1-positive tumor cells were found in pilocytic astrocytomas (66.7% of cases), diffuse astrocytomas (52.7%) WHO grade II (52.7%), anaplastic astrocytomas (83.4%) and glioblastomas (98.1%).
  • Overall, the majority of all astrocytic neoplasms (84.5%) expressed WT1.
  • Establishing a cut-off value of 0% immunoreactive tumor cells served to recognize neoplastic astrocytes with 100% specificity and 68% sensitivity and was associated with positive and negative predictive values of 1 and 0.68, respectively.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gliosis / metabolism. WT1 Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Endothelial Cells / metabolism. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 18371184.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / WT1 Proteins
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14. Comincini S, Chiarelli LR, Zelini P, Del Vecchio I, Azzalin A, Arias A, Ferrara V, Rognoni P, Dipoto A, Nano R, Valentini G, Ferretti L: Nuclear mRNA retention and aberrant doppel protein expression in human astrocytic tumor cells. Oncol Rep; 2006 Dec;16(6):1325-32
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  • [Title] Nuclear mRNA retention and aberrant doppel protein expression in human astrocytic tumor cells.
  • Besides, Dpl overexpression correlates with some prion-disease pathological features, such as ataxia and death of cerebellar neurons.
  • Recently, ectopic expression of doppel was found in two different tumor types, specifically in glial and haematological cancers.
  • In this study the doppel gene (PRND) mRNA and protein expression in PRT-HU2 and IPDDC-A2 astrocytoma-derived cell lines was investigated.
  • Northern blot analysis revealed two equally abundant PRND mRNA isoforms, while real-time PCR, on nuclear and cytoplasmic RNA fractions, and cRNA in situ hybridization, on astrocytoma cells and bioptical specimens, showed a nuclear retention of PRND transcripts.
  • Immunohistochemistry experiments demonstrated that Dpl was mainly localised in the cytoplasm of the astrocytic tumor cells, and that it failed to be GPI-anchored to the cell membrane.
  • This unusual cellular localization was also confirmed through EGFP-Dpl expression in astrocytomas; on the contrary, HeLa cells exhibited the expected Dpl membrane localization.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cell Nucleus / metabolism. Prions / biosynthesis. RNA, Messenger / metabolism
  • [MeSH-minor] Blotting, Northern. Blotting, Western. Cell Line, Tumor. Cytoplasm / metabolism. GPI-Linked Proteins. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Protein Biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transfection

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  • (PMID = 17089057.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / PRND protein, human; 0 / Prions; 0 / RNA, Messenger
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15. Arjona D, Rey JA, Taylor SM: Early genetic changes involved in low-grade astrocytic tumor development. Curr Mol Med; 2006 Sep;6(6):645-50
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  • [Title] Early genetic changes involved in low-grade astrocytic tumor development.
  • Astrocytomas represent the most common form of glial tumors.
  • The most malignant grade of these tumors, glioblastoma multiforme, may arise as a malignant progression from low-grade astrocytoma through anaplastic astrocytoma to secondary GBM, or else it may arise "de novo" as primary GBM.
  • Since malignant transformation is a multistep process, we summarize in this review the earliest genetic changes that seem to be involved in the appearance and development of low-grade astrocytic tumors, where early detection and treatment could be possible.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Glioblastoma / genetics. Models, Genetic. Tumor Suppressor Proteins / genetics

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  • (PMID = 17022734.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins
  • [Number-of-references] 80
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16. Cui XL, Zhao ZG, Ren XH, Sui DL, Chu JS, Tang K, Zeng C, Lin S: [Characteristics of combining loss of heterozygosity of 1p/19q in glioma]. Zhonghua Wai Ke Za Zhi; 2010 Jun 1;48(11):852-5
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  • [Title] [Characteristics of combining loss of heterozygosity of 1p/19q in glioma].
  • METHODS: The status of 1p and 19q of 138 glioma specimen from January 2009 to December 2009 was evaluated by Fluorescence in situ hybridization (FISH) method, and the frequencies of combining LOH of 1p/19q were compared between different pathologies, brain sub-regions, genders and ages.
  • RESULTS: The frequencies of combined LOH of 1p and 19q of oligodendroglial (81.3%) and oligo astrocytic tumors (55.8%) were significantly higher than that of astrocytic tumor (22.2%) (P < 0.01), and the frequency of oligodendroglial tumor was significantly higher than that of oligo astrocytic tumor (P < 0.05).
  • [MeSH-major] Brain Neoplasms / genetics. Glioma / genetics. Loss of Heterozygosity

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  • (PMID = 21163056.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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17. Srinivas BH, Uppin MS, Panigrahi MK, Vijaya Saradhi M, Jyotsna Rani Y, Challa S: Pleomorphic xanthoastrocytoma of the pineal region. J Clin Neurosci; 2010 Nov;17(11):1439-41
Genetic Alliance. consumer health - Pleomorphic xanthoastrocytoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pleomorphic xanthoastrocytomas are indolent, astrocytic tumors usually located in the superficial cerebral cortex.
  • We describe a patient with an astrocytic tumor arising in the pineal region that fulfilled all of the morphologic and immunohistochemical criteria of a pleomorphic xanthoastrocytoma.
  • To our knowledge, this is the first description of a pleomorphic xanthoastrocytoma located in the pineal region.
  • [MeSH-major] Astrocytoma / diagnosis. Pineal Gland / pathology. Pinealoma / diagnosis

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20655751.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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18. Lassman AB, Oligodendroglioma Study Group: Retrospective analysis of outcomes among more than 1,000 patients with newly diagnosed anaplastic oligodendroglial tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2014

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

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  • (PMID = 27964586.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. 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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20. Simonelli M, Banna G, Navarria P, Di Ieva A, Zucali P, De Vincenzo F, Gaetani P, Condorelli R, Rodriguez Y Baena R, Scorsetti M, Santoro A: Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13037

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

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

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

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  • (PMID = 27962826.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Tosoni A, Franceschi E, Ermani M, Bacci A, Volpin L, Lombardo L, Ravenna G, Pinna G, Poggi R, Brandes AA: MGMT methylation status as a prognostic factor in anaplastic astrocytomas. J Clin Oncol; 2009 May 20;27(15_suppl):2052

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

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  • (PMID = 27964674.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Desjardins A, Reardon DA, Gururangan S, Peters K, Threatt S, Friedman A, Friedman H, Vredenburgh J: Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG). J Clin Oncol; 2009 May 20;27(15_suppl):e13004

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

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  • (PMID = 27962751.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. 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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25. Witt H, Korshunov A, Remke M, Janzarik WG, Gnekow A, Scheurlen W, Kulozik AE, Lichter P, Pfister S: DNA methylation pattern of brain stem pilocytic astrocytomas in children. J Clin Oncol; 2009 May 20;27(15_suppl):10021

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

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

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

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

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

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

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

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  • (PMID = 27962817.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Rudnick JD, Phuphanich S, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Black KL, Wheeler C, Yu J: A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma. J Clin Oncol; 2009 May 20;27(15_suppl):2033

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

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  • (PMID = 27964627.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Potthast L, Chowdhary S, Pan E, Yu D, Zhu W, Brem S: The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab. J Clin Oncol; 2009 May 20;27(15_suppl):2057

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

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  • (PMID = 27964663.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Lin Y, Jiang T, Li G: MGMT expression in low-grade gliomas. J Clin Oncol; 2009 May 20;27(15_suppl):e13001

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

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  • (PMID = 27962757.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Huang X, Bai HM, Chen L, Li B, Lu YC: Reduced expression of LC3B-II and Beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors. J Clin Neurosci; 2010 Dec;17(12):1515-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced expression of LC3B-II and Beclin 1 in glioblastoma multiforme indicates a down-regulated autophagic capacity that relates to the progression of astrocytic tumors.
  • The aim of this study was to investigate the expression of microtubule-associated protein 1 light chain 3B (LC3B) and the autophagy-related gene Beclin 1 in astrocytic tumors and to analyze their expression profiles with respect to the development of astrocytic tumors.
  • The expression patterns of LC3B and Beclin 1 were analyzed by immunohistochemistry and/or western blotting in tumor samples from 62 patients with different grades of astrocytic tumor.
  • Western blot analysis indicated that the average optical densitometry (OD) ratio of Beclin 1 in high-grade astrocytic tumors (World Health Organization [WHO] grade III/IV) was lower than in low-grade astrocytic tumors (WHO grade I/II, p = 0.036).
  • The expression of LC3B-I exhibited no significant difference among the various grades of astrocytic tumor.
  • However, the average OD ratio of LC3B-II was lower in glioblastoma multiforme (GBM) than in other grades of astrocytic tumor (p = 0.030).
  • The progression of astrocytic tumors was related to a decrease in autophagic capacity represented by the loss of LC3B-II and Beclin 1 expression.
  • [MeSH-minor] Adult. Astrocytoma / metabolism. Astrocytoma / pathology. Autophagy. Blotting, Western. Disease Progression. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20863706.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / light chain 3, human
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33. Lee FY, Jan YJ, Wen MC, Li MC, Wang J, Wen-Hsien C: A 32-year-old man with a fourth ventricular mass. Brain Pathol; 2009 Apr;19(2):333-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our case is in the fourth ventricle of a 32 year-old man.Many areas showed tumor cells with a signet-ring appearance and focally formed perivascular arrangements.
  • There was strong positive immunoreactivity to GFAP and S-100 protein, even in those vacuolated tumor cells.The proliferation index was less than 10%.
  • These findings confirm that the vacuoles were lipid droplets in astrocytic tumor cells.
  • The features noted are suggestive of a probable better prognosis in this variant of low-grade astrocytoma.
  • [MeSH-major] Astrocytoma / pathology. Cerebral Ventricle Neoplasms / pathology

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  • (PMID = 19291000.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / S100 Proteins
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34. Fernandez A, Karavitaki N, Ansorge O, Fazal-Sanderson V, Wass JA: Acromegaly and anaplastic astrocytoma: coincidence or pathophysiological relation? Pituitary; 2008;11(3):325-30
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  • [Title] Acromegaly and anaplastic astrocytoma: coincidence or pathophysiological relation?
  • In astrocytic-cell tumors, the role of autocrine and paracrine IGF-I expression in enhancing tumoral progression is well established.
  • However, the influence of systemic IGF-I levels on the clinical behavior of astrocytic neoplasms remains an open subject of research.
  • We report the case of a 28-year-old man who presented simultaneously with acromegaly and an anaplastic astrocytoma, which had rapidly progressed from a low-grade astrocytoma.
  • The coexistence of systemic IGF-I hypersecretion with a quick progression in the histopathological grade of the astrocytoma raises the compelling question of whether the clinical behavior of the astrocytic tumor was influenced by the acromegalic status.
  • The role of IGF-I signaling in the pathogenesis of astrocytic-cell tumors and the experience with therapeutic strategies addressing this pathway in astrocytomas are also discussed.
  • [MeSH-major] Acromegaly / complications. Astrocytoma / complications. Brain Neoplasms / complications
  • [MeSH-minor] Adult. Cranial Irradiation. Craniotomy. Disease Progression. Ergolines / therapeutic use. Humans. Insulin-Like Growth Factor I / metabolism. Magnetic Resonance Imaging. Male. Neoplasm Staging. Peptides, Cyclic / therapeutic use. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Treatment Outcome. Up-Regulation

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  • (PMID = 18000757.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ergolines; 0 / Peptides, Cyclic; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I; LL60K9J05T / cabergoline
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35. Hlobilkova A, Ehrmann J, Sedlakova E, Krejci V, Knizetova P, Fiuraskova M, Kala M, Kalita O, Kolar Z: Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression? Neoplasma; 2007;54(4):334-41
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  • [Title] Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression?
  • The most frequent alterations found in astrocytomas are two major groups of signaling proteins: the cell cycle and the growth factor-regulated signaling pathways.
  • The aim of our study was to detect changes in expression of the following proteins: the tumor suppressors PTEN, p53, and p21Waf1/Cip1, glial fibrillary acidic protein (GFAP, as a marker of astroglial differentiation), the phosphorylated form of protein kinase B/Akt (PKB/Akt), which is downstream to the epidermal growth factor receptor (EGFR), and MDM2, which degrades p53.
  • Paraffin-embedded astrocytoma tissue samples from 89 patients were divided into low grade (grade I-II; 42 samples) and high grade astrocytomas (grade III-IV; 47 samples).
  • EGFR protein was detected in 29 % of low grade and in 60 % of high grade astrocytomas.
  • The expression of phosphorylated PKB/Akt was found in roughly the same proportions: in 86% of low grade and in 79% of high grade astrocytomas.
  • PTEN was not found in most of astrocytomas, 64% of low grade and 74% of high grade tumors showed no PTEN staining.
  • Overexpression of the mutated form of p53 or loss of p53 expression, however, was found in about 63% in both groups of astrocytomas with no differences between them.
  • GFAP expression was decreased in tumor astrocytes compared to normal astrocytes and this decreased with grading.
  • GFAP positive tumor cells were detected in only 50% of low grade, and 32% of high grade astrocytomas.
  • We conclude that EGFR expression increases with astrocytoma grading.
  • PTEN defects may also participate in aggressive tumor behaviour through activation of the PKB/Akt pathway.
  • The alteration of p53 supports the finding that the cell cycle regulation is also disrupted during development of astrocytomas.
  • EGFR is one of the factors, which drives the progression of astrocytomas from low to high grade stage.
  • [MeSH-major] Astrocytoma / metabolism. Cell Cycle. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Mutation / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / pathology. PTEN Phosphohydrolase / metabolism. Phosphorylation. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17822324.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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36. Xu GW, Mymryk JS, Cairncross JG: Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin. J Neurooncol; 2005 Sep;74(2):141-9
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  • [Title] Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin.
  • p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.
  • In this report, we examined the effect of p53 inactivation on the chemosensitivity of two additional human astrocytic glioma cell lines, D54 and A172, in order to assess whether sensitization is a general property of astrocytic tumor cells.
  • Sensitization to both BCNU and TMZ was associated with failure of p21(WAF1) induction, lack of a sustained G2 cell cycle arrest and significant tumor cell death.
  • These findings suggest that enhanced sensitivity to BCNU and TMZ is a general property of human astrocytic glioma cells in which p53 was disrupted.
  • In contrast, p53 inactivation rendered D54 and U87MG cells significantly more resistant to cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which high-grade astrocytomas sometimes respond.
  • These results indicate that p53 status influences the chemosensitivity of astrocytic glioma cells in a drug-type specific manner, a finding that may have implications for the selection of drug treatments for patients with astrocytic gliomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Carmustine / therapeutic use. Cisplatin / therapeutic use. Dacarbazine / analogs & derivatives. Gene Silencing. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. Tumor Cells, Cultured. Tumor Stem Cell Assay

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  • (PMID = 16193384.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Tumor Suppressor Protein p53; 7GR28W0FJI / Dacarbazine; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine; YF1K15M17Y / temozolomide
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37. Komatani H, Sugita Y, Arakawa F, Ohshima K, Shigemori M: Expression of CXCL12 on pseudopalisading cells and proliferating microvessels in glioblastomas: an accelerated growth factor in glioblastomas. Int J Oncol; 2009 Mar;34(3):665-72
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

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  • To elucidate the correlation between the CXCR4/CXCL12 axis and glioblastomas (GBs), the present study assessed CXCR4/CXCL12 expression in 44 astrocytic tumor tissues using immunohistochemical analyses.
  • Although low-grade, astrocytic tumors were rarely positive for CXCL12 immunohistochemically, all GBs showed moderate to intense immunostaining with CXCL12, with particularly intense immunostaining being observed in the pseudopalisading cells and the proliferating microvessels.
  • Regarding CXCR4, widespread positive immunoreactivity was noted in the tumor cells in almost all cases of GBs.
  • Taken together, these results suggest that secretion of CXCR4/CXCL12 by hypoxic pseudopalisading and proliferating microvascular cells contributes to an outward migration of tumor cells away from hypoxia, creating a peripherally moving wave and subsequent microvascular proliferation.
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / blood supply. Astrocytoma / pathology. Cell Growth Processes / physiology. Cell Line, Tumor. Cell Movement / physiology. Child. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Microvessels / metabolism. Microvessels / pathology. Middle Aged. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Young Adult

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  • (PMID = 19212671.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chemokine CXCL12
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38. Mertsch S, Schmitz N, Jeibmann A, Geng JG, Paulus W, Senner V: Slit2 involvement in glioma cell migration is mediated by Robo1 receptor. J Neurooncol; 2008 Mar;87(1):1-7
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  • [Title] Slit2 involvement in glioma cell migration is mediated by Robo1 receptor.
  • Because similar molecular mechanisms may be utilized in glioma cell invasion and neuroblast migration, we studied the expression of Slit2 and its transmembrane receptor Robo1 as well as their functional role in migration in glioma cells. qRT-PCR and immunohistochemistry of human specimens revealed that Slit2 was distinctly expressed by non-neoplastic neurons, but at only very low levels in fibrillary astrocytoma and glioblastoma.
  • Robo1 also was mainly restricted to neurons in the normal brain, whereas astrocytic tumor cells in situ as well as glioblastoma cell lines overexpressed Robo1 at mRNA and protein levels.
  • Recombinant human Slit2 in a concentration of 0.45 nM was repulsive for glioma cell lines in a modified Boyden chamber assay.
  • RNAi-mediated knockdown of Robo1 in glioma cell lines neutralized the repulsive effect of Slit2, demonstrating that Robo1 served as the major Slit2 receptor.
  • Our findings suggest that a chemorepulsive effect mediated by interaction of Slit2 and Robo1 participates in glioma cell guidance in the brain.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Glioma / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Nerve Tissue Proteins / metabolism. Receptors, Immunologic / metabolism
  • [MeSH-minor] Astrocytes / metabolism. Blotting, Western. Cell Line, Tumor. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Neurons / metabolism. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17968499.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Immunologic; 0 / Slit homolog 2 protein; 0 / roundabout protein
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39. Arismendi-Morillo G, Castellano-Ramírez A, Medina Z: Ultrastructural characterization of macrophage-like mononuclear leukocytes in human astrocytic tumors. Ultrastruct Pathol; 2010 Dec;34(6):321-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultrastructural characterization of macrophage-like mononuclear leukocytes in human astrocytic tumors.
  • The aim of this study was to describe the ultrastructural features of macrophage-like mononuclear leukocytes associated with human astrocytic tumors.
  • Tumoral biopsies of 10 patients with a pathological diagnosis of astrocytic tumor by means of transmission electron microscopy were examined.
  • The macrophage-like mononuclear leukocyte shows ultrastructural characteristics related with the physiologic phenotype of the alternatively activated macrophage (M2), localized principally around of tumoral vasculature and tumor milieu; classically activated macrophages (M1) in surrounding necrosis areas were observed.
  • The presence of these two ultrastructural kinds of macrophage-like mononuclear leukocytes into different areas of the tumor denotes that cellular response of TAMs is dependent of microenvironment stimuli in different parts of a tumor.
  • The process of transvascular emigration of monocyte/macrophage-like mononuclear leukocytes into tumor is presented.
  • Therefore, macrophage polarization toward anti-tumoral macrophage-like mononuclear leukocytes would be a potential target for therapeutic manipulation in human astrocytic tumors.
  • [MeSH-major] Astrocytoma / ultrastructure. Brain Neoplasms / ultrastructure. Leukocytes, Mononuclear / ultrastructure. Macrophages / ultrastructure

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  • (PMID = 20568985.001).
  • [ISSN] 1521-0758
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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40. Conti A, Aguennouz M, La Torre D, Tomasello C, Cardali S, Angileri FF, Maio F, Cama A, Germanò A, Vita G, Tomasello F: miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors. J Neurooncol; 2009 Jul;93(3):325-32
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors.
  • Recent evidence indicates that miRNAs can function both as tumor suppressors and as oncogenes.
  • Expression of miR-21, 221, 128a, 128b, 128c, 181a, 181b, 181c was studied using real-time quantitative reverse transcriptase polymerase chain reaction and northern blotting for human astrocytic tumors with different grade of malignancy. miR-21 and 221 were overexpressed in glioma samples, whereas miRNA 181b was downregulated compared with normal brain tissue. miRNA-21 was hyperexpressed in all tumor samples whereas higher levels of miRNA-221 were found in high-grade gliomas.
  • This study is the first analysis of miRNAs in astrocytic tumor at different stages of malignancy.

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  • (PMID = 19159078.001).
  • [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 / MIRN21 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs
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41. Khayal IS, Nelson SJ: Characterization of low-grade gliomas using RGB color maps derived from ADC histograms. J Magn Reson Imaging; 2009 Jul;30(1):209-13
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  • [Title] Characterization of low-grade gliomas using RGB color maps derived from ADC histograms.
  • PURPOSE: To use normalized apparent diffusion coefficient (nADC) histograms from patients with grade II oligodendroglioma (OD) and astrocytoma (AC) to generate RGB color maps that emphasize the differences between normal-appearing white matter (NAWM), oligo-like, and astro-like regions.
  • MATERIALS AND METHODS: NAWM and nonenhancing lesion (NEL) ADC values from 19 ODs and 11 ACs were summed to generate oligo-like (red), NAWM (green), and astro-like (blue) nADC histograms.
  • RESULTS: Color maps of oligodendroglial tumor regions were generally visualized in pink, while color maps of astrocytic tumor regions showed various shades of blue.
  • This technique was also applied to 23 patients with the more mixed subtype, oligoastrocytoma (OA), which showed a mixture of both blue and pink, which in many cases appeared to bleed into each other and were blotchy.
  • CONCLUSION: This technique allows for the visualization of biologically different regions within the whole tumor mass, which may aid in directing image-guided biopsies.
  • This can be used to ensure that the biopsy is directed to regions that can more accurately define the dominant tumor characteristics.
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology. Magnetic Resonance Imaging / methods

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19557741.001).
  • [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; AU0V1LM3JT / Gadolinium
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42. Stukel JM, Caplan MR: Targeted drug delivery for treatment and imaging of glioblastoma multiforme. Expert Opin Drug Deliv; 2009 Jul;6(7):705-18
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  • Glioblastoma multiforme is a grade IV astrocytic tumor with a very high mortality rate.
  • Although current treatment often includes surgical resection, this rarely removes all primary tumor cells, so is usually followed by radiation and/or chemotherapy.
  • Remaining migratory tumor cells invade surrounding healthy tissue and contribute to secondary and tertiary tumor recurrence; therefore, despite significant research into glioma removal and treatment, prognosis remains poor.

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  • (PMID = 19538036.001).
  • [ISSN] 1744-7593
  • [Journal-full-title] Expert opinion on drug delivery
  • [ISO-abbreviation] Expert Opin Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 118
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43. Tsuji K, Nakasu S, Tsuji A, Fukami T, Nozaki K: [Postoperative regression of desmoplastic infantile astrocytoma]. No Shinkei Geka; 2008 Nov;36(11):1035-9
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  • [Title] [Postoperative regression of desmoplastic infantile astrocytoma].
  • Desmoplastic infantile astrocytoma/ganglioglioma (DIA/DIG) is a rare tumor that is usually located superficially with a large cystic component.
  • In rare cases, postoperative regression of the residual tumor has been reported.
  • A CT scan showed a large cystic tumor in his left parieto-occipital lobe.
  • The histopathological examination revealed an astrocytic tumor with marked desmoplasia.
  • In the central portion of the tumor, anaplastic features, such as necrosis, mitosis, and high nucleus-cytoplasmic ratio, were noticed.
  • Six months later when he was admitted for the second-stage surgery, MRI showed regression of the tumor.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / surgery. Brain Neoplasms / pathology. Brain Neoplasms / surgery
  • [MeSH-minor] Gliosis. Humans. Infant. Male. Neoplasm Regression, Spontaneous

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  • (PMID = 19048924.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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44. 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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45. Pédeboscq S, L'Azou B, Passagne I, De Giorgi F, Ichas F, Pometan JP, Cambar J: Cytotoxic and apoptotic effects of bortezomib and gefitinib compared to alkylating agents on human glioblastoma cells. J Exp Ther Oncol; 2008;7(2):99-111
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  • Glioblastoma is a malignant astrocytic tumor with a median survival of about 12 months for which new therapeutic strategies are required.
  • [MeSH-minor] Animals. Bortezomib. Carboplatin / pharmacology. Carmustine / pharmacology. Cell Line, Tumor. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Dose-Response Relationship, Drug. Flow Cytometry. Glial Fibrillary Acidic Protein / genetics. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Indicators and Reagents. Mice. Proteasome Inhibitors. Rats. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, Epidermal Growth Factor / genetics. Tetrazolium Salts. Thiazoles

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  • (PMID = 18771084.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Boronic Acids; 0 / Glial Fibrillary Acidic Protein; 0 / Indicators and Reagents; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Quinazolines; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; 69G8BD63PP / Bortezomib; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; BG3F62OND5 / Carboplatin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib; U68WG3173Y / Carmustine
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46. Fu YJ, Miyahara H, Uzuka T, Natsumeda M, Okamoto K, Hirose T, Fujii Y, Takahashi H: Intraventricular pleomorphic xanthoastrocytoma with anaplastic features. Neuropathology; 2010 Aug;30(4):443-8
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  • Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic tumor that usually occurs in the superficial cerebral hemispheres of children and young adults and has a relatively favorable prognosis.
  • We report an unusual case of supratentorial, intraventricular tumor in a 52-year-old man.
  • The tumor was composed of pleomorphic cells, including giant cells, most of which were multinucleated, and small cells.
  • In addition, frequent xanthic changes in the cytoplasm of the tumor cells, and widespread reticulin deposits and lymphocytic infiltrates in the stroma were characteristic features.
  • Many tumor cells were positive for GFAP, and a number were positive for neurofilament protein and synaptophysin, indicating their neuronal differentiation.
  • In addition, occasional tumor cells were positive for CD34. p53 protein was entirely negative in the tumor cells.
  • In diagnosing this tumor histopathologically, differentiation between PXA and giant cell glioblastoma (GCG), a rare variant of glioblastoma, was problematic.
  • The present case indicates that PXA can occur as an intraventricular tumor, and suggests that in some instances, it would be very difficult to differentiate PXA and GCG histopathologically.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology

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  • (PMID = 20051018.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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47. Azzalin A, Del Vecchio I, Chiarelli LR, Valentini G, Comincini S, Ferretti L: Absence of interaction between doppel and GFAP, Grb2, PrPc proteins in human tumor astrocytic cells. Anticancer Res; 2005 Nov-Dec;25(6B):4369-74
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  • [Title] Absence of interaction between doppel and GFAP, Grb2, PrPc proteins in human tumor astrocytic cells.
  • Recently, Dpl was shown to be aberrantly expressed in astrocytic tumor specimens and in astrocytoma-derived cell lines, showing a peculiar cytoplasmic localization.
  • In particular, whether the tumor astrocytic environment is suitable for doppel interaction with GFAP and Grb2 proteins, as well as with the PrPC protein itself was investigated.
  • Our findings provided evidence that, in our astrocytoma cell-based model, Dpl does not share with PrP(C) the ability to interact with GFAP and Grb2.
  • CONCLUSION: Identifying Dpl ligands may provide new insights into the involvement of Dpl in astrocytoma tumor progression.
  • [MeSH-major] Astrocytoma / metabolism. GRB2 Adaptor Protein / metabolism. Glial Fibrillary Acidic Protein / metabolism. PrPC Proteins / metabolism. Prions / metabolism

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  • (PMID = 16309242.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / PRND protein, human; 0 / PrPC Proteins; 0 / Prions
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48. Rao AA, Laack NN, Giannini C, Wetmore C: Pleomorphic xanthoastrocytoma in children and adolescents. Pediatr Blood Cancer; 2010 Aug;55(2):290-4
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  • BACKGROUND: Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic tumor occurring primarily in children and young adults.
  • The superficial location of the tumor facilitates gross total resection (GTR) thus conferring a relatively favorable outcome with a reported 10-year overall survival (OS) of 70%.
  • [MeSH-major] Astrocytoma

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
  • (PMID = 20582976.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Min HS, Lee SH, Yoo H, Myung J, Hong EK, Park SH: Cytogenetic study of glioneuronal tumor with neuropil-like islands: a case report. Neuropathology; 2010 Aug;30(4):420-6
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  • [Title] Cytogenetic study of glioneuronal tumor with neuropil-like islands: a case report.
  • Glioneuronal tumor with neuropil-like islands (GTNI) is a recently recognized glioneuronal neoplasm but it was classified as an astrocytic tumor by the World Health Organization (WHO) in 2007.
  • Histopathologically, the tumor showed the biphasic feature of the predominating micronodular neuropil-like islands and the diffusely infiltrating glial component.
  • The remaining tumor after subtotal resection progressed 7 months later, despite combined chemo- and radiotherapy.
  • From the results, it seems that GTNI does not share pathologic or genetic features with conventional astrocytoma, suggesting a unique entity with aggressive behavior.

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  • (PMID = 19845863.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
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50. Taomoto K, Ohnishi H, Kamada Y, Kuga Y, Kohaya N, Nakashima K, Ichioka T, Tominaga T, Nakamura M, Nakazato Y: A rare case of malignant glioma suspected to have arisen from a cavernous sinus. Brain Tumor Pathol; 2007;24(2):75-80
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  • [Title] A rare case of malignant glioma suspected to have arisen from a cavernous sinus.
  • The extraparenchymal tumor located around the right trigeminal ganglion was totally removed, except for an intracavernous lesion, by the orbitozygomatic approach.
  • The solid tumor was completely separated from the brainstem and seemed to be a trigeminal schwannoma arising from the trigeminal ganglion or cavernous sinus at surgery.
  • A histological examination, however, found a typical malignant glioma that consisted primarily of astrocytic tumor cells.
  • Immunohistochemical staining showed the tumor cells stained intensely for GFAP, S-100 protein, and vimentin, but not for NFP, Schwann/2E, CD34, and CD68.
  • The tumor recurred after a short time, and then it rapidly disseminated into the subarachnoid space and left the cerebral hemisphere.
  • There are no previous reports of a malignant glioma arising from either the cavernous sinus or the trigeminal ganglion.
  • From the pathogenetic point of view, this malignant glioma is an extremely rare case that developed clinically and neuroradiologically from the cavernous sinus and was suspected be being derived from ectopic glial tissue.
  • [MeSH-major] Brain Neoplasms / pathology. Cavernous Sinus / pathology. Glioma / pathology. Neoplasm Recurrence, Local / pathology

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  • (PMID = 18095135.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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51. Chang HT, Latorre JG, Hahn S, Dubowy R, Schelper RL: Pediatric cerebellar pleomorphic xanthoastrocytoma with anaplastic features: a case of long-term survival after multimodality therapy. Childs Nerv Syst; 2006 Jun;22(6):609-13
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  • METHODS: Additional special stains and immunocytochemistry were performed on the paraffin embedded tumor sections.
  • However, the additional stains revealed that the tumor is a relatively well-circumscribed meningeal-based astrocytic tumor (positive for GFAP) with extensive reticulin deposit and focal neuronal differentiation (positive for synaptophysin).
  • A Ki67 labeling index is generally very low, but is positive in up to 5-10% of tumor cells focally.
  • In the light of the favorable clinical outcome and the overall histological features, this tumor may be best reclassified as a rare example of cerebellar pleomorphic xanthoastrocytoma with foci of anaplasia.

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  • (PMID = 16570197.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins
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52. Amos S, Redpath GT, Dipierro CG, Carpenter JE, Hussaini IM: Epidermal growth factor receptor-mediated regulation of urokinase plasminogen activator expression and glioblastoma invasion via C-SRC/MAPK/AP-1 signaling pathways. J Neuropathol Exp Neurol; 2010 Jun;69(6):582-92
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  • One of the major pathophysiological features of malignant astrocytomas is their ability to infiltrate surrounding brain tissue.
  • The epidermal growth factor receptor (EGFR) and proteases are known to be overexpressed in glioblastomas (GBMs), but the interaction between the activation of the EGFR and urokinase plasminogen activator (uPA) in promoting astrocytic tumor invasion has not been fully elucidated.
  • Here, we characterized the signal transduction pathway(s) by which EGF regulates uPA expression and promotes astrocytoma invasion.

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  • (PMID = 20467333.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090851; United States / NCI NIH HHS / CA / CA 090851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factor AP-1; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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53. Gologorsky Y, DeLaMora P, Souweidane MM, Greenfield JP: Cerebellar cryptococcoma in an immunocompetent child. Case report. J Neurosurg; 2007 Oct;107(4 Suppl):314-7
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  • This is the first report of a cerebellar cryptococcoma in a previously healthy, HIV-negative child.
  • Isolated cryptococcomas of the central nervous system (CNS) have been previously described in immunocompetent adults; however, this is the first report of a cryptococcoma in a child.
  • The patient underwent excision of the mass, and analysis of frozen sections suggested the presence of an astrocytic tumor with pilocytic features; therefore gross-total resection was performed.
  • Once the definitive diagnosis of a cryptococcal abscess was obtained, medical treatment with antifungal medications led to the resolution of all symptoms and the normalization of serum titers.
  • [MeSH-major] Cerebellar Diseases / diagnosis. Cryptococcosis / diagnosis. Immunocompetence. Magnetic Resonance Imaging. Neurosurgical Procedures. Tomography, X-Ray Computed

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  • (PMID = 17941497.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents
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54. Rickert CH, Riemenschneider MJ, Schachenmayr W, Richter HP, Bockhorn J, Reifenberger G, Paulus W: Glioblastoma with adipocyte-like tumor cell differentiation--histological and molecular features of a rare differentiation pattern. Brain Pathol; 2009 Jul;19(3):431-8
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  • [Title] Glioblastoma with adipocyte-like tumor cell differentiation--histological and molecular features of a rare differentiation pattern.
  • We report on three adult patients with primary glioblastomas showing prominent adipocytic (lipomatous) differentiation, hence referred to as "glioblastomas with adipocyte-like tumor cell differentiation."
  • Histologically, the tumors demonstrated typical features of glioblastoma but additionally contained areas consisting of glial fibrillary acidic protein (GFAP)-positive astrocytic tumor cells resembling adipocytes, that is, containing large intracellular lipid vacuoles.
  • The second tumor showed gains of chromosomes 3, 4, 8q and 12 as well as losses of chromosomes 10, 13, 15q, 19 and 22.
  • In addition, this tumor carried homozygous deletions of CDKN2A and p14(ARF) as well as point mutations in the TP53 and PTEN genes.
  • The third tumor also had a mutation in the PTEN gene.
  • Taken together, our results define a rare glioblastoma differentiation pattern and indicate that glioblastomas with adipocyte-like tumor cell differentiation share common molecular genetic features with other primary glioblastomas.


55. Witte HT, Jeibmann A, Klämbt C, Paulus W: Modeling glioma growth and invasion in Drosophila melanogaster. Neoplasia; 2009 Sep;11(9):882-8
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  • [Title] Modeling glioma growth and invasion in Drosophila melanogaster.
  • Glioblastoma is the most common and most malignant intrinsic human brain tumor, characterized by extensive invasion and proliferation of glial (astrocytic) tumor cells, frequent activation of tyrosine kinase receptor signaling pathways, relative resistance to chemotherapy and radiotherapy, and poor prognosis.
  • Using the Gal4-UAS system, we have produced glioma models in Drosophila by overexpressing homologs of human tyrosine kinase receptors under control of the glia-specific promoter reversed polarity (repo).
  • Glial overexpression of activated epidermal growth factor receptor (EGFR) resulted in enhanced proliferation and migration of larval glial cells with increased numbers in the eye imaginal disc, diffuse tumor-like enlargement of the optic stalk, and marked ectopic invasion of glial cells along the optic nerve.
  • We suggest that Drosophila models will be useful for deciphering signaling cascades underlying abnormal behavior of glioma cells for genetic screens to reveal interacting genes involved in gliomagenesis and for experimental therapy approaches.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Drosophila melanogaster / metabolism. Glioma / pathology
  • [MeSH-minor] Animals. Eye / cytology. Eye / metabolism. Humans. Immunoenzyme Techniques. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Platelet-Derived Growth Factor / metabolism. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Receptors, Platelet-Derived Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 19724682.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC2735809
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56. Soichi O, Masanori N, Hideo T, Kazunori A, Nobuya I, Jun-ichi K: Clinical significance of ABCA2' a possible molecular marker for oligodendrogliomas. Neurosurgery; 2007 Apr;60(4):707-14; discussion 714
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  • METHODS: To determine whether or not ABCA2 can distinguish oligodendrogliomas from astrocytic tumors, the authors investigated the expression of ABCA2 in a panel of 55 glioma tissues (13 oligodendrogliomas, nine anaplastic oligodendrogliomas, 12 anaplastic astrocytomas, and 21 glioblastomas) using real-time reverse-transcriptase polymerase chain reaction analysis, immunoblot analysis, and immunohistochemistry analysis.
  • RESULTS: The relative expression level of ABCA2 messenger ribonucleic acid determined by real-time quantitative polymerase chain reaction is significantly higher (by a factor of five) in oligodendroglioma than in anaplastic astrocytoma or glioblastoma.
  • In immunohistochemical analysis, ABCA2 exhibited remarkable immunopositivity in 11 out of 13 oligodendrogliomas showing a granular pattern in the cytoplasm of tumor cells.
  • However, ABCA2 was completely negative in most anaplastic astrocytomas (75%) and glioblastomas (76%).
  • However, Olig2 was strongly positive in most anaplastic astrocytomas (83%) and glioblastomas (71%).
  • Although there was no difference in the detection of oligodendroglial tumors, the specificity (negative in astrocytic tumor) was significantly higher in ABCA2 than in Olig2.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism. Oligodendroglioma / metabolism

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  • (PMID = 17415208.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCA2 protein, human; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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57. Crespo-Rodríguez AM, Smirniotopoulos JG, Rushing EJ: MR and CT imaging of 24 pleomorphic xanthoastrocytomas (PXA) and a review of the literature. Neuroradiology; 2007 Apr;49(4):307-15
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  • INTRODUCTION: The aim of our study was to review the imaging appearance of PXA, a rare and usually low-grade, astrocytic tumor that typically occurs in young adults.
  • Two morphologic patterns were defined according to imaging features.
  • Apart from the classical PXA appearance of a cystic lesion with an enhancing mural nodule, a second pattern consisting of a predominantly solid mass was recognized.
  • [MeSH-major] Astrocytoma / diagnosis. Magnetic Resonance Imaging / methods. Supratentorial Neoplasms / diagnosis. Tomography, X-Ray Computed / methods

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  • (PMID = 17205313.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 44
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58. Bodey B, Siegel SE, Kaiser HE: Cyclooxygenase-2 (COX-2) overexpression in childhood brain tumors. In Vivo; 2006 Jul-Aug;20(4):519-25
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  • A sensitive, 4-step, alkaline phosphatase conjugated antigen detection technique was used and a specific monoclonal antibody for medulloblastomas/ primitive neuroectodermal tumors (MEDs/PNETs), anaplastic, high-grade astrocytomas (ASTRs) and in glioblastoma multiformes (GMs) was employed.
  • However, of the 14 subtypes of astrocytic tumors examined, the COX-2 receptor expression level did not even approach those of the MEDs/PNETs levels.
  • In two low grade pilocytic ASTRs, the expression level never exceeded 20%, while in high grade glial tumors (6 anaplastic ASTRs and 6 GMs) 30 to 50% of the tumor cells overexpressed COX-2 receptors, documenting an increase in COX-2 receptor overexpression with the increasing grade of the astrocytic tumor.
  • In view of these findings, it would appear likely that COX-2 inhibitors may represent a chemo-preventive tool in treating childhood brain tumors, which are the leading cause of solid tumor cancer death in children under the age of 20.
  • [MeSH-major] Brain Neoplasms / enzymology. Brain Neoplasms / metabolism. Cyclooxygenase 2 / metabolism. Glioma / enzymology. Glioma / metabolism

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  • (PMID = 16900783.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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59. Kotoula V, Cheva A, Barbanis S, Papadimitriou CS, Karkavelas G: hTERT immunopositivity patterns in the normal brain and in astrocytic tumors. Acta Neuropathol; 2006 Jun;111(6):569-78
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  • [Title] hTERT immunopositivity patterns in the normal brain and in astrocytic tumors.
  • Accumulating data about the impact of hTERT in astrocytic tumor carcinogenesis and recent evidence about its association with disease outcome prompt the evaluation of this molecule with methods applicable in routine pathology practice.
  • In this study, we investigated hTERT protein expression with immunohistochemistry (IHC) and the NCL-hTERT antibody in 49 astrocytic tumors.
  • Low- and high-grade astrocytic tumors were found positive for hTERT in 74 and 85% of cases, respectively.
  • The prevailing nuclear IPs differed significantly between pilocytic astrocytomas (pattern As) and the rest of histologic types up to glioblastoma (patterns Am and B) (P<0.0001).
  • Positive endothelial cells were found in astrocytic tumors of all grades, even when tumor cells showed no hTERT immunoreactivity.
  • The nuclear hTERT IPs described here may reflect the functional status of non-neoplastic brain and neoplastic astrocytic cells and support the model of a continuum in the development of glioblastomas from diffuse fibrillary astrocytomas.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Brain Chemistry / physiology. Brain Neoplasms / metabolism. Telomerase / genetics. Telomerase / metabolism
  • [MeSH-minor] Adult. Aged. Child. Endothelial Cells / pathology. Female. Fixatives. Formaldehyde. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Paraffin Embedding. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16614861.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fixatives; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 1HG84L3525 / Formaldehyde; EC 2.7.7.49 / Telomerase
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60. Beppu T, Sato Y, Uesugi N, Kuzu Y, Ogasawara K, Ogawa A: Desmoplastic infantile astrocytoma and characteristics of the accompanying cyst. Case report. J Neurosurg Pediatr; 2008 Feb;1(2):148-51
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  • [Title] Desmoplastic infantile astrocytoma and characteristics of the accompanying cyst. Case report.
  • A desmoplastic infantile astrocytoma (DIA) is an extremely rare tumor that comprises a solid astrocytic tumor accompanied by a large cyst and involves the superficial cerebral cortex and leptomeninges in infants.
  • The solid part of this type of tumor has been well described in various reports and books, but characteristics of the cystic portion have remained unclear.
  • The authors report on the clinical and histological features of the cyst in a case of a DIA.
  • Contrast-enhanced magnetic resonance imaging revealed a strongly enhancing single-lobed large cyst located in the deep white matter, under the solid part of the tumor attached to the dura mater of the left frontal lobe.
  • Both the solid and cystic portions of the tumor were surgically removed.
  • Histologically, the cyst wall was composed of gliosis representing a rough accumulation of reactive astrocytes, lymphocytes, and small capillary vessels in edematous parenchyma, but no tumor cells.
  • The present case and previous reports suggest that the cyst does not contain tumor cells, even if strongly depicted on contrast-enhanced neuroimaging, and that a thickly enhancing cyst wall indicates gliosis with accumulation of numerous small vessels.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Diseases / diagnosis. Brain Neoplasms / diagnosis. Cysts / diagnosis

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  • (PMID = 18352787.001).
  • [ISSN] 1933-0707
  • [Journal-full-title] Journal of neurosurgery. Pediatrics
  • [ISO-abbreviation] J Neurosurg Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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61. Asano K, Miyamoto S, Kubo O, Kikkukawa T, Yagihashi A, Ohkuma H: A case of anaplastic pleomorphic xanthoastrocytoma presenting with tumor bleeding and cerebrospinal fluid dissemination. Brain Tumor Pathol; 2006 Apr;23(1):55-63
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  • [Title] A case of anaplastic pleomorphic xanthoastrocytoma presenting with tumor bleeding and cerebrospinal fluid dissemination.
  • Pleomorphic xanthoastrocytoma (PXA) has been considered an astrocytic tumor with a relatively favorable prognosis.
  • The present case was a 59-year-old woman who presented with tumor bleeding onset and cerebrospinal fluid dissemination.
  • After emergency surgery had removed the hematoma, postoperative contrast-enhanced CT scan revealed a left temporal tumor.
  • A second surgery was therefore performed for initial tumor removal 2 months later.
  • Histopathological findings showed that the tumor was typical PXA with strong pleomorphism and xanthomatous changes and contained an ependymoma-like component in the center area.
  • This case report is the first case in which PXA presented with tumor bleeding onset.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Carcinoma / pathology. Hematoma / pathology
  • [MeSH-minor] Biomarkers, Tumor. Fatal Outcome. Female. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Middle Aged. Mitosis / physiology. Neoplasm Recurrence, Local. Tomography, X-Ray Computed

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  • (PMID = 18095120.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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62. Jung SI, Cho HS, Lee CH, Kim KD, Ha JO, Kim MK, Lee KH, Hyun MS: Two cases of trisomy 19 as a sole chromosomal abnormality in myeloid disorders. Korean J Lab Med; 2008 Jun;28(3):174-8

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  • [Title] Two cases of trisomy 19 as a sole chromosomal abnormality in myeloid disorders.
  • Trisomy 19 is frequently encountered in cases of chronic myeloid leukemia (CML) as a secondary abnormality: however, trisomy 19 rarely occurs as a sole chromosomal abnormality and, to date, it has only been reported in 48 hematopoietic malignancies, 1 case of adenocarcinoma and 1 case of astrocytic tumor.
  • Four months later, her peripheral blood smears suggested that the disease had progressed, but she refused further evaluation.
  • Based on a review of the existing literature and the results of this report, trisomy 19 not only as a secondary abnormality but also as a sole karyotypic aberration is strongly associated with myeloid disorder; however, it is not preferentially found in specific FAB subgroups of myelodysplasic syndrome or acute myeloid leukemia.
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Female. Humans. Infant. Karyotyping. Male

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  • (PMID = 18594167.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
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63. Begnami MD, Rushing EJ, Evangelista R, Santi M, Quezado M: Evaluation of RB gene and cyclin-dependent kinase inhibitors P21 and P27 in pleomorphic xantoastrocytoma. Int J Surg Pathol; 2006 Apr;14(2):113-8
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  • Pleomorphic xantoastrocytoma (PXA) is a rare, circumscribed astrocytic tumor that usually occurs in the superficial cerebral hemispheres in children and young adults.
  • In diffuse gliomas, approximately one third demonstrate mutations of the RB gene.
  • Low expression level and high activity of p27 are known to constitute an independent prognostic factor in patients with malignant gliomas, while p21 expressions have variable labeling ranges.
  • Nine PXAs expressed homogeneous pRb positivity in the most nuclei of the tumor cells.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Retinoblastoma Protein / metabolism

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  • (PMID = 16703171.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Retinoblastoma Protein; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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64. Järvelä S, Rantala I, Rodriguez A, Kallio H, Parkkila S, Kinnula VL, Soini Y, Haapasalo H: Specific expression profile and prognostic significance of peroxiredoxins in grade II-IV astrocytic brain tumors. BMC Cancer; 2010;10:104
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  • [Title] Specific expression profile and prognostic significance of peroxiredoxins in grade II-IV astrocytic brain tumors.
  • METHODS: We studied the expression of Prx I-VI and their relationship to patient survival in 383 grade II-IV diffuse astrocytic brain tumors.
  • CONCLUSION: The expression of Prx I and Prx II correlates with astrocytic tumor features, such as grade and patient age and proliferation activity (Prx I), and accordingly with patient survival.
  • [MeSH-major] Astrocytoma / enzymology. Brain Neoplasms / enzymology. Peroxiredoxins / biosynthesis

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  • (PMID = 20307276.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.11.1.15 / Peroxiredoxins
  • [Other-IDs] NLM/ PMC2858108
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65. Gelpi E, Popovic M, Preusser M, Budka H, Hainfellner J: Pleomorphic xanthoastrocytoma with anaplastic features presenting without GFAP immunoreactivity: implications for differential diagnosis. Neuropathology; 2005 Sep;25(3):241-6
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  • Pleomorphic xanthoastrocytoma (PXA) is an uncommon, usually low-grade, astrocytic tumor.
  • Characteristic histological features include tumor cell pleomorphism and lipidization of tumor cells.
  • A 43-year-old woman was operated on for a left occipital parasagital tumor attached to the dura.
  • Histopathology showed a pleomorphic tumor with moderate mitotic activity and necrosis, lack of GFAP immunoreactivity and ultrastructural detection of premelanosome-like structures.
  • Three years later she had local tumor recurrence and underwent another operation.
  • The recurrent tumor showed similar plain histology as the first specimen.
  • In contrast, anti-GFAP immunoreactivity was now detectable in pleomorphic tumor cells.
  • Focal GFAP staining of tumor cells was now achieved.
  • We conclude that non-standard GFAP staining protocols may enhance sensitivity and thus lead to detection of a low level of GFAP expression in tumor specimens, in which PXA is considered in the differential diagnosis.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Glial Fibrillary Acidic Protein / metabolism
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods. Melanoma / pathology. Microscopy, Confocal. Microscopy, Electron, Transmission. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology

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  • (PMID = 16193842.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein
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66. McCarthy BJ, Propp JM, Davis FG, Burger PC: Time trends in oligodendroglial and astrocytic tumor incidence. Neuroepidemiology; 2008;30(1):34-44
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  • [Title] Time trends in oligodendroglial and astrocytic tumor incidence.
  • BACKGROUND: We hypothesized that the incidences of oligodendrogliomas, anaplastic oligodendrogliomas, and mixed gliomas have significantly increased from the early 1990 s forward, while the incidences of anaplastic and grade II astrocytic tumors have significantly decreased.
  • METHODS: Data for the years 1973-2004 from the Surveillance, Epidemiology and End Results (SEER) public-use data and for 1985-2004 from six collaborating registries of the Central Brain Tumor Registry of the US (CBTRUS) were obtained.
  • RESULTS: Using CBTRUS data, the incidences (per 100,000 person-years) of oligodendrogliomas (APC = 4.7), mixed gliomas (APC = 3.9) and anaplastic oligodendrogliomas (APC = 12.5) have all increased over time, while the incidences of astrocytoma not otherwise specified (APC = -8.1) and fibrillary astrocytoma (APC = -2.1) have decreased.
  • CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18259099.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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67. Marton E, Feletti A, Orvieto E, Longatti P: Malignant progression in pleomorphic xanthoastrocytoma: personal experience and review of the literature. J Neurol Sci; 2007 Jan 31;252(2):144-53
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  • Pleomorphic xanthoastrocytoma (PXA) is a rare primary low-grade astrocytic tumor, recently classified as a neuroglial tumor.
  • Pleomorphic xanthoastrocytomas with malignant transformation have been reported in three out of eight patients operated on for this type of tumor in our department in the last 15 years.
  • Mean recurrence time was 5.7 years, with the original xanthoastrocytoma evolving to glioblastoma in two cases and anaplastic astrocytoma in the third.
  • Two died from tumor progression and one from brain edema after intracerebral haemorrhage.
  • A review of the available PXA literature dating back to 1979 revealed 16 cases of primary anaplastic astrocytoma and 21 cases of PXA with malignant transformation.
  • Our experience adds three more cases of malignant transformations, outlining once again the potential malignancy of pleomorphic xanthoastrocytomas and the fact that prognosis in these cases is the same as for primary anaplastic astrocytoma and glioblastoma.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic. Child. Disease Progression. Fatal Outcome. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Neoplasm Recurrence, Local / pathology. Tomography, X-Ray Computed


68. Aoyama T, Hida K, Ishii N, Seki T, Ikeda J, Iwasaki Y: Intramedullary spinal cord germinoma--2 case reports. Surg Neurol; 2007 Feb;67(2):177-83; discussion 183
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  • Astrocytic tumor was initially suspected, and partial removal was performed.
  • Because the lesion did not respond to steroid pulse therapy, spinal cord tumor was suspected and biopsy was performed.
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Chorionic Gonadotropin, beta Subunit, Human / analysis. Chorionic Gonadotropin, beta Subunit, Human / metabolism. Female. Humans. Magnetic Resonance Imaging. Neurosurgical Procedures. Paraparesis / etiology. Radiotherapy. Treatment Outcome. Urination Disorders / etiology

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  • (PMID = 17254883.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human
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69. Pédeboscq S, L'Azou B, Liguoro D, Pometan JP, Cambar J: Interindividual differences in anticancer drug cytotoxicity in primary human glioblastoma cells. Exp Toxicol Pathol; 2007 Jan;58(4):247-53
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  • Glioblastoma multiforme is a malignant astrocytic tumor characterized by rapid growth, extensive invasiveness and high vascularity.
  • [MeSH-minor] Aged. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 17123803.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Glial Fibrillary Acidic Protein; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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70. Liu J, Lu H, Ohgaki H, Merlo A, Shen Z: Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas. BMC Cancer; 2009 Aug 04;9:268
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  • [Title] Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas.
  • BACKGROUND: Loss of heterozygosity of chromosome 10q26 has been shown to be associated with the aggressiveness of astrocytic tumors (or astrocytomas), but the responsible gene(s) residing in this region has not been fully identified.
  • In this study, we investigated whether BCCIP is altered in astrocytomas.
  • METHODS: Genomic DNA from 45 cases of grade IV astrocytic tumor (glioblastoma) tissues and 12 cases of normal tissues were analyzed by quantitative PCR.
  • The BCCIP protein expression in 96 cases of grade II-IV astrocytic tumors was detected by immunohistochemistry (IHC).
  • IHC staining of glial fibrillary acid protein (GFAP), a marker for astrocytic cells, was used to identify cells of the astrocytic lineage.
  • However, BCCIP protein expression was not detectable in approximately 45% of all astrocytic tumors, and in > 60% in the grade IV glioblastoma.
  • Furthermore, the frequency of lacking BCCIP expression is associated with the aggressiveness of astrocytic tumors.
  • CONCLUSION: Our data implicate a role of BCCIP in astrocytic tumorigenesis, and lack of BCCIP may be used as a marker for astrocytomas.

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  • (PMID = 19653894.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115488
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCCIP protein, human; 0 / BRCA2 Protein; 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2736977
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71. Arvanitis DL, Arvanitis LD, Panourias IG, Kitsoulis P, Kanavaros P: The expression of the epitope H recognized by the monoclonal antibody H is higher in astrocytomas compared to anaplastic astrocytomas and glioblastomas. Histol Histopathol; 2005 10;20(4):1057-63

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  • [Title] The expression of the epitope H recognized by the monoclonal antibody H is higher in astrocytomas compared to anaplastic astrocytomas and glioblastomas.
  • In the present study we used the mAbH to investigate the immunohistochemical expression of the epitope H in 41 cases of astrocytic tumors including 19 cases of astrocytomas, 8 cases of anaplastic astrocytomas and 14 cases of glioblastomas.
  • Seven out of 19 cases (37%) of astrocytomas showed weak staining, 10 cases (53%) moderate staining and 2 cases (10%) intense staining.
  • Two out of 8 cases (25%) of anaplastic astrocytomas appeared negative, 3 cases (37.5%) showed weak staining and 3 cases (37.5%) moderate staining.
  • There was a statistically significant elevation of the expression of the epitope H in astrocytomas compared to anaplastic astrocytomas and glioblastomas (p=0.047).
  • These results indicate that the expression of the epitope H decreases in parallel with the increase of the grade of astrocytic tumors from low to higher grade neoplasms.
  • This could be of interest for predicting the progression of an astrocytic tumor since it is documented that astrocytomas progress to tumors of higher grade of malignancy.
  • Further investigation of the antigens bearing the epitope H might help to gain further insight into the mechanisms which regulate the progression of astrocytic tumors and to examine the relevance of the mAbH staining with respect to the prognosis of these neoplasms.
  • [MeSH-major] Antibodies, Monoclonal / metabolism. Astrocytoma / immunology. Epitopes / biosynthesis. Glioblastoma / immunology

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  • (PMID = 16136487.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Glial Fibrillary Acidic Protein
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72. Heimberger AB, McGary EC, Suki D, Ruiz M, Wang H, Fuller GN, Bar-Eli M: Loss of the AP-2alpha transcription factor is associated with the grade of human gliomas. Clin Cancer Res; 2005 Jan 1;11(1):267-72
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  • [Title] Loss of the AP-2alpha transcription factor is associated with the grade of human gliomas.
  • The purpose of our study was to determine AP-2alpha expression distribution among grades of gliomas and any possible effect on prognosis.
  • EXPERIMENTAL DESIGN: A tissue microarray was assembled from all surgical glioma cases with available tissue samples at M.D.
  • Anderson Cancer Center since 1986 to include 72 glioblastomas, 49 anaplastic astrocytomas, 9 low-grade astrocytoma, 37 oligodendrogliomas, 37 anaplastic oligodendrogliomas, 15 mixed oligoastrocytomas, 20 anaplastic mixed oligoastrocytomas, and 7 gliosarcomas.
  • RESULTS: AP-2alpha expression was lost on 99% (P < 0.001) and 98% (P < 0.001) of glioblastomas and anaplastic astrocytomas, respectively, compared with grade 2 astrocytomas and normal brain, all of which (100%) maintained expression of AP-2alpha.
  • The loss of AP-2alpha was a negative prognostic indicator within the overall category of gliomas by univariate analysis (rate ratio, 4.30; 95% confidence interval, 2.60-7.10; P < 0.001).
  • However, there was no significant effect of loss of AP-2alpha expression on survival observed after adjustment for patient age, Karnofsky Performance Scale score, tumor grade, and extent of resection (rate ratio, 1.2; 95% confidence interval, 0.6-2.2; P = 0.6).
  • CONCLUSIONS: AP-2alpha expression correlates inversely with glioma grade, suggesting a direct role in glioma tumorigenicity, possibly through subsequent deregulation of target genes.
  • Of all the previously characterized markers of progression, the loss of AP-2alpha would be the most common (96.2%) molecular marker as an astrocytic tumor evolves from grade 2 to 3.
  • [MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic. Glioma / metabolism. Transcription Factors / biosynthesis. Transcription Factors / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Motifs. Antigens, CD / biosynthesis. Antigens, CD146. Astrocytoma / metabolism. Brain / metabolism. Cell Cycle Proteins / biosynthesis. Cell Line, Tumor. Child. Child, Preschool. Cyclin-Dependent Kinase Inhibitor p21. Disease Progression. Humans. Immunohistochemistry. Matrix Metalloproteinase 2 / biosynthesis. Middle Aged. Neural Cell Adhesion Molecules / biosynthesis. Oligodendroglioma / metabolism. Oligonucleotide Array Sequence Analysis. Prognosis. Proportional Hazards Models. Proto-Oncogene Proteins c-kit / biosynthesis. Time Factors. Transcription Factor AP-2. Treatment Outcome. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 15671555.001).
  • [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 / PHS HHS / / T-32-09666
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD146; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / MCAM protein, human; 0 / Neural Cell Adhesion Molecules; 0 / TFAP2A protein, human; 0 / Transcription Factor AP-2; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.24.24 / Matrix Metalloproteinase 2
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73. Dörner L, Fritsch MJ, Hugo HH, Mehdorn HM: Primary diffuse leptomeningeal gliomatosis in a 2-year-old girl. Surg Neurol; 2009 Jun;71(6):713-9, discussion 719
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  • BACKGROUND: Primary diffuse leptomeningeal gliomatosis is a rare tumor disease affecting the leptomeninx of the CNS.
  • Cerebrospinal fluid diagnostic studies showed a mild pleocytosis and elevated protein levels but no tumor cells or evidence of infection.
  • A spinal biopsy was taken and subsequently a paucicellular astrocytic tumor was diagnosed corresponding to a WHO I diffuse leptomeningeal gliomatosis.
  • Chemotherapy with vincristine, carboplatin, and etoposide was initiated (Protocol SIOP-LGG 2004) but was stopped by the parents when the child was in partial remission after 50 weeks because of a neurologic deterioration.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / therapy. Meningeal Neoplasms / diagnosis. Meningeal Neoplasms / therapy

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  • (PMID = 18423532.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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74. Kato T, Shinoda J, Nakayama N, Miwa K, Okumura A, Yano H, Yoshimura S, Maruyama T, Muragaki Y, Iwama T: Metabolic assessment of gliomas using 11C-methionine, [18F] fluorodeoxyglucose, and 11C-choline positron-emission tomography. AJNR Am J Neuroradiol; 2008 Jun;29(6):1176-82
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  • [Title] Metabolic assessment of gliomas using 11C-methionine, [18F] fluorodeoxyglucose, and 11C-choline positron-emission tomography.
  • BACKGROUND AND PURPOSE: Positron-emission tomography (PET) is a useful tool in oncology.
  • The aim of this study was to assess the metabolic activity of gliomas using (11)C-methionine (MET), [(18)F] fluorodeoxyglucose (FDG), and (11)C-choline (CHO) PET and to explore the correlation between the metabolic activity and histopathologic features.
  • MATERIALS AND METHODS: PET examinations were performed for 95 primary gliomas (37 grade II, 37 grade III, and 21 grade IV).
  • We measured the tumor/normal brain uptake ratio (T/N ratio) on each PET and investigated the correlations among the tracer uptake, tumor grade, tumor type, and tumor proliferation activity.
  • In addition, we compared the ease of visual evaluation for tumor detection.
  • RESULTS: All 3 of the tracers showed positive correlations with astrocytic tumor (AT) grades (II/IV and III/IV).
  • Tumor grade and type influenced MET uptake only.
  • MET T/N ratios of more than 2.0 were seen in 87% of all of the gliomas.
  • In terms of visual evaluation of tumor localization, MET PET is superior to FDG and CHO PET in all of the gliomas, due to its straightforward detection of "hot lesions".
  • [MeSH-major] Brain Neoplasms / metabolism. Choline / pharmacokinetics. Fluorodeoxyglucose F18 / pharmacokinetics. Glioma / metabolism. Methionine / pharmacokinetics. Positron-Emission Tomography / methods

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  • [CommentIn] Nat Clin Pract Neurol. 2008 Sep;4(9):470-1 [18628750.001]
  • [CommentIn] AJNR Am J Neuroradiol. 2008 Nov;29(10):e96 [19008320.001]
  • (PMID = 18388218.001).
  • [ISSN] 1936-959X
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AE28F7PNPL / Methionine; N91BDP6H0X / Choline
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75. Torii K, Tsuyuguchi N, Kawabe J, Sunada I, Hara M, Shiomi S: Correlation of amino-acid uptake using methionine PET and histological classifications in various gliomas. Ann Nucl Med; 2005 Dec;19(8):677-83
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  • [Title] Correlation of amino-acid uptake using methionine PET and histological classifications in various gliomas.
  • OBJECTIVE: The uptake of L-methyl-11C-methionine (MET) by gliomas is greater than that by intact tissue, making methionine very useful for evaluation of tumor extent.
  • METHODS: We performed this study on 67 glioma patients between 3 and 69 years of age (36 males and 31 females).
  • Tumors included diffuse astrocytoma, anaplastic astrocytoma, glioblastoma, ependymoma, oligodendroglioma, medulloblastoma, dysembryoplastic neuroepithelial tumor, choroid plexus papilloma, central neurocytoma, optic glioma, gliomatosis cerebri, pleomorphic xanthoastrocytoma, and ganglioglioma.
  • Tumor activity and degree of malignancy were evaluated using Ki-67LI (LI: labeling index) and Kaplan-Meier survival curves.
  • The correlations between methionine uptake and tumor proliferation (tumor versus contralateral gray matter ratio (T/N) and Ki-67LI) were determined for the group of all subjects.
  • The existence of significant correlations between T/N and Ki-67LI and between SUV and Ki-67LI was determined for astrocytic tumors.
  • Receiver operating characteristics (ROC) analysis of T/N and standardized uptake value (SUV) was performed for the group of astrocytic tumors.
  • RESULTS: For the 67 cases of glioma, the degree of accumulation was variable.
  • Ki-67LI differed significantly between the high-grade group and low-grade group at T/N levels between 1.5 and 1.8 on analysis using tumor proliferative potential (p = 0.019-0.031).
  • CONCLUSIONS: When analysis was confined to cases of astrocytic tumor, a correlation was noted between methionine accumulation and Ki-67LI.
  • For the astrocytic tumors, T/N ratio seemed to be more useful as a diagnostic indicator than SUV.
  • The cut-off level of T/N ratio for distinction between high-grade and low-grade astrocytoma appears to lie between 1.5 and 1.6.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / radionuclide imaging. Glioma / pathology. Glioma / radionuclide imaging. Methionine / pharmacokinetics. Positron-Emission Tomography / methods

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  • (PMID = 16444993.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 58576-49-1 / carbon-11 methionine; AE28F7PNPL / Methionine
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76. 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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77. Puget S, Crimmins DW, Garnett MR, Grill J, Oliveira R, Boddaert N, Wray A, Lelouch-Tubiana A, Roujeau T, Di Rocco F, Zerah M, Sainte-Rose C: Thalamic tumors in children: a reappraisal. J Neurosurg; 2007 May;106(5 Suppl):354-62
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  • METHODS: The records of 69 children who presented with a thalamic tumor between 1989 and 2003 were retrospectively reviewed.
  • In the patients in whom a unilateral thalamic tumor was diagnosed, 33 had an astrocytic tumor.
  • Of the 54 patients, 32 had a low-grade and 22 had a high-grade tumor.
  • The survival rate was significantly better for patients with the following characteristics: symptom duration longer than 2 months (p < 0.001), lesions with low-grade histological features (p = 0.003), and tumor excision greater than 90% at surgery (p = 0.04).
  • The thalamopeduncular tumors were mostly pilocytic astrocytomas, which had a good prognosis following surgery.
  • The bilateral thalamic tumors in this series were mainly low-grade astrocytic lesions, and more than half of the children attained long-term survival (mean follow-up duration 4.5 years).
  • CONCLUSIONS: The majority of tumors arising in the thalamus are astrocytic, of which less than half are high-grade lesions.
  • [MeSH-minor] Adolescent. Astrocytoma / diagnosis. Astrocytoma / therapy. Cerebrospinal Fluid Shunts. Child. Child, Preschool. Female. Glioma / diagnosis. Glioma / therapy. Humans. Hydrocephalus / etiology. Hydrocephalus / surgery. Infant. Kaplan-Meier Estimate. Magnetic Resonance Imaging. Male. Neurosurgical Procedures. Prognosis. Retrospective Studies. Tomography, X-Ray Computed

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  • (PMID = 17566201.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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78. Nawashiro H, Otani N, Shinomiya N, Fukui S, Ooigawa H, Shima K, Matsuo H, Kanai Y, Endou H: L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors. Int J Cancer; 2006 Aug 1;119(3):484-92
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  • [Title] L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors.
  • LAT1 has been identified as a light chain of the CD98 heterodimer from C6 glioma cells.
  • We have investigated for the first time, the expression of the transporter in the human primary astrocytic tumor tissue from 60 patients.
  • On the basis of these findings, we also investigated the effect of the specific inhibitor to LAT1, 2-aminobicyclo-2 (2,2,1)-heptane-2-carboxylic acid (BCH), on the survival of C6 glioma cells in vitro and in vivo using a rat C6 glioma model.
  • BCH inhibited the growth of C6 glioma cells in vitro and in vivo in a dose-dependent manner.
  • These findings suggest that LAT1 could be one of the molecular targets in glioma therapy.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Large Neutral Amino Acid-Transporter 1 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acids, Cyclic / pharmacology. Animals. Antigens, CD98 Heavy Chain / analysis. Cell Line, Tumor. Cell Survival / drug effects. Child. Female. Glioma / drug therapy. Glioma / mortality. Glioma / pathology. Humans. Immunohistochemistry. Infant, Newborn. Male. Middle Aged. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / mortality. Neoplasms, Experimental / pathology. Rats. Rats, Wistar. Survival Analysis. Survival Rate

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16496379.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Cyclic; 0 / Antigens, CD98 Heavy Chain; 0 / Large Neutral Amino Acid-Transporter 1; 20448-79-7 / 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid
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79. Hayashi S, Yamamoto M, Tachibana K, Ueno Y, Bu G, Fukushima T: Mechanism of photofrin-enhanced ultrasound-induced human glioma cell death. Anticancer Res; 2009 Mar;29(3):897-905
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  • [Title] Mechanism of photofrin-enhanced ultrasound-induced human glioma cell death.
  • BACKGROUND: Low-intensity ultrasound showed tumor cell killing by a non-thermal effect in human leukemia cells.
  • The aim of our study was to investigate the efficacy of low-intensity ultrasound on malignant astrocytic tumor cells with the photosensitizer, Photofrin, which is taken up by the cell surface receptor, low density lipoprotein receptor-related protein/alpha2-macroglobulin receptor (LRP/alpha2MR).
  • MATERIALS AND METHODS: Cells were sonicated with continuous wave ultrasound with or without the presence of Photofrin (75 mg/ml) at an intensity of 0.3 W/cm(2) for a duration of 5, 15, or 30 s.
  • RESULTS: Ultrasound alone induced instant cell killing immediately after sonication in both U251MG and U105MG malignant gliomas cells.
  • CONCLUSION: This is the first report to demonstrate the usefulness of low-intensity ultrasound for the cell killing of malignant glioma cells.
  • [MeSH-major] Brain Neoplasms / therapy. Cell Survival / drug effects. Dihematoporphyrin Ether / therapeutic use. Glioma / therapy. Photosensitizing Agents / therapeutic use. Ultrasonic Therapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Low Density Lipoprotein Receptor-Related Protein-1 / genetics. Low Density Lipoprotein Receptor-Related Protein-1 / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. alpha-Macroglobulins / genetics. alpha-Macroglobulins / metabolism

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  • (PMID = 19414325.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Low Density Lipoprotein Receptor-Related Protein-1; 0 / Photosensitizing Agents; 0 / RNA, Messenger; 0 / alpha-Macroglobulins; 97067-70-4 / Dihematoporphyrin Ether
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80. Komotar RJ, Carson BS, Rao C, Chaffee S, Goldthwaite PT, Tihan T: Pilomyxoid Astrocytoma of the Spinal Cord: Report of Three Cases. Neurosurgery; 2005 Jan 01;56(1):E206-E210

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

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  • (PMID = 28184642.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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81. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • In addition, we summarize the key genetic alterations that have been attributed to astrocytoma patho-genesis and progression.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • Novel animal models will provide us with the opportunity to comprehensively study this multilayered disease and explore novel therapeutic approaches in vivo.
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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82. Korkolopoulou P, Perdiki M, Thymara I, Boviatsis E, Agrogiannis G, Kotsiakis X, Angelidakis D, Rologis D, Diamantopoulou K, Thomas-Tsagli E, Kaklamanis L, Gatter K, Patsouris E: Expression of hypoxia-related tissue factors in astrocytic gliomas. A multivariate survival study with emphasis upon carbonic anhydrase IX. Hum Pathol; 2007 Apr;38(4):629-38

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

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  • (PMID = 17367605.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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83. Mizoguchi M, Betensky RA, Batchelor TT, Bernay DC, Louis DN, Nutt CL: Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival. J Neuropathol Exp Neurol; 2006 Dec;65(12):1181-8
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  • [Title] Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas: correlation with EGFR status, tumor grade, and survival.
  • Diffuse astrocytic gliomas are the most common human glial tumors with glioblastoma being the most malignant form.
  • In this study, we investigated the activation status of these 3 signaling molecules as well as wild-type (EGFRwt) and mutant (EGFRvIII) EGFR in 82 malignant astrocytic gliomas (55 glioblastomas and 27 anaplastic astrocytomas) using immunohistochemistry.
  • The distribution of these 3 activated molecules varied significantly with tumor grade; although activation of STAT3 was essentially identical between anaplastic astrocytomas and glioblastomas, an increase in the activation of MAPK and AKT appeared to correlate with the progression of anaplastic astrocytoma to glioblastoma.
  • Taken together, these findings begin to elucidate the interrelationship between these signaling pathways in astrocytic gliomas in vivo.
  • [MeSH-major] Astrocytoma / enzymology. Brain Neoplasms / enzymology. Glioblastoma / enzymology. Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Epidermal Growth Factor / biosynthesis. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Disease Progression. Enzyme Activation / genetics. Genetic Predisposition to Disease / genetics. Humans. Immunohistochemistry. Mutation / genetics. Predictive Value of Tests. Prognosis. Signal Transduction / physiology. Survival Rate / trends. Transcriptional Activation / genetics

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  • (PMID = 17146292.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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84. Ritch PS, Carroll SL, Sontheimer H: Neuregulin-1 enhances survival of human astrocytic glioma cells. Glia; 2005 Aug 15;51(3):217-28
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  • [Title] Neuregulin-1 enhances survival of human astrocytic glioma cells.
  • Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.
  • In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.
  • Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.
  • We then verify receptor expression in a panel of human glioma cell lines.
  • Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.
  • Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.
  • Moreover, Nrg-1beta activates an inhibitor of apoptosis, Akt, implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas.
  • This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

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  • (PMID = 15812817.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247-010003; United States / NINDS NIH HHS / NS / R01 NS036692-05A1; United States / NCI NIH HHS / CA / CA097247-010003; United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50CA97247; United States / NINDS NIH HHS / NS / NS036692-05A1; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01-NS36692; United States / NINDS NIH HHS / NS / R01 NS036692-06; United States / NINDS NIH HHS / NS / NS036692-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuregulin-1; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS25075; NLM/ PMC2548407
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85. Blough MD, Zlatescu MC, Cairncross JG: O6-methylguanine-DNA methyltransferase regulation by p53 in astrocytic cells. Cancer Res; 2007 Jan 15;67(2):580-4
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  • [Title] O6-methylguanine-DNA methyltransferase regulation by p53 in astrocytic cells.
  • In this study, we tested the hypothesis that MGMT is regulated by p53 in astrocytic cells, the precursors of which may give rise to glioblastoma. p53 is of interest because, in addition to often being mutated in glioblastoma, inactivation sensitizes some astrocytoma cell lines to temozolomide.
  • MGMT expression was examined in neonatal murine astrocytes and SF767 human astrocytic glioma cells following p53 inactivation by knockout (murine only) or RNAi methods.
  • In SF767 human astrocytic glioma cells, transient knockdown of p53 led to the down-regulation of MGMT gene expression.
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA Methylation. Gene Silencing. Glioma / enzymology. Glioma / genetics. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. Promoter Regions, Genetic

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  • (PMID = 17234766.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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86. Götze S, Wolter M, Reifenberger G, Müller O, Sievers S: Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas. Int J Cancer; 2010 Jun 1;126(11):2584-93
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  • [Title] Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas.
  • Recent studies suggested a role of Wnt signaling in gliomas, the most common primary brain tumors.
  • We investigated 70 gliomas of different malignancy grades for promoter hypermethylation in 8 genes encoding members of the secreted frizzled-related protein (SFRP1, SFRP2, SFRP4, SFRP5), dickkopf (DKK1, DKK3) and naked (NKD1, NKD2) families of Wnt pathway inhibitors.
  • While none of the tumors carried CTNNB1 mutations, we found frequent promoter hypermethylation of Wnt pathway inhibitor genes, with at least one of these genes being hypermethylated in 6 of 16 diffuse astrocytomas (38%), 4 of 14 anaplastic astrocytomas (29%), 7 of 10 secondary glioblastomas (70%) and 23 of 30 primary glioblastomas (77%).
  • Furthermore, SFRP1-hypermethylated gliomas showed significantly lower expression of the respective transcripts when compared with unmethylated tumors.
  • Taken together, our results suggest an important role of epigenetic silencing of Wnt pathway inhibitor genes in astrocytic gliomas, in particular, in glioblastomas, with distinct patterns of hypermethylated genes distinguishing primary from secondary glioblastomas.
  • [MeSH-major] Astrocytoma / genetics. DNA Methylation / genetics. Promoter Regions, Genetic. Wnt Proteins / genetics
  • [MeSH-minor] Carrier Proteins / genetics. Cell Line, Tumor. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Exons. Eye Proteins / genetics. Glioblastoma / genetics. Glioblastoma / secondary. Glioma / genetics. Glioma / pathology. Humans. Intercellular Signaling Peptides and Proteins / genetics. Membrane Proteins / genetics. Mutation. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. beta Catenin / genetics

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  • (PMID = 19847810.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NKD1 protein, human; 0 / NKD2 protein, human; 0 / Proto-Oncogene Proteins; 0 / SFRP1 protein, human; 0 / SFRP2 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
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87. Shostak KO, Dmitrenko VV, Vudmaska MI, Naidenov VG, Beletskii AV, Malisheva TA, Semenova VM, Zozulya YP, Demotes-Mainard J, Kavsan VM: Patterns of expression of TSC-22 protein in astrocytic gliomas. Exp Oncol; 2005 Dec;27(4):314-8
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  • [Title] Patterns of expression of TSC-22 protein in astrocytic gliomas.
  • AIM: To evaluate expression patterns of protein product of putative tumor suppressor gene TSC-22 in human astrocytic tumors by immunohistochemical approach.
  • Immunohistochemical analysis of TSC-22 and GFAP expression with the use of anti-human-TSC-22- and anti-human-GFAP-antibodies was performed on histological slides of astrocytic tumors.
  • RESULTS: Immunohistochemical analysis has shown that the number of cells expressing TSC-22 was significantly lower in glioblastoma tissues than that in diffuse astrocytoma.
  • Double immunohistochemical staining of astrocytic tumors using anti-human-TSC-2- and anti-human-GFAP-antibodies showed that both TSC-22 and GFAP expression is co-localized in astrocytes.
  • In more aggressive forms of astrocytic tumors decreased expression of TSC-22 mRNA correlates with its lowered expression on protein level.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Repressor Proteins / biosynthesis
  • [MeSH-minor] Amino Acid Sequence. Astrocytes / metabolism. Base Sequence. Biomarkers, Tumor / analysis. Gene Expression Profiling. Glial Fibrillary Acidic Protein / biosynthesis. Humans. Immunohistochemistry. Microglia / metabolism. Molecular Sequence Data. Recombinant Proteins / biosynthesis. Recombinant Proteins / genetics

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  • (PMID = 16404353.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / TSC22D1 protein, human
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88. Katsetos CD, Reddy G, Dráberová E, Smejkalová B, Del Valle L, Ashraf Q, Tadevosyan A, Yelin K, Maraziotis T, Mishra OP, Mörk S, Legido A, Nissanov J, Baas PW, de Chadarévian JP, Dráber P: Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines. J Neuropathol Exp Neurol; 2006 May;65(5):465-77
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  • [Title] Altered cellular distribution and subcellular sorting of gamma-tubulin in diffuse astrocytic gliomas and human glioblastoma cell lines.
  • Centrosome amplification is a pivotal mechanism underlying tumorigenesis but its role in gliomas is underinvestigated.
  • The present study specifically examines the expression and distribution of the centrosome-associated cytoskeletal protein gamma-tubulin in 56 primary diffuse astrocytic gliomas (grades II-IV) and in 4 human glioblastoma cell lines (U87MG, U118MG, U138MG, and T98G).
  • In tumors in adults (n = 46), varying degrees of localization were detected in all tumor grades, but immunoreactivity was significantly increased in high-grade anaplastic astrocytomas and glioblastomas multiforme as compared to low-grade diffuse astrocytomas (p = 0.0001).
  • A similar trend was noted in diffuse gliomas in children but the sample of cases was too small as to be statistically meaningful.
  • Our results indicate that overexpression and ectopic cellular distribution of gamma-tubulin in astrocytic gliomas may be significant in the context of centrosome protein amplification and may be linked to tumor progression and anaplastic potential.
  • [MeSH-minor] Antigens / metabolism. Blotting, Northern / methods. Cell Line, Tumor. Humans. Immunohistochemistry / methods

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  • (PMID = 16772870.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
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89. Zhou YH, Hess KR, Liu L, Linskey ME, Yung WK: Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables. Neuro Oncol; 2005 Oct;7(4):485-94
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  • [Title] Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables.
  • The disparate lengths of survival among patients with malignant astrocytic gliomas (anaplastic astrocytomas [AAs] and glioblastoma multiforme [GBM]) cannot be adequately accounted for by clinical variables (patient age, histology, and recurrent status).
  • We previously explicated the expression and prognostic value of PAX6, PTEN, VEGF, and EGFR in these glioma tissues and established a comprehensive prognostic model (Zhou et al., 2003).
  • This study attempts to improve that model by including four additional genetic markers, which exhibited a differential expression (P < 0.001) among tumor grades and between tumor and normal tissues.
  • This finding suggests that the expression of IGFBP2 is associated with pathways activated specifically in GBMs that result in enhancing invasiveness and angiogenesis.
  • [MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical

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  • (PMID = 16212813.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ribosomal Proteins; 0 / ribosomal protein S9; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC1871729
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90. 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.
  • We observed that morphologically different parts of a glioma could carry different or similar mutations in the p53 gene and could be either associated or not associated with the locus of heterozygosity at the mutant site.
  • 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.
  • Our results are of importance for a further understanding of the molecular mechanisms behind failure to treat glioma patients.
  • [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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91. Elsir T, Eriksson A, Orrego A, Lindström MS, Nistér M: Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas. J Neuropathol Exp Neurol; 2010 Feb;69(2):129-38
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  • [Title] Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas.
  • PROX1 is a prospero-related transcription factor that plays a critical role in the development of various organs including the mammalian lymphatic and central nervous systems; it controls cell proliferation and differentiation through different transcription pathwaysand has both oncogenic and tumor-suppressive functions.
  • We investigated PROX1 expression patterns in 56 human astrocytic gliomas of different grades using immunohistochemistry.
  • An average of 79% of cells in World Health Organization Grade IV (glioblastoma, n = 15) and 57% of cells in World Health Organization Grade III (anaplastic astrocytoma, n = 13) were strongly PROX1 positive; low-grade diffuse astrocytomas (Grade II, n = 13) had 21% of cells that were strongly positive; Grade I tumors (n = 15) had 1.5%; and non-neoplastic brain tissue (n = 15) had 3.7% of cells that were PROX1 positive.
  • Analyses of coexpression with proliferation markers suggest that PROX1+ cells have a marginally lower rate of proliferation than other tumor cells but are still mitotically active.
  • We conclude that PROX1 may constitute a useful tool for the diagnosis and grading ofastrocytic gliomas and for distinguishing Grade III and Grade IV tumors from Grade I and Grade II tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Homeodomain Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Antigens, Nuclear / metabolism. Biomarkers / metabolism. Brain Diseases / metabolism. Cell Proliferation. Humans. Immunohistochemistry. Microtubule-Associated Proteins / metabolism. Microvessels / metabolism. Mitosis. Nerve Tissue Proteins / metabolism. Tubulin / metabolism

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  • (PMID = 20084020.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / neuronal nuclear antigen NeuN, human; 0 / prospero-related homeobox 1 protein
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92. Li H, Wang Q, Gao F, Zhu F, Wang X, Zhou C, Liu C, Chen Y, Ma C, Sun W, Zhang L: Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas. Oncol Rep; 2008 Sep;20(3):573-9
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  • [Title] Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas.
  • However, the expression level of PDCD5 in human gliomas has not been investigated.
  • In the present study, we examined the expression of PDCD5 in 88 human glioma samples at both mRNA and protein levels by RT-PCR, Western blotting and immunohistochemistry.
  • We found that 53.3% (16/30) of the glioma samples had a reduced expression of PDCD5 mRNA and 70.5% (62/88) had a reduced expression of the PDCD5 protein as compared to normal brain tissue.
  • Furthermore, we studied the correlation of the expression level of PDCD5 with the clinicopathological grade and survival of patients with astrocytomas.
  • Although longitudinal studies of a cohort of patients with astrocytoma revealed that PDCD5 expression was not able to predict clinical outcome (p>0.05), a decreased expression of PDCD5 correlated significantly with high-grade astrocytomas (p<0.001).
  • In conclusion, our data suggest that reduced PDCD5 expression may contribute to the pathogenesis of human gliomas.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Female. Humans. Immunoenzyme Techniques. Male. Neoplasm Staging. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tumor Cells, Cultured

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  • (PMID = 18695908.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / RNA, Messenger
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93. Arjona D, Bello MJ, Alonso ME, Isla A, De Campos JM, Vaquero J, Sarasa JL, Gutierrez M, Rey JA: Real-time quantitative PCR analysis of regions involved in gene amplification reveals gene overdose in low-grade astrocytic gliomas. Diagn Mol Pathol; 2005 Dec;14(4):224-9

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  • [Title] Real-time quantitative PCR analysis of regions involved in gene amplification reveals gene overdose in low-grade astrocytic gliomas.
  • We have studied gene amplification of genes located in 1q32 (GAC1, ELF3, MDM4, and ren1), 4q11 (PDGFR-alpha), and in 12q13-14 (MDM2 and CDK4) using quantitative real-time PCR in a group of 86 tumors consisting of 44 WHO grade IV glioblastomas (GBM) (34 primary and 10 secondary tumors), 21 WHO grade III anaplastic astrocytomas (AA), and 21 WHO grade II astrocytomas (AII).
  • GAC1 (51%) and MDM4 (27%) were the most frequently amplified genes within the 1q32 amplicon, and their higher amplification frequency was statistically significant (P<0.05, chi) in the low-grade astrocytomas.
  • The present study shows that gene amplification in the studied regions is already present in low-grade astrocytic tumors and that amplification of some genes may represent another molecular marker to differentiate primary from secondary GBM.
  • [MeSH-major] Astrocytoma / genetics. Gene Amplification. Gene Dosage. Proto-Oncogenes / genetics
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Polymerase Chain Reaction

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  • (PMID = 16319692.001).
  • [ISSN] 1052-9551
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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94. Kitai R, Horita R, Sato K, Yoshida K, Arishima H, Higashino Y, Hashimoto N, Takeuchi H, Kubota T, Kikuta K: Nestin expression in astrocytic tumors delineates tumor infiltration. Brain Tumor Pathol; 2010 Apr;27(1):17-21
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  • [Title] Nestin expression in astrocytic tumors delineates tumor infiltration.
  • Nestin is an intermediate filament protein expressed in undifferentiated cells during central nervous system development, and glioma is known to be a highly infiltrative tumor.
  • We determined whether nestin was expressed in astrocytic tumors and could identify infiltrating tumor cells.
  • We screened 65 archival, paraffin-embedded adult astrocytic tumors using immunohistochemical staining and computerized overlaid photographs.
  • The intensity of nestin expression corresponded to the tumor grade.
  • All 33 glioblastoma cases showed positive and extensive staining, which was less positive in diffuse astrocytoma.
  • Overlaid images showed that nestin immunostaining delineated tumor invasion into adjacent gray and white matter.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Intermediate Filament Proteins / metabolism. Intermediate Filament Proteins / physiology. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Child. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Nestin. Young Adult

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  • (PMID = 20425043.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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95. Qu M, Olofsson T, Sigurdardottir S, You C, Kalimo H, Nistér M, Smits A, Ren ZP: Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas. Acta Neuropathol; 2007 Feb;113(2):129-36
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  • [Title] Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas.
  • Oligoastrocytomas are glial tumours consisting of a mixture of neoplastic astrocytic and oligodendroglial cells.
  • Genetic alterations of oligoastrocytomas include loss of heterozygosity of chromosomes 1p and/or 19q (LOH 1p/19q), typically occurring in oligodendrogliomas, and mutations of TP53, frequently occurring in astrocytomas.
  • In the majority of cases (9/11), the oligodendroglial and astrocytic components of an individual oligoastrocytoma displayed the same genotype.
  • In one case, the oligodendroglial part of the tumour showed LOH19q, whereas the astrocytic part showed TP53 mutation (codon 273).
  • In another case, we found LOH 1p/19q in the oligodendroglial component, but two retained areas on chromosome 1p in the astrocytic component of the tumour.
  • The two cases of biphasic oligoastrocytomas in our sample that display a different genotype in the astrocytic and oligodendroglial part of the tumour show that different components of an oligoastrocytoma may be derived from different cell clones during neoplastic transformation.
  • [MeSH-major] Astrocytoma / classification. Astrocytoma / genetics. Brain Neoplasms / classification. Brain Neoplasms / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17031656.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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96. Dong L, Pu PY, Wang H, Wang GX, Kang CS, Jiao DR: [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):232-6
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  • [Title] [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].
  • OBJECTIVE: To study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas. METHODS:.
  • (1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.
  • RESULTS: The frequency of p53 mutation in diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas and secondary glioblastomas was 1/10, 4/19 (21.1%), 4/6 and 2/2, respectively and the frequency of EGFR overexpression was 5/10, 10/19 (52.6%), 5/6 and 2/2, respectively.
  • Both p53 accumulation and EGFR overexpression increased accompanied by a successive increase of degree of the glioma malignancy.
  • CONCLUSIONS: EGFR overexpression is not infrequently seen, however, p53 mutation is rarely seen in the low grade gliomas.
  • Consequently, EGFR overexpression and p53 gene mutation are not mutually exclusive in astrocytic gliomagenesis but synergistically to promote the glioma progression.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16776982.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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97. Sarkar C, Karak AK, Nath N, Sharma MC, Mahapatra AK, Chattopadhyay P, Sinha S: Apoptosis and proliferation: correlation with p53 in astrocytic tumours. J Neurooncol; 2005 Jun;73(2):93-100
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  • [Title] Apoptosis and proliferation: correlation with p53 in astrocytic tumours.
  • We, as well as several other groups, have earlier demonstrated the association of p53 immunopositivity with increased degree of cell proliferation in astrocytic tumours.
  • Here we have studied the extent of apoptosis in 62 primary human astrocytic tumours [25 Diffuse Astrocytoma (DA), 9 Anaplastic Astrocytoma (AA) and 28 Glioblastoma multiforme (GBM)] in relation to tumour grade, proliferative status and p53 protein expression.
  • Taking p53 negativity in IHC as evidence of a functional gene/protein, this extends the link between proliferation and apoptosis, hitherto observed only in cultured cells with functional p53, to a subset of solid tumours.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glioblastoma / metabolism. Glioblastoma / pathology. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15981097.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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98. Haapasalo J, Hilvo M, Nordfors K, Haapasalo H, Parkkila S, Hyrskyluoto A, Rantala I, Waheed A, Sly WS, Pastorekova S, Pastorek J, Parkkila AK: Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas. Neuro Oncol; 2008 Apr;10(2):131-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of an alternatively spliced isoform of carbonic anhydrase XII in diffusely infiltrating astrocytic gliomas.
  • CA XII has been proposed to be involved in acidification of the extracellular milieu, creating an appropriate microenvironment for rapid tumor growth.
  • Because RNA sequence databases have indicated that two isoforms of CA XII might exist in human tissues, and because alternatively spliced protein forms have been linked to aggressive behavior of cancer cells, we designed a study to evaluate the presence of the two forms of CA XII in diffuse astrocytomas, a tumor type known for its aggressive and often noncurable behavior.
  • Reverse transcription PCR of tumor samples surprisingly revealed that CA XII present in diffuse astrocytomas is mainly encoded by a shorter mRNA variant.
  • We further showed by Western blotting that anti-CA XII antibody recognized both isoforms in the glioblastoma cell lines, and we then evaluated the expression of CA XII in astrocytomas using immunohistochemistry and correlated the results with various clinicopathological and molecular factors.
  • Of 370 diffusely infiltrating astrocytomas, 363 cases (98%) showed immunoreactions for CA XII.
  • From these results, we conclude that CA XII is commonly expressed in diffuse astrocytomas and that it might be used as a biomarker of poor prognosis.
  • The absence of 11 amino acids in the shorter isoform, which seems to be common in astrocytomas, may affect the normal quaternary structure and biological function of CA XII.
  • [MeSH-major] Astrocytoma / enzymology. Biomarkers, Tumor / analysis. Brain Neoplasms / enzymology. Carbonic Anhydrases / genetics. Carbonic Anhydrases / metabolism

  • MedlinePlus Health Information. consumer health - Brain Tumors.
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  • (PMID = 18322268.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Isoenzymes; EC 4.2.1.1 / CA13 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2613815
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99. Hagemann C, Gloger J, Anacker J, Said HM, Gerngras S, Kühnel S, Meyer C, Rapp UR, Kämmerer U, Vordermark D, Flentje M, Roosen K, Vince GH: RAF expression in human astrocytic tumors. Int J Mol Med; 2009 Jan;23(1):17-31
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  • [Title] RAF expression in human astrocytic tumors.
  • Only for A-RAF no link to tumorigenesis has been published so far.
  • Malignant gliomas are the most prevalent primary brain tumors of adults.
  • Although a role of the mitogenic Ras-RAF-MEK-ERK signalling cascade in brain tumor development is well established, there are only few reports available addressing alterations in RAF sequence or protein expression and function in human gliomas.
  • We analysed the mutational status of A-RAF and B-RAF in human glioblastomas (GBM) by sequencing.
  • Then we checked for RAF gene amplification by dot blot hybridization and examined RAF mRNA and protein expression patterns in human astrocytic gliomas of WHO grade II (LGA) and IV (GBM) by semiquantitative RT-PCR and Western blotting, respectively.
  • Finally, we performed functional assays to address a putative function of A-RAF in glioma cell proliferation and migration.
  • A-raf gene amplification was more often detected and overexpression of all three RAF proteins on mRNA and protein level was regularly found in human malignant gliomas.
  • Since neither A-RAF, nor C-RAF expression had any influence on proliferation and migration of GBM cells, putative functions of C-RAF in angiogenesis and of A-RAF in regulation of metabolism are discussed.
  • [MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Proto-Oncogene Proteins A-raf / genetics. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins c-raf / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Cell Proliferation. Gene Expression Regulation. Humans. Mutant Proteins / genetics. Prognosis. RNA, Messenger / genetics. Sequence Analysis, DNA

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  • (PMID = 19082503.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / RNA, Messenger; EC 2.7.11.1 / Proto-Oncogene Proteins A-raf; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
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100. Fathi AR, Vassella E, Arnold M, Curschmann J, Reinert M, Vajtai I, Weis J, Deiana G, Mariani L: Objective response to radiation therapy and long-term survival of patients with WHO grade II astrocytic gliomas with known LOH 1p/19q status. Strahlenther Onkol; 2007 Sep;183(9):517-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Objective response to radiation therapy and long-term survival of patients with WHO grade II astrocytic gliomas with known LOH 1p/19q status.
  • BACKGROUND: WHO grade II gliomas are often approached by radiation therapy (RT).
  • However, little is known about tumor response and its potential impact on long-term survival.
  • PATIENTS AND METHODS: Patients subjected to RT were selected from the own database of WHO grade II gliomas diagnosed between 1991 and 2000.
  • The volumetric tumor response after RT was assessed based on magnetic resonance imaging and graded according to standard criteria as complete, partial (PR, >or= 50%), or minor (MR, 25% to <50%).
  • RESULTS: There were 24 astrocytomas and three oligoastrocytomas.
  • CONCLUSION: Approximately 50% of patients with astrocytic WHO grade II gliomas respond to RT despite the absence of LOH for 1p/19q.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / radiotherapy. Chromosomes, Human, Pair 1 / radiation effects. Chromosomes, Human, Pair 19 / radiation effects. Cranial Irradiation. Loss of Heterozygosity / radiation effects. Supratentorial Neoplasms / genetics. Supratentorial Neoplasms / radiotherapy. Survivors
  • [MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Magnetic Resonance Imaging. Male. Microsatellite Repeats. Middle Aged. Neoplasm Staging. Radiotherapy Dosage. Retrospective Studies. Survival Analysis

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  • (PMID = 17762927.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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