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6. Liebrich M, Guo LH, Schluesener HJ, Schwab JM, Dietz K, Will BE, Meyermann R: Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors. Arch Immunol Ther Exp (Warsz); 2007 Jan-Feb;55(1):41-7
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  • [Title] Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors.
  • MATERIALS AND METHODS: Expression of IL-16 was analyzed by immunohistochemistry in human astrocytic brain tumors and the rat C6 glioblastoma tumor model.
  • IL-16 was detected in both human astrocytic brain tumors and rat C6 glioma.
  • RESULTS: Compared with human control brains, a significant increase in the percentages of parenchymal IL-16+ macrophages/microglia was observed already in grade II astrocytomas, indicating that IL-16+ immunostaining could be a descriptor of a macrophage/microglia subset in astrocytic brain tumors.
  • This increase in IL-16 immunoreactivity correlated with WHO grades of human astrocytic brain tumors.
  • [MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Glioblastoma / immunology. Interleukin-16 / biosynthesis. Macrophages / immunology. Microglia / immunology
  • [MeSH-minor] Adult. Aged. Animals. Cell Line, Tumor. Female. Humans. Inflammation Mediators / metabolism. Male. Middle Aged. Rats. Rats, Sprague-Dawley

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  • (PMID = 17221335.001).
  • [ISSN] 0004-069X
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Inflammation Mediators; 0 / Interleukin-16
  • [Other-IDs] NLM/ PMC3234149
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7. Martínez C, Molina JA, Alonso-Navarro H, Jiménez-Jiménez FJ, Agúndez JA, García-Martín E: Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma. BMC Neurol; 2010;10:71
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  • [Title] Two common nonsynonymous paraoxonase 1 (PON1) gene polymorphisms and brain astrocytoma and meningioma.
  • Aiming to identify genetic variations related to the risk of developing brain tumors, we investigated the putative association between common nonsynonymous PON1 polymorphisms and the risk of developing astrocytoma and meningioma.
  • METHODS: Seventy one consecutive patients with brain tumors (43 with astrocytoma grade II/III and 28 with meningioma) with ages ranging 21 to 76 years, and 220 healthy controls subjects were analyzed for the frequency of the nonsynonymous PON1 genotypes L55M rs854560 and Q192R rs662.
  • RESULTS: The frequencies of the PON1 genotypes and allelic variants of the polymorphisms PON1 L55M and PON1 Q192R did not differ significantly between patients with astrocytoma and meningioma and controls.
  • The minor allele frequencies were as follows: PON1 55L, 0.398, 0.328 and 0.286 for patients with astrocytoma, meningioma and control individuals, respectively; PON1 192R, 0.341, 0.362 and 0.302 for patients with astrocytoma, meningioma and control individuals, respectively.
  • Haplotype association analyses did not identify any significant association with the risk of developing astrocytoma or meningioma.
  • CONCLUSIONS: Common nonsynonymous PON1 polymorphisms are not related with the risk of developing astrocytoma and meningioma.
  • [MeSH-major] Aryldialkylphosphatase / genetics. Astrocytoma / genetics. Brain Neoplasms / genetics. Meningeal Neoplasms / genetics. Meningioma / genetics

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  • (PMID = 20723250.001).
  • [ISSN] 1471-2377
  • [Journal-full-title] BMC neurology
  • [ISO-abbreviation] BMC Neurol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.8.1 / Aryldialkylphosphatase; EC 3.1.8.1 / PON1 protein, human
  • [Other-IDs] NLM/ PMC2936881
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8. Karmakar S, Banik NL, Patel SJ, Ray SK: 5-Aminolevulinic acid-based photodynamic therapy suppressed survival factors and activated proteases for apoptosis in human glioblastoma U87MG cells. Neurosci Lett; 2007 Mar 30;415(3):242-7
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  • Glioblastoma is the most common astrocytic brain tumor in humans.
  • We used 5-aminolevulinic acid (5-ALA) as a photosensitizer for PDT to induce apoptosis in human malignant glioblastoma U87MG cells and to understand the underlying molecular mechanisms.

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  • (PMID = 17335970.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS057811-01A1; United States / NCI NIH HHS / CA / R01 CA091460-04; United States / NCI NIH HHS / CA / R01 CA091460; United States / NINDS NIH HHS / NS / R01 NS 57811; United States / NCI NIH HHS / CA / R01 CA 91460; United States / NINDS NIH HHS / NS / R01 NS057811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Apoptosis Inducing Factor; 0 / Apoptosis Regulatory Proteins; 0 / BIRC3 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / NF-kappa B; 88755TAZ87 / Aminolevulinic Acid; EC 3.4.- / Peptide Hydrolases; EC 3.4.22.- / Calpain; EC 3.4.22.- / Caspases; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ NIHMS20981; NLM/ PMC2533742
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9. Li M, Jia ZZ, Gu HM, Zhou XJ, Tang LM: [Application of apparent diffusion coefficient and fractional anisotropy in identification of tumor component and grading of brain astrocytoma]. Zhonghua Yi Xue Za Zhi; 2008 Dec 23;88(47):3352-5
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  • [Title] [Application of apparent diffusion coefficient and fractional anisotropy in identification of tumor component and grading of brain astrocytoma].
  • OBJECTIVE: To evaluate the value of apparent diffusion coefficient (ADC) and fractional anisotropy (FA) in identification of tumor element and grading of brain astrocytoma.
  • METHODS: Thirty-three patients with histologically confirmed astrocytoma underwent diffusion weighted imaging (DWI), diffusion tensor imaging (DTI), and conventional MRI before operation.
  • The values of ADC and FA of different regions in the same tumor and of astrocytoma of different grades were measured and compared.
  • RESULTS: The ADC values of the tumor parenchyma, necrotic region, peritumoral edema region were (1.28 +/- 0.44), (1.97 +/- 0.53), and (1.74 +/- 0.47) respectively, all significantly higher than that of the corresponding normal brain tissues [(0.80 +/- 0.18), P = 0.009, P = 0.000, P = 0.000] with significantly differences between the tumor parenchyma and necrotic region and peritumoral edema region (both P < 0.05), however, there was not significant difference between the necrotic region and peritumoral edema region.
  • The FA values of the tumor parenchyma, necrotic region, and peritumoral edema region were (0.18 +/- 0.07), (0.14 +/- 0.05), and (0.16 +/- 0.05) respectively, all significantly higher than that of the corresponding normal brain tissues [(0.58 +/- 0.10), all P = 0.000], without significant differences among the former 3 groups.
  • There were no significant differences in the ADC and FA values among the tumors at different grades, however, there was a tendency of ADC to decrease and of FA to increase along the increase of grade of tumor, although not significantly.
  • CONCLUSION: ADC value plays an important part in distinguishing tumor components and determining tumor boundary, and plays a certain role in judging the grade of astrocytomas.
  • FA value is vital to determine the tumor boundary, and has certain value in differentiating high-grade from low-grade astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Anisotropy. Female. Humans. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 19257968.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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10. Kostic A, Mihailovic D, Veselinovic S, Tasic G, Radulovic D, Stefanovic I: Peritumoral edema and karyometric variables in astrocytoma of the brain. J BUON; 2007 Apr-Jun;12(2):239-43
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  • [Title] Peritumoral edema and karyometric variables in astrocytoma of the brain.
  • PURPOSE: The aim of this study was to evaluate karyometry as a quantitative and objective histological method by showing correlation of some karyometric variables with the severity of peritumoral edema in patients with brain astrocytoma.
  • The patients were diagnosed with astrocytoma of the brain, histologically confirmed on the surgically removed material.
  • Maximal tumor excision was performed in all patients, who were postoperatively treated according to current oncologic therapeutic protocols.
  • The intensity of perifocal edema (preoperative CT scan) was correlated to the duration of survival and the values of 9 karyometric tumor variables: area, density, maximal axis, mean axis, circumference, roundness, integrated optical density and number of nuclei.
  • Correlation of karyometric variables with CT findings revealed that higher degrees of tumor cellularity and nuclear wrinkling with increased integrated optical density is associated with larger peritumoral edema.
  • [MeSH-major] Astrocytoma / pathology. Brain Edema / pathology. Brain Neoplasms / pathology

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  • (PMID = 17600879.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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11. Lu ZQ, Wang YM, Cao YY, Zhang QJ, Zhang XH, Li YH, Wang HS, Xie HL, Jiao BH, Zhang JH: [Correlations of polymorphisms in matrix metalloproteinase-3 and -7 promoters to susceptibility to brain astrocytoma]. Ai Zheng; 2007 May;26(5):463-8
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  • [Title] [Correlations of polymorphisms in matrix metalloproteinase-3 and -7 promoters to susceptibility to brain astrocytoma].
  • BACKGROUND & OBJECTIVE: Matrix metalloproteinases (MMPs) are key enzymes involved in tumor development, invasion and metastasis.
  • The single nucleotide polymorphisms (SNPs) in the promoter regions of MMP genes may influence tumor development and progression via modulating mRNA transcription and protein expression.
  • This study was to explore the correlations of the promoter SNPs in MMP-3 and MMP-7 genes to susceptibility to brain astrocytoma.
  • METHODS: The genotype of MMP-3 -1171 5A/6A and MMP-7 -181A/G polymorphisms in 236 patients with brain astrocytoma and 366 healthy controls was detected by polymerase chain reaction-restrictive fragment length polymorphism (PCR-RFLP).
  • RESULTS: The allelotype and overall genotype distribution of MMP-3 SNP among the astrocytoma patients and healthy controls were similar (P>0.05).
  • Stratified by sex, age, and histological grade, the susceptibility to brain astrocytoma among the subjects with 5A/5A and 5A/6A genotypes and the subjects with 6A/6A genotype were similar(P>0.05).
  • The overall genotype distribution of MMP-7 SNP among the astrocytoma patients and healthy controls were significantly different (P = 0.001).
  • Compared with the A/A genotype, both the G/G and the A/G genotypes significantly increased the susceptibility to astrocytoma [sex-and age-adjusted odds ratio (OR) = 2.77 and 1.69, 95% confidence interval (CI)=1.27-6.02 and 1.01-2.84, respectively].
  • Stratification analysis showed that the G/G genotype significantly increased the susceptibility to astrocytoma in men (adjusted OR = 3.24, 95% CI = 1.12-9.41) and in the individuals younger than 45 years (adjusted OR = 3.16, 95% CI = 1.09-9.16).
  • When stratified by histological grade, the A/G genotype increased the susceptibility to grade II astrocytoma by about 2 folds (adjusted OR = 2.06, 95% CI = 1.05 - 4.05), while the G/G genotype increased the susceptibility to grade II-IV astrocytoma by about 3 folds.
  • CONCLUSION: MMP-7 -181A/G polymorphism may influence the susceptibility to astrocytoma, while MMP-3-1171 5A/6A polymorphism has no correlation to the susceptibility.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genetic Predisposition to Disease. Matrix Metalloproteinase 3 / genetics. Matrix Metalloproteinase 7 / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 17672933.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 3.4.24.17 / MMP3 protein, human; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.23 / MMP7 protein, human; EC 3.4.24.23 / Matrix Metalloproteinase 7
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12. Lee WH, Jin JS, Tsai WC, Chen YT, Chang WL, Yao CW, Sheu LF, Chen A: Biological inhibitory effects of the Chinese herb danggui on brain astrocytoma. Pathobiology; 2006;73(3):141-8
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  • [Title] Biological inhibitory effects of the Chinese herb danggui on brain astrocytoma.
  • In nude mice, the growth of the tumor was inhibited by 30% by AS-CH or AS-AC (20 mg/kg; p < 0.05) and by 60% by AS-CH or AS-AC (60 mg/kg; p < 0.05).
  • CONCLUSIONS: Danggui may inhibit tumor growth by reducing the level of VEGF and the proapoptotic protein, cathepsin B.
  • [MeSH-major] Angelica sinensis / chemistry. Antineoplastic Agents / pharmacology. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Drugs, Chinese Herbal / pharmacology. Phytotherapy
  • [MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cathepsin B / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Female. Formazans / metabolism. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Plant Extracts / pharmacology. Tetrazolium Salts / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17085958.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Chinese Herbal; 0 / Formazans; 0 / Plant Extracts; 0 / Tetrazolium Salts; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 23305-68-2 / MTT formazan; EC 3.4.22.1 / Cathepsin B
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13. Olivera M, Martínez C, Molina JA, Alonso-Navarro H, Jiménez-Jiménez FJ, García-Martín E, Benítez J, Agúndez JA: Increased frequency of rapid acetylator genotypes in patients with brain astrocytoma and meningioma. Acta Neurol Scand; 2006 May;113(5):322-6
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  • [Title] Increased frequency of rapid acetylator genotypes in patients with brain astrocytoma and meningioma.
  • We investigated the association between the genetic NAT2 polymorphism and brain tumors by analysis of genomic DNA from 71 brain tumor patients and 258 healthy controls.
  • A higher number of individuals carrying functional NAT2 genes, and therefore with a rapid acetylation phenotype, was found in brain tumor patients vs healthy volunteers (OR 1.79, 95% CI 1.05-3.05; P < 0.05).
  • This is observed either for patients suffering from meningioma or astrocytoma, and this is due to an increase of the wild-type NAT2*4 allelic variant frequency (OR 1.48, 95% CI 0.99-2.19), and a reduction of the commonest defective allelic variant NAT2*5B in the brain tumor patients, compared with healthy subjects (OR 0.54, 95% CI 0.37-0.80).
  • CONCLUSIONS: This observation indicates that NAT2 could be considered as a low-penetrance gene for brain tumors, and that individuals carrying rapid acetylation alleles are at increased risk of developing brain tumors.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Astrocytoma / genetics. Brain Neoplasms / genetics. Meningeal Neoplasms / genetics. Meningioma / genetics. Polymorphism, Single Nucleotide / genetics

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  • (PMID = 16629768.001).
  • [ISSN] 0001-6314
  • [Journal-full-title] Acta neurologica Scandinavica
  • [ISO-abbreviation] Acta Neurol. Scand.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human
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1
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4. Liu RS, Chang CP, Chu LS, Chu YK, Hsieh HJ, Chang CW, Yang BH, Yen SH, Huang MC, Liao SQ, Yeh SH: PET imaging of brain astrocytoma with 1-11C-acetate. Eur J Nucl Med Mol Imaging; 2006 Apr;33(4):420-7
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  • [Title] PET imaging of brain astrocytoma with 1-11C-acetate.
  • Images were analysed by visual interpretation and determination of the tumour to cortex ratio (T/C ratio) and standardised uptake value (SUV).
  • The tumour uptake was visually scored into three grades as compared with the contralateral cortex: clearly lower (-), almost equal (+) and clearly higher (++).
  • ACE is complementary to FDG for the diagnosis and characterisation of astrocytoma.
  • [MeSH-major] Acetates. Astrocytoma / diagnostic imaging. Brain Neoplasms / diagnostic imaging. Carbon. Fluorodeoxyglucose F18. Positron-Emission Tomography / methods. Radiopharmaceuticals

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  • (PMID = 16404596.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Acetates; 0 / Radiopharmaceuticals; 0 / carbon-11 acetate; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 7440-44-0 / Carbon
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15. Banerjee HN, Zhang L: Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy. Mol Cell Biochem; 2007 Jan;295(1-2):237-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy.
  • To explore the biochemical differences between brain cancer cells Astrocytoma and normal cells Astrocyte, we investigated the Raman spectra of single cell from these two cell types and analyzed the difference in spectra and intensity.
  • The Raman spectra of brain cancer cells was similar to those of normal cells, but the Raman intensity of cancer cells was much higher than that of normal cells.
  • The Raman spectra of brain cancer Astrocytoma shows that the structural changes of cancer cells happen so that many biological functions of these cells are lost.
  • The results indicate that Raman spectra can offer the experimental basis for the cancer diagnosis and treatment.
  • [MeSH-major] Astrocytes / chemistry. Astrocytoma / chemistry. Brain Neoplasms / chemistry. Spectroscopy, Near-Infrared. Spectrum Analysis, Raman

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  • (PMID = 16924417.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / G11HD 34280-05
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
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16. Riemenschneider MJ, Reifenberger G: Astrocytic tumors. Recent Results Cancer Res; 2009;171:3-24
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  • [Title] Astrocytic tumors.
  • Astrocytic gliomas are the most common primary brain tumors and account for up to two thirds of all tumors of glial origin.
  • In this review we outline the basic histological and epidemiological aspects of the different astrocytoma subtypes in adults.
  • In addition, we summarize the key genetic alterations that have been attributed to astrocytoma patho-genesis and progression.
  • Also, the first steps have been taken in refining classical histopathological diagnosis by use of molecular predictive markers, for example, MGMT promoter hypermethylation in glioblastomas.
  • Finally, the tumor stem cell hypothesis has challenged our way of understanding astrocytoma biology by emphasizing intratumoral heterogeneity.
  • [MeSH-major] Brain Neoplasms / genetics
  • [MeSH-minor] Animals. Astrocytoma / chemistry. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / pathology. Disease Models, Animal. Humans. Immunohistochemistry. Neoplasm Invasiveness. Signal Transduction

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  • (PMID = 19322535.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 109
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17. Weber RG, Hoischen A, Ehrler M, Zipper P, Kaulich K, Blaschke B, Becker AJ, Weber-Mangal S, Jauch A, Radlwimmer B, Schramm J, Wiestler OD, Lichter P, Reifenberger G: Frequent loss of chromosome 9, homozygous CDKN2A/p14(ARF)/CDKN2B deletion and low TSC1 mRNA expression in pleomorphic xanthoastrocytomas. Oncogene; 2007 Feb 15;26(7):1088-97
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  • The molecular pathogenesis of pleomorphic xanthoastrocytoma (PXA), a rare astrocytic brain tumor with a relatively favorable prognosis, is still poorly understood.
  • Interphase fluorescence in situ hybridization to tissue sections confirmed the presence of tumor cells with homozygous 9p21.3 deletions.
  • [MeSH-major] Astrocytoma / genetics. Chromosome Deletion. Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Deletion. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Proteins / deficiency

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  • (PMID = 16909113.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein
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18. Qu M, Olofsson T, Sigurdardottir S, You C, Kalimo H, Nistér M, Smits A, Ren ZP: Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas. Acta Neuropathol; 2007 Feb;113(2):129-36
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  • [Title] Genetically distinct astrocytic and oligodendroglial components in oligoastrocytomas.
  • Oligoastrocytomas are glial tumours consisting of a mixture of neoplastic astrocytic and oligodendroglial cells.
  • To investigate whether these neoplastic cell types in oligoastrocytomas have different genetic profiles, we examined the two different components of oligoastrocytomas in comparison with the histological diagnosis of the specific tumour area for LOH 1p/19q and TP53 mutations by using microdissection technique.
  • We found a variety of lost markers for 1p and 19q, and the presence of two different TP53 mutations in the tumour samples.
  • In the majority of cases (9/11), the oligodendroglial and astrocytic components of an individual oligoastrocytoma displayed the same genotype.
  • We present two cases of biphasic oligoastrocytomas with aberrant findings, suggesting the coexistence of genetically and morphologically distinct tumour cell clones in these tumours.
  • In one case, the oligodendroglial part of the tumour showed LOH19q, whereas the astrocytic part showed TP53 mutation (codon 273).
  • In another case, we found LOH 1p/19q in the oligodendroglial component, but two retained areas on chromosome 1p in the astrocytic component of the tumour.
  • No evidence was found for the coexistence of tumour cells with the two genotypical changes within the same morphological region of one individual tumour.
  • The two cases of biphasic oligoastrocytomas in our sample that display a different genotype in the astrocytic and oligodendroglial part of the tumour show that different components of an oligoastrocytoma may be derived from different cell clones during neoplastic transformation.
  • [MeSH-major] Astrocytoma / classification. Astrocytoma / genetics. Brain Neoplasms / classification. Brain Neoplasms / genetics. Oligodendroglioma / genetics
  • [MeSH-minor] Adult. Aged. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17031656.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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19. Kitai R, Horita R, Sato K, Yoshida K, Arishima H, Higashino Y, Hashimoto N, Takeuchi H, Kubota T, Kikuta K: Nestin expression in astrocytic tumors delineates tumor infiltration. Brain Tumor Pathol; 2010 Apr;27(1):17-21
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  • [Title] Nestin expression in astrocytic tumors delineates tumor infiltration.
  • Nestin is an intermediate filament protein expressed in undifferentiated cells during central nervous system development, and glioma is known to be a highly infiltrative tumor.
  • We determined whether nestin was expressed in astrocytic tumors and could identify infiltrating tumor cells.
  • We screened 65 archival, paraffin-embedded adult astrocytic tumors using immunohistochemical staining and computerized overlaid photographs.
  • Normal biopsied brains and metastatic brain tumors were also examined.
  • The intensity of nestin expression corresponded to the tumor grade.
  • 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.
  • Nestin is a useful marker for examining the infiltration of malignant cells into surrounding tissue.
  • [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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20. 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.
  • Apoptosis and cell proliferation occur simultaneously in tumour tissue with tumour suppressor gene, p53 being one of the key players in the complex relationship between these two key phenomena.
  • 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.
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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21. 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.
  • Alterations of C-RAF expression are discussed to play a role in lung cancer.
  • 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.
  • 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.
  • 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.
  • [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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22. Gathinji M, McGirt MJ, Attenello FJ, Chaichana KL, Than K, Olivi A, Weingart JD, Brem H, Quinones-Hinojosa A: Association of preoperative depression and survival after resection of malignant brain astrocytoma. Surg Neurol; 2009 Mar;71(3):299-303, discussion 303
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  • [Title] Association of preoperative depression and survival after resection of malignant brain astrocytoma.
  • It remains unclear if clinical depression affects survival after surgical management of malignant brain astrocytoma.
  • We set out to determine whether patients with a diagnosis of clinical depression before surgery experienced decreased survival independent of treatment modality or degree of disability.
  • METHODS: One thousand fifty-two patients undergoing surgical management for malignant brain astrocytoma (WHO grade 3 or 4) performed at a single institution from 1995 to 2006 were retrospectively reviewed.
  • Forty-nine patients (5%) carried the diagnosis of depression at the time of surgery.
  • CONCLUSION: In our experience, patients who are actively depressed at the time of surgery were associated with decreased survival after surgical management of malignant astrocytoma, independent of degree of disability, tumor grade, or subsequent treatment modalities.
  • [MeSH-major] Astrocytoma / mortality. Brain Neoplasms / mortality. Depression / mortality

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  • (PMID = 18786716.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. 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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24. Mennel HD, Lell B: Ganglioside (GD2) expression and intermediary filaments in astrocytic tumors. Clin Neuropathol; 2005 Jan-Feb;24(1):13-8
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  • [Title] Ganglioside (GD2) expression and intermediary filaments in astrocytic tumors.
  • The search of proliferation markers in astrocytic tumors that may serve as targets for therapeutic interventions, is in full progress.
  • Gangliosides are lipid-sugar compounds localized on the cell membrane that are thought to modify pertinent signals and, therefore, may influence a variety of functions in normal and pathologic conditions including those that act upon tumor growth.
  • Intracranial supratentorial astrocytic gliomas of the adult represent a tumor group, that may be divided into three grades of malignancy, the most anaplastic member being the glioblastoma.
  • Yet, the results were only partly congruent and the correlation to tumor grades rather loose.
  • Thus, the conclusion must be drawn that the correlation of ganglioside patterns to the proliferation of astrocytic tumors is as poor as that of GFAP or vimentin expression, respectively.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gangliosides / metabolism. Intermediate Filaments / metabolism

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  • (PMID = 15696779.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Gangliosides; 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin; 65988-71-8 / ganglioside, GD2
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25. Eckerich C, Zapf S, Ulbricht U, Müller S, Fillbrandt R, Westphal M, Lamszus K: Contactin is expressed in human astrocytic gliomas and mediates repulsive effects. Glia; 2006 Jan 1;53(1):1-12
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  • [Title] Contactin is expressed in human astrocytic gliomas and mediates repulsive effects.
  • Particularly high levels of contactin are present during brain development.
  • Using subtractive cloning, we identified contactin transcripts as overexpressed in glioblastomas compared with normal brain.
  • Analyzing different types of astrocytic tumors, we detected an association between increasing malignancy grade and contactin expression.
  • The repulsive properties of contactin may be a key factor in glioma disaggregation, and may contribute to the diffuse infiltration pattern characteristic of glioma cells in human brain.
  • [MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Cell Adhesion Molecules, Neuronal / metabolism
  • [MeSH-minor] Cell Adhesion / physiology. Cell Aggregation / physiology. Cell Communication / physiology. Cell Line, Tumor. Cell Movement / physiology. Cell Proliferation. Contactins. Extracellular Matrix Proteins / metabolism. Gene Expression Regulation, Neoplastic / physiology. Glial Fibrillary Acidic Protein / metabolism. Humans. Ligands. Neoplasm Invasiveness. Protein Tyrosine Phosphatases / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16078236.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules, Neuronal; 0 / Contactins; 0 / Extracellular Matrix Proteins; 0 / Glial Fibrillary Acidic Protein; 0 / Ligands; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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26. Necesalová E, Vranová V, Kuglík P, Cejpek P, Jarosová M, Pesáková M, Relichová J, Veselská R: Incidence of the main genetic markers in glioblastoma multiforme is independent of tumor topology. Neoplasma; 2007;54(3):212-8
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  • [Title] Incidence of the main genetic markers in glioblastoma multiforme is independent of tumor topology.
  • Glioblastoma multiforme (GBM) is the most common as well as the most aggressive type of primary brain tumor of astrocytic origin in adults.
  • Trisomy/polysomy of chromosome 7, monosomy of chromosome 10, EGFR gene amplification and p53 deletion have been described as the typical genetic markers for tumor classification and prediction of possible response to therapy.
  • Chromosomal abnormalities in tumor samples from a group of 21 patients surgically treated for GBM were characterized by means of the interphase-fluorescence in situ hybridization (I-FISH) technique using sets of centromere and locus-specific DNA probes.
  • In addition, we performed a detailed analysis of one selected tumor sample using a genomic microarray system (GenoSensor Array 300) to characterize copy number changes of specific sequences and refine results obtained by I-FISH.
  • However, the data show no significant differences in occurrence of the described genetic markers in either part of the tumor.
  • [MeSH-major] Brain Neoplasms / genetics. Chromosomes, Human, Pair 10 / genetics. Glioblastoma / genetics. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / genetics. Chromosome Aberrations. Chromosome Mapping. Female. Gene Amplification. Gene Dosage. Genetic Markers / genetics. Humans. In Situ Hybridization, Fluorescence. Incidence. Karyotyping. Male. Middle Aged. Nucleic Acid Hybridization. Polymerase Chain Reaction. Prognosis

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  • (PMID = 17447852.001).
  • [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 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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27. 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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28. Ren ZP, Olofsson T, Qu M, Hesselager G, Soussi T, Kalimo H, Smits A, Nistér M: Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors. J Neuropathol Exp Neurol; 2007 Oct;66(10):944-54
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  • [Title] Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors.
  • We investigated genetic heterogeneity of astrocytic gliomas using p53 gene mutations as a marker.
  • Different parts of morphologically heterogeneous astrocytic gliomas were microdissected, and direct DNA sequencing of p53 gene exons 5 through 8 was performed.
  • Thirty-five glioma samples and tumor-adjacent normal-appearing brain tissue from 11 patients were analyzed.
  • The mutations were present in grade II, III, and IV astrocytic glioma areas.
  • Both severe functionally dead mutants and mutants with remaining transcriptional activity could be observed in the same tumor.
  • Coexistence of p53 gene mutations and the locus of heterozygosity was common, at least in astrocytomas grade III and in glioblastomas, and also occurred in astrocytoma grade II areas.
  • These results support the notion that intratumoral heterogeneity in brain tumors originates from different molecular defects.
  • [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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29. 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.
  • Positive endothelial cells were found in astrocytic tumors of all grades, even when tumor cells showed no hTERT immunoreactivity.
  • A subset of mature normal neurons was positive for hTERT (pattern As), suggesting a role for this molecule in neuronal maintenance in the adult brain.
  • 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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30. 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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31. 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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32. 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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33. 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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  • [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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34. 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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  • [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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35. Murakami H, Sawa H, Kamada H: [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors]. No To Shinkei; 2006 Jan;58(1):43-9

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  • [Title] [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors].
  • Cyclooxygenase (COX)-2 of astrocytic tumors was studied by immunohistochemistry.
  • COX-2 was expressed in 8 of 12 (75%) glioblastoma multiforme, 1 of 7 (14%) anaplastic astrocytoma, but none in astrocytoma.
  • The result showed that COX-2 expression may be related with histological grades and COX-2 inhibitors will be one of promising therapeutic tools in human astrocytic tumors.
  • [MeSH-major] Astrocytoma / enzymology. Cyclooxygenase 2 / analysis. Cyclooxygenase 2 Inhibitors / therapeutic use
  • [MeSH-minor] Adult. Aged. Etodolac / pharmacology. Female. Glioblastoma / drug therapy. Glioblastoma / enzymology. Humans. Immunoblotting. Immunohistochemistry. Male. Middle Aged. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured

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  • (PMID = 16482921.001).
  • [ISSN] 0006-8969
  • [Journal-full-title] Nō to shinkei = Brain and nerve
  • [ISO-abbreviation] No To Shinkei
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitrobenzenes; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 2M36281008 / Etodolac; EC 1.14.99.1 / Cyclooxygenase 2
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36. Rossi D, Volterra A: Astrocytic dysfunction: insights on the role in neurodegeneration. Brain Res Bull; 2009 Oct 28;80(4-5):224-32
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  • [Title] Astrocytic dysfunction: insights on the role in neurodegeneration.
  • The additional observation that glutamate release from astrocytes is controlled by molecules linked to inflammatory reactions, such as the cytokine tumor necrosis factor alpha (TNFalpha) and prostaglandins (PGs), suggests that glia-to-neuron signalling may be sensitive to changes in the production of these mediators occurring in pathological conditions.
  • Indeed, a local, parenchymal brain inflammatory reaction (neuroinflammation) characterized by astrocytic and microglial activation has been reported in several neurodegenerative disorders, including AIDS dementia complex, Alzheimer's disease and amyotrophic lateral sclerosis.
  • The findings reported in this review suggest that a better comprehension of the glutamatergic interplay between neurons and astrocytes may provide information about normal brain function and also highlight potential molecular targets for therapeutic interventions in pathology.

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  • (PMID = 19631259.001).
  • [ISSN] 1873-2747
  • [Journal-full-title] Brain research bulletin
  • [ISO-abbreviation] Brain Res. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 3KX376GY7L / Glutamic Acid; SY7Q814VUP / Calcium
  • [Number-of-references] 123
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37. Kumar AJ, Leeds NE, Kumar VA, Fuller GN, Lang FF, Milas Z, Weinberg JS, Ater JL, Sawaya R: Magnetic resonance imaging features of pilocytic astrocytoma of the brain mimicking high-grade gliomas. J Comput Assist Tomogr; 2010 Jul;34(4):601-11
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  • [Title] Magnetic resonance imaging features of pilocytic astrocytoma of the brain mimicking high-grade gliomas.
  • OBJECTIVE: The typical magnetic resonance/computed tomographic imaging appearance of pilocytic astrocytoma (PA) is that of a cyst with an intensely enhancing mural nodule.
  • METHODS: One hundred patients referred to the cancer center with brain tumors histologically proven to be PA were retrospectively reviewed (95 by magnetic resonance imaging and 5 by computed tomographic imaging) and analyzed.
  • Tumor locations consisted of the following: optic chiasm (22), lateral ventricle (3), thalamus (12), basal ganglia (1), cerebral hemisphere (10), corpus callosum (2), brain stem (26), fourth ventricle (1), and cerebellum (23).
  • CONCLUSIONS: It is important to recognize the aggressive imaging appearance of PA (grade 1 astrocytoma) because it can be mistaken for high-grade gliomas and may thus lead to inappropriate therapy.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis. Glioma / diagnosis. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Brain / pathology. Brain / radiography. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Retrospective Studies. Tomography, X-Ray Computed / methods. Young Adult

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  • (PMID = 20657231.001).
  • [ISSN] 1532-3145
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Burzynski SR: Treatments for astrocytic tumors in children: current and emerging strategies. Paediatr Drugs; 2006;8(3):167-78
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  • [Title] Treatments for astrocytic tumors in children: current and emerging strategies.
  • Strategies for the treatment of childhood cancer have changed considerably during the last 50 years and have led to dramatic improvements in long-term survival.
  • Astrocytic tumors form the most common histologic group among childhood brain tumors.
  • Radiation therapy is generally recommended for children with progressive LGA, or after failure of chemotherapy, accomplishing tumor control at 10 years in over 60% of patients.
  • OPG is the most common type of brain tumor associated with NF1.
  • Tumor growth in some of these patients is slow with no treatment recommended for an extended period of time.
  • Diffuse intrinsic BSG are among the most difficult-to-treat brain tumors.
  • Careful evaluation of histology, location of the tumor, patient age, and consideration of treatment-related morbidity play an important part in selecting between clinical observation, surgery, radiation, chemotherapy, or investigational agents.
  • The goals of treatment for astrocytic tumors should extend well beyond objective responses and increased survival.
  • [MeSH-major] Astrocytoma / therapy. Central Nervous System Neoplasms / therapy

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  • (PMID = 16774296.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Number-of-references] 155
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39. Zhang H, Rödiger LA, Zhang G, Oudkerk M: Differentiation between Supratentorial Single Brain Metastases and High Grade Astrocytic Tumors: an Evaluation of Different DSC MRI Measurements. Neuroradiol J; 2009 Aug 29;22(4):369-77

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  • [Title] Differentiation between Supratentorial Single Brain Metastases and High Grade Astrocytic Tumors: an Evaluation of Different DSC MRI Measurements.
  • This study evaluated the role of different perfusion MRI measurements in the pre-operative differentiation between single brain metastases and high grade astrocytic tumors.
  • 24 high-grade astrocytic tumors and 29 single metastases were studied.
  • Relative cerebral blood volume, cerebral blood flow and mean transit time in both tumor parenchyma (T rCBV, T rCBF and T rMTT) and peritumoral edema (P rCBV, P rCBF and P rMTT) were measured.
  • Mann-Whitney tests were used to assess differences between single brain metastases and high grade astrocytic tumors.
  • Receiver operating characteristic analyses were performed to determine optimum thresholds for tumor differentiation.
  • Sensitivity, specificity and accuracy for identifying brain metastases were calculated.
  • Mean T rCBV, T rCBF, P rCBV and P CBF of brain metastases (2.75±1.72, 2.51±2.09, 1.05±0.53, 0.87±0.40) differed statistically (P <0.05) from those of high grade astrocytic tumors (6.00±2.17, 5.68±2.35, 1.77±1.19 and 1.58±0.99).
  • Based on the area under the ROC curves (AUC), the efficiency of T rCBV and T rCBF for correct diagnosis of brain metastases is almost identical (AUC: 0.899, 0.890 respectively) and superior to other measurements.
  • Different perfusion measurements can be used to differentiate single metastases from high-grade astrocytic tumors.

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  • (PMID = 24207139.001).
  • [ISSN] 1971-4009
  • [Journal-full-title] The neuroradiology journal
  • [ISO-abbreviation] Neuroradiol J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. 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).
  • The RCAS1 protein was not detected in normal brain tissues by immunohistochemical staining.
  • 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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41. 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.

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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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42. 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.
  • 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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43. Chu SH, Yuan XH, Jiang PC, Li ZQ, Zhang J, Wen ZH, Zhao SY, Chen XJ, Cao CJ: [The expression of hepatocyte growth factor and its receptor in brain astrocytomas]. Zhonghua Yi Xue Za Zhi; 2005 Mar 30;85(12):835-8
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  • [Title] [The expression of hepatocyte growth factor and its receptor in brain astrocytomas].
  • OBJECTIVE: To investigate the expression of hepatocyte growth factor (HGF) mRNA and its receptor (c-Met) mRNA in brain astrocytomas and their relationships with tumor proliferation, angiogenesis, clinical pathology and prognosis.
  • METHODS: The expression of HGF mRNA, c-Met mRNA in the resected tumor tissues of 76 patients with brain astrocytomas, 43 males and 33 females, aged 20 - 71, were detected by in situ hybridization.
  • RESULTS: The positive rates of expression of HGF, c-Met and PCNA in low pathologic grades of brain astrocytoma were 34.5%, 44.8% and 15% +/- 9% respectively, and in high pathologic grades of brain astrocytoma were 34.5%, 44.8% and 48% +/- 12% respectively (P < 0.05).
  • MVD in low and high pathologic grades of brain astrocytoma were 17 +/- 7 and 31 +/- 13 respectively (P < 0.05).
  • The expression of HGF, c-Met, PCNA and CD34 was not related to sex, age, position of tumor and diameter of tumor.
  • The expression of c-Met was related to the expression of HGF, PCNA and the MVD in the tumor tissues of these patients.
  • The pathological grade, position of tumor, HGF, c-Met, PCNA, MVD had a significant influence on the survival time.
  • CONCLUSION: HGF/c-Met plays an important role in the formation and progression of the brain astrocytoma and can promote tumor proliferation and intratumoral microvascular formation, and is closely related to the prognosis of the patients.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Hepatocyte Growth Factor / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Receptors, Growth Factor / biosynthesis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor. Female. Humans. Male. Middle Aged. Neovascularization, Pathologic. Proto-Oncogene Proteins c-met. RNA, Messenger / biosynthesis. RNA, Messenger / genetics


44. Seng TJ, Ichimura K, Liu L, Tingby O, Pearson DM, Collins VP: Complex chromosome 22 rearrangements in astrocytic tumors identified using microsatellite and chromosome 22 tile path array analysis. Genes Chromosomes Cancer; 2005 Jun;43(2):181-93
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  • [Title] Complex chromosome 22 rearrangements in astrocytic tumors identified using microsatellite and chromosome 22 tile path array analysis.
  • Many studies have reported chromosome 22 as being abnormal in astrocytic tumors.
  • In an attempt to map precisely the abnormal region or regions that potentially harbor tumor-suppressor genes or oncogenes, we constructed a chromosome 22 tile path array covering 82% of 22q with the use of 441 chromosome 22 clones.
  • A total of 126 astrocytic tumors-5 diffuse astrocytomas (A), 29 anaplastic astrocytomas (AA), and 92 glioblastomas (GB)-were examined for chromosome 22 alterations both by microsatellite analysis (using 28 markers to identify allelic imbalance) and with the tile path array.
  • The results showed that chromosome 22 alterations in astrocytic tumors could be complex.
  • This study demonstrated the advantages of combining array comparative genomic hybridization and microsatellite analysis in elucidating complex genomic rearrangements in primary human tumor tissue.
  • Supplementary material for this article can be found on the Genes, Chromosomes and Cancer website at http://www.interscience.wiley.com/jpages/1045-2257/suppmat/index.html.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 22. Microsatellite Repeats / genetics

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15770670.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers
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45. 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.
  • 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.
  • [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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46. da Cruz-Höfling MA, Rapôso C, Verinaud L, Zago GM: Neuroinflammation and astrocytic reaction in the course of Phoneutria nigriventer (armed-spider) blood-brain barrier (BBB) opening. Neurotoxicology; 2009 Jul;30(4):636-46
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  • [Title] Neuroinflammation and astrocytic reaction in the course of Phoneutria nigriventer (armed-spider) blood-brain barrier (BBB) opening.
  • Phoneutria nigriventer spider venom (PNV) causes uneven BBB permeability throughout different cerebral regions.
  • A clear explanation for this differential modulation is unclear, but likely result from regional differences in astrocytic/neuronal populations, BBB tightness, and/or extent/distribution of microvasculature and/or ion channels density/distribution.
  • [MeSH-major] Astrocytes / drug effects. Blood-Brain Barrier / drug effects. Cytokines / metabolism. Spider Venoms / toxicity
  • [MeSH-minor] Animals. Glial Fibrillary Acidic Protein / metabolism. Interferon-alpha / metabolism. Male. Neuroimmunomodulation / drug effects. Rats. Rats, Wistar. S100 Proteins / metabolism. Time Factors. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19393263.001).
  • [ISSN] 1872-9711
  • [Journal-full-title] Neurotoxicology
  • [ISO-abbreviation] Neurotoxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / Glial Fibrillary Acidic Protein; 0 / Interferon-alpha; 0 / S100 Proteins; 0 / Spider Venoms; 0 / Tumor Necrosis Factor-alpha
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47. Srivastava T, Chosdol K, Chattopadhayay P, Sarkar C, Mahapatra AK, Sinha S: Frequent loss of heterozygosity encompassing the hMLH1 locus in low grade astrocytic tumors. J Neurooncol; 2007 Feb;81(3):249-55
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  • [Title] Frequent loss of heterozygosity encompassing the hMLH1 locus in low grade astrocytic tumors.
  • In astrocytic tumors, the heterozygosity status of these genes with reference to tumor grade has not yet been determined.
  • We have analyzed the heterozygosity status and locus specific instability in 43 glial tumors comprising 22 low grades diffuses astrocytoma (WHO Grade II, DA) and 21 glioblastoma multiforme (Grade IV GBM) using 10 microsatellite markers at 2p and 3p to elucidate the involvement of these loci in astrocytic tumorigenesis.
  • Our results suggest that in the astrocytic tumorigenesis, LOH at the hMLH1 gene locus is an early event in tumorigenesis.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Carrier Proteins / genetics. Loss of Heterozygosity. Nuclear Proteins / genetics

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  • (PMID = 17019533.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / DNA Primers; 0 / MLH1 protein, human; 0 / Nuclear Proteins
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48. Chosdol K, Misra A, Puri S, Srivastava T, Chattopadhyay P, Sarkar C, Mahapatra AK, Sinha S: Frequent loss of heterozygosity and altered expression of the candidate tumor suppressor gene 'FAT' in human astrocytic tumors. BMC Cancer; 2009;9:5
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  • [Title] Frequent loss of heterozygosity and altered expression of the candidate tumor suppressor gene 'FAT' in human astrocytic tumors.
  • BACKGROUND: We had earlier used the comparison of RAPD (Random Amplification of Polymorphic DNA) DNA fingerprinting profiles of tumor and corresponding normal DNA to identify genetic alterations in primary human glial tumors.
  • METHODS: In this study we used RAPD-PCR to identify novel genomic alterations in the astrocytic tumors of WHO grade II (Low Grade Diffuse Astrocytoma) and WHO Grade IV (Glioblastoma Multiforme).
  • RESULTS: Bands consistently altered in the RAPD profile of tumor DNA in a significant proportion of tumors were identified.
  • One such 500 bp band, that was absent in the RAPD profile of 33% (4/12) of the grade II astrocytic tumors, was selected for further study.
  • Its sequence corresponded with a region of FAT, a putative tumor suppressor gene initially identified in Drosophila.
  • CONCLUSION: These results point to a role of the FAT in astrocytic tumorigenesis and demonstrate the use of RAPD analysis in identifying specific alterations in astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Cadherins / genetics. Central Nervous System Neoplasms / genetics. Genes, Tumor Suppressor. Loss of Heterozygosity

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  • (PMID = 19126244.001).
  • [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] 0 / Cadherins; 0 / DNA Primers; 0 / FAT1 protein, human
  • [Other-IDs] NLM/ PMC2631005
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49. Faria MH, Gonçalves BP, do Patrocínio RM, de Moraes-Filho MO, Rabenhorst SH: Expression of Ki-67, topoisomerase IIalpha and c-MYC in astrocytic tumors: correlation with the histopathological grade and proliferative status. Neuropathology; 2006 Dec;26(6):519-27
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  • [Title] Expression of Ki-67, topoisomerase IIalpha and c-MYC in astrocytic tumors: correlation with the histopathological grade and proliferative status.
  • Recently, the determination of the proliferative index of astrocytic tumors by different methods has been proposed as a valuable tool for tumor grading and also as a prognostic marker.
  • The aim of the present study was to evaluate the expression of cell proliferation-related proteins in human astrocytic tumors of different histopathological grades (WHO).
  • An immunohistochemical study of the Ki-67, Topoisomerase IIalpha (Topo IIalpha) and c-MYC proteins using the avidin-biotin-peroxidase method was performed in 55 astrocytomas (13 grade I, 14 grade II, 7 grade III and 21 grade IV) and five samples of non-tumor brain tissue (control group).
  • Ki-67, Topo IIalpha and c-MYC positive indices tended to increase according to malignant progression, were absent in non-tumor brain tissue and showed maximum values in high-grade astrocytomas (III and IV).
  • Ki-67 antigen detection in more than 8.0% of the tumor cells distinguished astrocytoma grade IV, while a labeling index between 1.5 and 8.0% characterized astrocytomas grade III and values below 1.5% discriminated low-grade tumors (I and II).
  • Moreover, Ki-67 antigen was found to be the best marker of cellular proliferation, and its expression predicts the grade of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, Neoplasm / metabolism. Cell Division. Child. Child, Preschool. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. Female. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. Infant. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins c-myc / metabolism

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  • (PMID = 17203587.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-myc; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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50. Shostak KO, Dmitrenko VV, Vudmaska MI, Naidenov VG, Beletskii AV, Malisheva TA, Semenova VM, Zozulya YP, Demotes-Mainard J, Kavsan VM: Patterns of expression of TSC-22 protein in astrocytic gliomas. Exp Oncol; 2005 Dec;27(4):314-8
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  • [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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56. Arismendi-Morillo G, Castellano A: Tumoral micro-blood vessels and vascular microenvironment in human astrocytic tumors. A transmission electron microscopy study. J Neurooncol; 2005 Jul;73(3):211-7
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  • [Title] Tumoral micro-blood vessels and vascular microenvironment in human astrocytic tumors. A transmission electron microscopy study.
  • The development of peritumoral edema is thought to be due to extravasation of plasma water and macromolecules through a defective blood-brain barrier (BBB), but the exact mechanism by which occurs is poorly understood.
  • The aim of this study was analyze at submicroscopic level the morphological changes in both micro-blood vessels and vascular microenvironment of astrocytic tumors in an attempt of understanding the pathological aspects that may help in the future researches for the design of future therapeutic strategies.
  • Biopsies of 25 patients with pathological diagnosis of astrocytic tumors were examined with the transmission electron microscope.
  • Both open and close tight junctions were observed in the micro-blood vessels, inclusive in a same tumor.
  • Pericytes exhibited edema and phagocytoced material, astrocytic perivascular-feet showed signs of oncosis and necrosis, co-option vessels totally surrounding by neoplastic cells also were seen.
  • The ultrastructural abnormalities observed in both junctional complexes and vascular microenvironment suggest a multi-factorial pathobiology process, probably hypoxia intratumoral, calcium overload in endothelial cells, and degradative effects of metalloproteinases over the basal membrane appear as determinant factors that leading to structural modifications of junctional complexes, therefore, treatment with both HIF-1alpha and metalloproteinases inhibitors possibly can contribute with the pharmacological handling of the peritumoral edema associated with astrocytic tumors.
  • [MeSH-major] Astrocytoma / blood supply. Brain Neoplasms / blood supply. Capillaries / pathology. Capillaries / ultrastructure. Tight Junctions / pathology

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  • (PMID = 15980971.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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57. Li X, Wang Y, Wang Y, Zhen H, Yang H, Fei Z, Zhang J, Liu W, Wang Y, Zhang X: Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis. Tumour Biol; 2007;28(3):165-72
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  • [Title] Expression of EphA2 in human astrocytic tumors: correlation with pathologic grade, proliferation and apoptosis.
  • A high expression of EphA2 has been detected in many non-central nervous system tumors; however, the EphA2 expression in brain astrocytic tumors remains unclear.
  • In this study, we investigated the expression of EphA2 mRNA and protein in 90 cases of human astrocytic tumors by reverse transcription polymerase chain reaction and immunohistochemistry, respectively.
  • The proliferative index (PI) of tumor cells was evaluated by Ki-67 immunohistochemistry, and the apoptotic index (AI) was determined by TdT-mediated dUTP nick end labeling assay.
  • The correlation between EphA2 expression, pathologic grade, proliferation and apoptosis of astrocytic tumors was further analyzed.
  • Therefore, EphA2 may be a new biomarker for astrocytic tumors.
  • It may also affect the proliferation and apoptosis of tumor cells and be an attractive therapy target for astrocytic tumors.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Receptor, EphA2 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Cell Division. Child. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / genetics

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17519535.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, EphA2
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58. 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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59. Rousseau A, Nutt CL, Betensky RA, Iafrate AJ, Han M, Ligon KL, Rowitch DH, Louis DN: Expression of oligodendroglial and astrocytic lineage markers in diffuse gliomas: use of YKL-40, ApoE, ASCL1, and NKX2-2. J Neuropathol Exp Neurol; 2006 Dec;65(12):1149-56
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  • [Title] Expression of oligodendroglial and astrocytic lineage markers in diffuse gliomas: use of YKL-40, ApoE, ASCL1, and NKX2-2.
  • The phenotypic heterogeneity of astrocytic and oligodendroglial tumor cells complicates establishing accurate diagnostic criteria, and lineage-specific markers would facilitate diagnosis of glioma subtypes.
  • For the astrocytic lineage markers (GFAP, YKL-40, and ApoE), GFAP expression was significantly higher in the astrocytic component of oligoastrocytomas compared with the oligodendroglial part; similar patterns were detected for YKL-40 and ApoE, although the differences were not significant.
  • In addition to GFAP, therefore, YKL-40, ApoE, ASCL1, and NKX2-2 represent promising tumor cell markers to distinguish oligodendrogliomas from astrocytomas.
  • [MeSH-major] Astrocytes / pathology. Biomarkers, Tumor / metabolism. Brain Neoplasms / diagnosis. Cell Lineage / genetics. Glioma / diagnosis. Oligodendroglia / pathology
  • [MeSH-minor] Adipokines. Apolipoproteins E / analysis. Apolipoproteins E / metabolism. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / analysis. Basic Helix-Loop-Helix Transcription Factors / metabolism. Diagnosis, Differential. Glial Fibrillary Acidic Protein / analysis. Glial Fibrillary Acidic Protein / metabolism. Glycoproteins / analysis. Glycoproteins / metabolism. Homeodomain Proteins / analysis. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Lectins. Oligodendroglioma / diagnosis. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Predictive Value of Tests. Transcription Factors / analysis. Transcription Factors / metabolism

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  • (PMID = 17146289.001).
  • [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 / ASCL1 protein, human; 0 / Adipokines; 0 / Apolipoproteins E; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / CHI3L1 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Glycoproteins; 0 / Homeodomain Proteins; 0 / Lectins; 0 / Nkx-2.2 homedomain protein; 0 / Transcription Factors; 0 / apolipoprotein E1
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60. Erdamar S, Bagci P, Oz B, Dirican A: Correlation of endothelial nitric oxide synthase and vascular endothelial growth factor expression with malignancy in patients with astrocytic tumors. J BUON; 2006 Apr-Jun;11(2):213-6
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  • [Title] Correlation of endothelial nitric oxide synthase and vascular endothelial growth factor expression with malignancy in patients with astrocytic tumors.
  • PURPOSE: Many characteristics of malignant brain tumors (increased vascular permeability, vasodilatation, neovascularisation and free radical injury to the tumor and adjacent normal tissues) are believed to be mediated by nitric oxide (NO) synthetized by endothelial NO synthase (eNOS).
  • Our aim was to study immunohistochemically the coexpression of eNOS and VEGF in astrocytic tumors and to analyse their possible correlation with tumor grade, angiogenesis and proliferation index.
  • MATERIALS AND METHODS: Sections from 120 randomly selected patients with supratentorial astrocytic tumors [38 glioblastomas (GB), 22 anaplastic astrocytomas (AA) and 20 low-grade astrocytomas (LA)], also including oligodendrogliomas (n=20) and mixed oligoastrocytomas (n=20), were immunostained with monoclonal antibodies for eNOS and VEGF using the avidin-biotin method.
  • The proliferative potential was assessed as the MIB-1 staining index for tumor cells.
  • CONCLUSION: Overexpressions of eNOS and VEGF in astrocytic tumors were significantly correlated with histological grade, proliferative potential and malignant transformation.
  • The expression of VEGF in a necrotic and ischemic tumor such as GB is more intense and diffuse than low-grade astrocytomas.
  • These findings suggest that eNOS overexpression in tumor vasculature would be precipitated by transformation into an angiogenic phenotype in the process of neovascularisation in astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Nitric Oxide Synthase Type III / biosynthesis. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 17318973.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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61. Jiang L, Huang CG, Lu YC, Luo C, Hu GH, Liu HM, Chen JX, Han HX: Expression of ubiquitin-conjugating enzyme E2C/UbcH10 in astrocytic tumors. Brain Res; 2008 Mar 27;1201:161-6
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  • [Title] Expression of ubiquitin-conjugating enzyme E2C/UbcH10 in astrocytic tumors.
  • However, its role in astrocytic carcinogenesis is not well defined.
  • NM_007019) was detected in astrocytomas and normal brain tissues by RT-PCR and sequence analysis.
  • These data suggest that overexpression of UbcH10 may serve as one important molecular mechanism that underlies the astrocytic carcinogenesis.
  • [MeSH-major] Astrocytoma / enzymology. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Ubiquitin-Conjugating Enzymes / genetics. Ubiquitin-Conjugating Enzymes / metabolism
  • [MeSH-minor] Alternative Splicing / genetics. Astrocytes / enzymology. Astrocytes / pathology. Brain / enzymology. Brain / pathology. Brain / physiopathology. Gene Expression Regulation, Enzymologic / genetics. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Isoenzymes / genetics. Isoenzymes / metabolism. Ki-67 Antigen / metabolism. Prognosis. RNA, Messenger / analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Ubiquitin / metabolism. Up-Regulation / genetics

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  • (PMID = 18331723.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Ki-67 Antigen; 0 / RNA, Messenger; 0 / Ubiquitin; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
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62. Higano S, Yun X, Kumabe T, Watanabe M, Mugikura S, Umetsu A, Sato A, Yamada T, Takahashi S: Malignant astrocytic tumors: clinical importance of apparent diffusion coefficient in prediction of grade and prognosis. Radiology; 2006 Dec;241(3):839-46
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  • [Title] Malignant astrocytic tumors: clinical importance of apparent diffusion coefficient in prediction of grade and prognosis.
  • PURPOSE: To retrospectively assess the apparent diffusion coefficient (ADC) for prediction of malignancy and prognosis of malignant astrocytic tumors.
  • Findings from 37 consecutive patients (21 men, 16 women; mean age, 43 years) with pathologically proved malignant astrocytic tumors that included 22 glioblastomas (GBMs) and 15 anaplastic astrocytomas (AAs) were retrospectively evaluated.
  • The minimum ADC value of each tumor was preoperatively determined from several regions of interest defined in the tumor, preferably with avoidance of cystic or necrotic components, on ADC maps derived from isotropic diffusion-weighted images.
  • CONCLUSION: The minimum ADC of malignant astrocytomas can provide additional information about their clinical malignancy related to posttreatment prognosis.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Combined Modality Therapy. Female. Humans. Image Processing, Computer-Assisted. Ki-67 Antigen / analysis. Male. Predictive Value of Tests. Prognosis. ROC Curve. Retrospective Studies. Treatment Outcome

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  • [Copyright] (c) RSNA, 2006.
  • (PMID = 17032910.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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63. Lapointe M, Lanthier J, Moumdjian R, Régina A, Desrosiers RR: Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors. Brain Res Mol Brain Res; 2005 Apr 27;135(1-2):93-103
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  • [Title] Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors.
  • Here we investigated PIMT regulation in astrocytic tumors, which are the most common human brain tumors.
  • PIMT expression and enzyme activity were significantly decreased in all grades of human astrocytic tumors.
  • Furthermore, the reduced PIMT levels correlated closely with a decrease in the number of neuron cells in astrocytic tumors as assessed by measuring the neuron-specific enolase level.
  • Many proteins with abnormal aspartyl residues accumulated in brain tumors and some were specific to individual grades of astrocytic tumors.
  • Similar results were obtained, either by measuring the reduction in PIMT activity and expression or by measuring the formation of abnormal proteins, in an orthotopic rat brain tumor model implanted with invasive CNS-1 glioma cells.
  • The novelty of these findings was to provide the first evidence for a marked reduction of PIMT expression and activity during stage progression of astrocytic tumors in humans.
  • [MeSH-major] Brain / enzymology. Brain Neoplasms / enzymology. Gene Expression Regulation, Neoplastic / physiology. Glioma / enzymology. Protein D-Aspartate-L-Isoaspartate Methyltransferase / metabolism
  • [MeSH-minor] Animals. Blotting, Northern. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry / methods. Male. Methylation. Neoplasm Transplantation / methods. Phosphopyruvate Hydratase / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred Lew. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 15857672.001).
  • [ISSN] 0169-328X
  • [Journal-full-title] Brain research. Molecular brain research
  • [ISO-abbreviation] Brain Res. Mol. Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / RNA, Messenger; EC 2.1.1.77 / Protein D-Aspartate-L-Isoaspartate Methyltransferase; EC 4.2.1.11 / Phosphopyruvate Hydratase
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64. Haapasalo JA, Nordfors KM, Hilvo M, Rantala IJ, Soini Y, Parkkila AK, Pastoreková S, Pastorek J, Parkkila SM, Haapasalo HK: Expression of carbonic anhydrase IX in astrocytic tumors predicts poor prognosis. Clin Cancer Res; 2006 Jan 15;12(2):473-7
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  • [Title] Expression of carbonic anhydrase IX in astrocytic tumors predicts poor prognosis.
  • Normal human brain tissue shows only slight or no expression of CA IX.
  • The CA IX immunoreactivity showed strong association with tumor malignancy grades (P < 0.0001).
  • Our results suggest that CA IX is a useful biomarker for predicting poor prognosis of astrocytic tumors.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Astrocytoma / enzymology. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Carbonic Anhydrases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Apoptosis. Cell Proliferation. Female. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Recurrence, Local / enzymology. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / pathology. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / metabolism. Survival Rate. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16428489.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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65. Guo D, Nilsson J, Haapasalo H, Raheem O, Bergenheim T, Hedman H, Henriksson R: Perinuclear leucine-rich repeats and immunoglobulin-like domain proteins (LRIG1-3) as prognostic indicators in astrocytic tumors. Acta Neuropathol; 2006 Mar;111(3):238-46
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  • [Title] Perinuclear leucine-rich repeats and immunoglobulin-like domain proteins (LRIG1-3) as prognostic indicators in astrocytic tumors.
  • We have previously characterized three human leucine-rich repeats and immunoglobulin-like domains (LRIG) genes and proteins, named LRIG1-3 and proposed that they may act as suppressors of tumor growth.
  • In this study, we evaluated the mRNA expression level of LRIG1-3 in human glioma cell lines and control-matched glioma tissues, characterized the sub-cellular localization of an LRIG3-GFP fusion protein, and analyzed the relationship between sub-cellular localization of LRIG1-3 and clinical parameters in 404 astrocytic tumors by immunohistochemistry.
  • Perinuclear staining of LRIG3 was associated with a lower proliferation index and was in addition to tumor grade, an independent prognostic factor.
  • These results indicate that expression and sub-cellular localization of LRIG1-3 might be of importance in the pathogenesis and prognosis of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Cell Proliferation. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Infant, Newborn. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Survival Rate


66. Ohgaki H, Kleihues P: Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas. J Neuropathol Exp Neurol; 2005 Jun;64(6):479-89
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  • [Title] Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.
  • This review summarizes data on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland (approximately 1.16 million inhabitants).
  • While survival rates for pilocytic astrocytomas were excellent (96% at 10 years), the prognosis of diffusely infiltrating gliomas was poorer, with median survival times (MST) of 5.6 years for low-grade astrocytoma WHO grade II, 1.6 years for anaplastic astrocytoma grade III, and 0.4 years for glioblastoma.
  • [MeSH-major] Astrocytoma. Brain Neoplasms. Loss of Heterozygosity. Oligodendroglioma. Tumor Suppressor Protein p53 / genetics


67. Facoetti A, Nano R, Zelini P, Morbini P, Benericetti E, Ceroni M, Campoli M, Ferrone S: Human leukocyte antigen and antigen processing machinery component defects in astrocytic tumors. Clin Cancer Res; 2005 Dec 1;11(23):8304-11
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  • [Title] Human leukocyte antigen and antigen processing machinery component defects in astrocytic tumors.
  • PURPOSE: To determine the frequency of abnormalities in human leukocyte antigen (HLA) and antigen processing machinery (APM) component expression in malignant brain tumors.
  • This information may contribute to our understanding of the immune escape mechanisms used by malignant brain tumors because HLA antigens mediate interactions of tumor cells with the host's immune system.
  • EXPERIMENTAL DESIGN: Eighty-eight surgically removed malignant astrocytic tumors, classified according to the WHO criteria, were stained in immunoperoxidase reactions with monoclonal antibody recognizing monomorphic, locus-specific, and allospecific determinants of HLA class I antigens, beta2-microglobulin, APM components (LMP2, LMP7, TAP1, TAP2, calnexin, calreticulin, and tapasin), and HLA class II antigens.
  • RESULTS: HLA class I antigens were lost in approximately 50% of the 47 glioblastoma multiforme (GBM) lesions and in approximately 20% of the 18 grade 2 astrocytoma lesions stained.
  • Selective HLA-A2 antigen loss was observed in approximately 80% of the 24 GBM lesions and in approximately 50% of the 12 grade 2 astrocytoma lesions stained.
  • HLA class I antigen loss was significantly (P < 0.025) correlated with tumor grade.
  • Among the APM components investigated, tapasin expression was down-regulated in approximately 20% of the GBM lesions analyzed; it was associated, although not significantly, with HLA class I antigen down-regulation and tumor grade.
  • CONCLUSION: The presence of HLA antigen defects in malignant brain tumors may provide an explanation for the relatively poor clinical response rates observed in the majority of the T cell-based immunotherapy clinical trials conducted to date in patients with malignant brain tumors.
  • [MeSH-major] Antiporters / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. HLA-A2 Antigen / metabolism. Histocompatibility Antigens Class I / metabolism. Immunoglobulins / metabolism
  • [MeSH-minor] ATP-Binding Cassette Transporters / metabolism. Antibodies, Monoclonal. Antigen Presentation. Biomarkers, Tumor / metabolism. Calnexin / metabolism. Calreticulin / metabolism. Cysteine Endopeptidases / metabolism. Down-Regulation. Humans. Membrane Transport Proteins. Multienzyme Complexes / metabolism. Proteasome Endopeptidase Complex. beta 2-Microglobulin / metabolism

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  • (PMID = 16322289.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056; United States / NCI NIH HHS / CA / R01 CA67108; United States / NCI NIH HHS / CA / T32 CA85183
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antiporters; 0 / Biomarkers, Tumor; 0 / Calreticulin; 0 / HLA-A2 Antigen; 0 / Histocompatibility Antigens Class I; 0 / Immunoglobulins; 0 / Membrane Transport Proteins; 0 / Multienzyme Complexes; 0 / TAP1 protein, human; 0 / beta 2-Microglobulin; 0 / tapasin; 139873-08-8 / Calnexin; 144416-78-4 / LMP-2 protein; 145892-13-3 / TAP2 protein, human; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.25.1 / LMP7 protein; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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68. Shrestha P, Saito T, Hama S, Arifin MT, Kajiwara Y, Yamasaki F, Hidaka T, Sugiyama K, Kurisu K: Geminin: a good prognostic factor in high-grade astrocytic brain tumors. Cancer; 2007 Mar 1;109(5):949-56
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  • [Title] Geminin: a good prognostic factor in high-grade astrocytic brain tumors.
  • For this study, the authors investigated geminin expression in high-grade astrocytic tumors, including anaplastic astrocytoma (AA) and glioblastoma multiforme (GBM), with a view to predicting clinical outcomes on this basis in patients with these malignant brain tumors.
  • METHODS: Immunohistochemistry was used to detect geminin expression in 51 patients with high-grade astrocytic tumors (19 AA and 32 GBM).
  • The relation of geminin expression to clinical outcome in these malignant brain tumors was analyzed by using the Kaplan-Meier method and a Cox proportional hazards regression model.
  • Similarly, the Cox regression analysis showed that geminin expression has a significant correlation with survival in patients with high-grade astrocytoma (P = .0278), especially in an early stage.
  • CONCLUSIONS: Although it is an inhibitor of DNA proliferation and, thus, is a cell cycle inhibitor, geminin expression was found in all malignant astrocytic tumors.
  • The geminin LI was a significant predictive factor of outcomes in patients with high-grade astrocytoma, with higher expression indicating a good prognosis.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cell Cycle Proteins / metabolism

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  • (PMID = 17262828.001).
  • [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 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / GMNN protein, human; 0 / Geminin
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69. 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.
  • 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.
  • 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).
  • [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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70. Peria FM, Neder L, Marie SK, Rosemberg S, Oba-Shinjo SM, Colli BO, Gabbai AA, Malheiros SM, Zago MA, Panepucci RA, Moreira-Filho CA, Okamoto OK, Carlotti CG Jr: Pleiotrophin expression in astrocytic and oligodendroglial tumors and it's correlation with histological diagnosis, microvascular density, cellular proliferation and overall survival. J Neurooncol; 2007 Sep;84(3):255-61
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  • [Title] Pleiotrophin expression in astrocytic and oligodendroglial tumors and it's correlation with histological diagnosis, microvascular density, cellular proliferation and overall survival.
  • BACKGROUND: Pleiotrophin (PTN) is a secreted cytokine with several properties related with tumor development, including differentiation, angiogenesis, invasion, apoptosis and metastasis.
  • There is evidence that PTN has also a relevant role in primary brain neoplasms and its inactivation could be important to treatment response.
  • Astrocytic and oligodendroglial tumors are the most frequent primary brain neoplasms.
  • Astrocytic tumors are classified as pilocytic astrocytoma (PA), diffuse astrocytoma (DA), anaplastic astrocytoma (AA) and glioblastoma (GBM).
  • The aim of the present study was to compare PTN expression, in astrocytomas and oligodendrogliomas and its association with the histological diagnosis, microvascular density, proliferate potential and clinical outcome.
  • The histological diagnosis in accordance with WHO classification was: 13PA, 18DA, 8AA, 15GBM, 16O and 8AO.
  • [MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Brain Neoplasms / pathology. Carrier Proteins / biosynthesis. Cytokines / biosynthesis. Oligodendroglioma / pathology

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  • (PMID = 17443289.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Cytokines; 134034-50-7 / pleiotrophin
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71. Landriscina M, Schinzari G, Di Leonardo G, Quirino M, Cassano A, D'Argento E, Lauriola L, Scerrati M, Prudovsky I, Barone C: S100A13, a new marker of angiogenesis in human astrocytic gliomas. J Neurooncol; 2006 Dec;80(3):251-9
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  • [Title] S100A13, a new marker of angiogenesis in human astrocytic gliomas.
  • We investigated the expression of S100A13 in human astrocytic gliomas in relation to tumour grading and vascularization.
  • A series of 26 astrocytic gliomas was studied to evaluate microvessel density and to assess FGF1, S100A13 and VEGF-A expression.
  • Moreover, both S100A13 and VEGF-A expression significantly correlated with microvessel density and tumour grading.
  • These data suggest that the up-regulation of S100A13 and VEGF-A expression correlates with the activation of angiogenesis in high-grade human astrocytic gliomas.
  • [MeSH-major] Astrocytoma / blood supply. Biomarkers, Tumor / metabolism. Brain Neoplasms / blood supply. Neovascularization, Pathologic / metabolism. S100 Proteins / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16773219.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL32348; United States / NHLBI NIH HHS / HL / HL35627; United States / NCRR NIH HHS / RR / RR1555
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / S100 Proteins; 0 / S100A13 protein, human; 0 / Vascular Endothelial Growth Factor A; 62031-54-3 / Fibroblast Growth Factors
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72. Gavillet M, Allaman I, Magistretti PJ: Modulation of astrocytic metabolic phenotype by proinflammatory cytokines. Glia; 2008 Jul;56(9):975-89
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  • [Title] Modulation of astrocytic metabolic phenotype by proinflammatory cytokines.
  • In previous experiments, we showed that long-term treatment with interleukin 1alpha (IL-1alpha) or tumor necrosis factor-alpha (TNFalpha) alone increases glucose utilization in primary culture of mouse astrocytes.

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  • (PMID = 18383346.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Glutamates; 0 / Inflammation Mediators; IY9XDZ35W2 / Glucose
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73. Lin ZX, Yang LJ, Huang Q, Fu J: Activated vascular endothelia regulate invasion of glioma cells through expression of fibronectin. Chin Med J (Engl); 2010 Jul;123(13):1754-61
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  • BACKGROUND: Previous researches have indicated that glioma invasion may occur within a tumor-host microecology, and that fibronectin may be involved in glioma invasion as an important component of the extracellular matrix.
  • However, how the interaction between tumor cells and vascular endothelial cells affects glioma invasion is poorly understood.
  • The aim of this study was to investigate the effects of the interaction between tumor cells and vascular endothelial cells on glioma invasion, and the relationship of this interaction to fibronectin.
  • METHODS: The localization of fibronectin in different brain astrocytoma tissues was determined by immunohistochemistry.
  • Additionally, the influence of the interaction between tumor cells and vascular endothelial cells on glioma cell invasion was determined by an in vitro rapid invasion test.
  • RESULTS: In brain astrocytoma tissues, fibronectin was present on the endothelial cells, in the extracellular matrix.
  • [MeSH-minor] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Cell Movement / physiology. Cells, Cultured. Coculture Techniques. Enzyme-Linked Immunosorbent Assay. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20819642.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Fibronectins
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74. Gu X, Jones L, Lowery-Norberg M, Fowler M: Expression of eukaryotic initiation factor 4E in astrocytic tumors. Appl Immunohistochem Mol Morphol; 2005 Jun;13(2):178-83
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  • [Title] Expression of eukaryotic initiation factor 4E in astrocytic tumors.
  • In this immunohistochemical study, eIF4E protein expression was investigated in human brain tissue from patients without central nervous system diseases and brain biopsy tissues from patients with anaplastic astrocytoma and glioblastoma multiforme.
  • In anaplastic astrocytoma and glioblastoma multiforme, there was diffuse uniform expression of eIF4E immunoreactivity in malignant astrocytes.
  • This study provides evidence that eIF4E is upregulated in high-grade astrocytic tumors.
  • As in other malignancies, a high level of eIF4E may play an important role in the neoplastic transformation, angiogenesis, and tumor growth in astrocytic tumors.
  • Because eIF4E is crucial in regulation of tumor growth, eIF4E could be a potential target for inhibitors as an adjuvant therapy for brain tumors.

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  • (PMID = 15894932.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Eukaryotic Initiation Factor-4E
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75. Axelsen JB, Lotem J, Sachs L, Domany E: Genes overexpressed in different human solid cancers exhibit different tissue-specific expression profiles. Proc Natl Acad Sci U S A; 2007 Aug 7;104(32):13122-7
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  • The cancers analyzed include brain (astrocytoma and glioblastoma), breast, colon, endometrium, kidney, liver, lung, ovary, prostate, skin, and thyroid cancers.
  • Different types of cancers, including different brain cancers arising from the same lineage, showed differences in the tissue-selective genes they overexpressed.
  • Melanomas overexpressed the highest number of brain-selective genes and this may contribute to melanoma metastasis to the brain.
  • Of all of the genes with tissue-selective expression, those selectively expressed in testis showed the highest frequency of genes that are overexpressed in at least two types of cancer.
  • Cancers aberrantly expressing such genes may acquire phenotypic alterations that contribute to cancer cell viability, growth, and metastasis.

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  • (PMID = 17664417.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1941809
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76. Lu Z, Cao Y, Wang Y, Zhang Q, Zhang X, Wang S, Li Y, Xie H, Jiao B, Zhang J: Polymorphisms in the matrix metalloproteinase-1, 3, and 9 promoters and susceptibility to adult astrocytoma in northern China. J Neurooncol; 2007 Oct;85(1):65-73
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  • [Title] Polymorphisms in the matrix metalloproteinase-1, 3, and 9 promoters and susceptibility to adult astrocytoma in northern China.
  • The single nucleotide polymorphisms (SNPs) in the promoter region of matrix metalloproteinase (MMP) genes may influence tumor occurrence and progression via modifying mRNA transcription and protein expression.
  • The study aims to explore the association of the SNPs in MMP-1, 3 and MMP-9 promoters with susceptibility to adult brain astrocytoma in northern China.
  • Genotyping for the MMP-1 -1607 2G/1G, MMP-3 -1171 5A/6A, and MMP-9 -1562 C/T SNPs were performed by PCR-RFLP methods among 236 adult astrocytoma patients and 366 healthy controls.
  • The results showed that the overall distribution of the MMP-1 allelotype and genotype among astrocytoma patients and healthy controls was significantly different (P = 0.002 and P < 0.001, respectively).
  • Compared with the 2G/2G genotype, the 1G/1G genotype significantly decreased the risk of astrocytoma development (adjusted OR = 0.58, 95% CI = 0.42-0.79).
  • The similar results were obtained when stratified by gender and age at tumor diagnosis (< or =45 or >45 years).
  • The association between MMP-3 -1171 5A/6A or MMP-9 -1562 C/T SNPs and susceptibility to astrocytoma was not observed in this study.
  • However, MMP-1 1G-MMP-3 6A haplotype significantly reduced the risk of astrocytoma development when using MMP-1 2G-MMP-3 6A haplotype as a reference (OR = 0.45, 95% CI = 0.29-0.67).
  • The present study suggested that, the MMP-1 -1607 1G/1G genotype and MMP-1 1G-MMP-3 6A haplotype may play protective role in the development of adult astrocytoma in northern Chinese, whereas the MMP-3 -1171 5A/6A and MMP-9 -1562 C/T polymorphisms may not be independent factors to influence susceptibility to adult astrocytoma in this population.
  • [MeSH-major] Astrocytoma / epidemiology. Astrocytoma / genetics. Brain Neoplasms / epidemiology. Brain Neoplasms / genetics. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 3 / genetics. Matrix Metalloproteinase 9 / genetics. Polymorphism, Genetic / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adult. Case-Control Studies. China / epidemiology. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / genetics. Genetic Linkage / genetics. Genotype. Haplotypes. Humans. Polymorphism, Single Nucleotide. Risk

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  • (PMID = 17502998.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
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77. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
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  • [Chemical-registry-number] EC 1.11.1.15 / Peroxiredoxins
  • [Other-IDs] NLM/ PMC2858108
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78. Dimitriadi M, Poulogiannis G, Liu L, Bäcklund LM, Pearson DM, Ichimura K, Collins VP: p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumours. Br J Cancer; 2008 Oct 07;99(7):1144-52
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  • [Title] p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumours.
  • We used RT-PCR to study P1- and P2-MDM2 transcript expression in astrocytic tumours, xenografts and cell lines with known MDM2, TP53 and p14(ARF) gene status.
  • Examination of SNP309 in glioblastoma patients showed a borderline association with survival but no apparent correlation with age at diagnosis nor with TP53 and p14(ARF) status of their tumours.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins c-mdm2 / genetics. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 18781178.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [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] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2567066
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79. Faria MH, Khayat AS, Burbano RR, Rabenhorst SH: c -MYC amplification and expression in astrocytic tumors. Acta Neuropathol; 2008 Jul;116(1):87-95
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  • [Title] c -MYC amplification and expression in astrocytic tumors.
  • The aim of this study was to evaluate the nuclear and cytoplasmic expression of c-MYC protein in human astrocytic tumors of different histopathological grades and to determine whether its expression correlates with c-MYC gene amplification.
  • An immunohistochemical study of c-MYC protein was performed in 140 paraffin-embedded astrocytic tumors of different grades.
  • The distribution of the positive cases according to the tumor grade increased in both nuclear and cytoplasmic staining with malignancy.
  • The median nuclear LI also increased with tumor grade, with highest c-MYC nuclear expression in grade III.
  • These results indicate that c-MYC expression in astrocytic tumors is strongly associated with increased c-MYC gene copy number and suggest that c-MYC plays a role in the early tumorigenesis of astrocytomas.
  • [MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Genes, myc

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  • (PMID = 18369647.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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80. Plotkin M, Amthauer H, Eisenacher J, Wurm R, Michel R, Wust P, Stockhammer F, Röttgen R, Gutberlet M, Ruf J, Felix R: Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours. Neuroradiology; 2005 Jan;47(1):18-26
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  • [Title] Value of 123I-IMT SPECT for diagnosis of recurrent non-astrocytic intracranial tumours.
  • The value of single-photon emission tomography (SPECT) using iodine-123-alpha-methyl-tyrosine (IMT) for the diagnosis of recurrent or residual gliomas is well established.
  • In the current study we investigated whether IMT-SPECT could also be useful in the follow-up of brain metastases and other intracranial tumours of non-astrocytic origin.
  • The study included 22 patients with suspected recurrent intracranial tumours of non-astrocytic origin (12 brain metastases, one supratentorial primitive neuroendocrine tumour (PNET), one rhabdoid tumour, two clivus chordomas, three ependymomas, two pituitary tumours, one anaplastic meningioma) who had previously been treated by surgery and/or radio/chemotherapy.
  • We concluded that the IMT-SPECT is a promising complementary imaging tool for the detection of recurrences of non-astrocytic intracranial tumours and their distinguishing from treatment-induced changes.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Iodine Radioisotopes. Methyltyrosines. Neoplasm Recurrence, Local / diagnostic imaging. Radiopharmaceuticals. Tomography, Emission-Computed, Single-Photon / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Chordoma / diagnostic imaging. Ependymoma / diagnostic imaging. False Negative Reactions. False Positive Reactions. Female. Follow-Up Studies. Glioma / diagnostic imaging. Humans. Magnetic Resonance Imaging. Male. Meningioma / diagnostic imaging. Middle Aged. Neuroendocrine Tumors / diagnostic imaging. Pituitary Neoplasms / diagnostic imaging. Retrospective Studies. Rhabdoid Tumor / diagnostic imaging. Sensitivity and Specificity. Supratentorial Neoplasms / diagnostic imaging

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  • (PMID = 15630586.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Methyltyrosines; 0 / Radiopharmaceuticals; A77N8J5H5T / 3-iodo-alpha-methyltyrosine
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81. Gong Y, Zhang Z: CellFrame: a data structure for abstraction of cell biology experiments and construction of perturbation networks. Ann N Y Acad Sci; 2007 Dec;1115:249-66
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  • We have implemented an initial version of CellFrame, which contains data collected from reported experiments on human brain astrocytoma and colorectal cancer cell lines (http://cellframe.bioknowledge.org).

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  • (PMID = 17925354.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteome
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82. Yao Y, Kubota T, Takeuchi H, Sato K: Prognostic significance of microvessel density determined by an anti-CD105/endoglin monoclonal antibody in astrocytic tumors: comparison with an anti-CD31 monoclonal antibody. Neuropathology; 2005 Sep;25(3):201-6
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  • [Title] Prognostic significance of microvessel density determined by an anti-CD105/endoglin monoclonal antibody in astrocytic tumors: comparison with an anti-CD31 monoclonal antibody.
  • There are conflicting reports as to whether the degree of angiogenesis as measured by microvessel density (MVD) has a prognostic value in astrocytic tumors.
  • To clarify the validity of anti-CD105 antibody in the evaluation of angiogenesis, we assessed MVD using an anti-CD105 monoclonal antibody (mAb) (CD105-MVD) and an anti-CD31 mAb (CD31-MVD) in a series of 50 astrocytic tumors, and correlated MVD with expression of the key angiogenic factor vascular endothelial growth factor (VEGF) and prognosis.
  • The mean CD31-MVD and CD105-MVD was 36.7 and 24.8 for low-grade astrocytoma (LGA), 48.0 and 42.7 for anaplastic astrocytoma, 55.3 and 51.9 for glioblastoma multiforme (GBM), respectively.
  • Whereas the MST of patients with higher CD31-MVD tumors seemed to be shorter than that of lower CD31-MVD patients within each tumor grade, the differences were not statistically significant.
  • These findings suggest that anti-CD105 mAb may be a better marker than anti-CD31 mAb in evaluation of angiogenesis and prediction of prognosis in astrocytic tumors.
  • [MeSH-major] Antibodies, Monoclonal. Astrocytoma / blood supply. Biomarkers, Tumor / analysis. Brain Neoplasms / mortality. Neovascularization, Pathologic / metabolism

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  • (PMID = 16193836.001).
  • [ISSN] 0919-6544
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD31; 0 / Biomarkers, Tumor; 0 / ENG protein, human; 0 / Receptors, Cell Surface; 0 / Vascular Cell Adhesion Molecule-1; 0 / Vascular Endothelial Growth Factor A
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83. Jha P, Agarwal S, Pathak P, Srivastava A, Suri V, Sharma MC, Chosdol K, Srivastava T, Gupta D, Gupta A, Suri A, Sarkar C: Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India. Cancer Genet Cytogenet; 2010 Apr 15;198(2):126-34
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  • [Title] Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India.
  • There are few reports of loss of heterozygosity (LOH) of 1p and 19q in astrocytic tumors, especially glioblastoma multiforme (GBM).
  • Thus, 1p and 19q LOH can occur in astrocytic tumors, most commonly in secondary GBMs without morphological correlation with an oligodendroglial histology.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Gene Amplification. Genes, erbB-1. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20362227.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] 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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84. 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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85. 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).
  • Using real-time quantitative reverse transcription-polymerase chain reaction, we quantified the expression of four genes that were putative prognostic markers (CDK4, IGFBP2, MMP2, and RPS9) in a set of 43 AAs, 41 GBMs, and seven adjacent normal brain tissues.
  • 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.
  • [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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86. Donato G, Iofrida G, Lavano A, Volpentesta G, Signorelli F, Pallante PL, Berlingieri MT, Pierantoni MG, Palmieri D, Conforti F, Maltese L, Tucci L, Amorosi A, Fusco A: Analysis of UbcH10 expression represents a useful tool for the diagnosis and therapy of astrocytic tumors. Clin Neuropathol; 2008 Jul-Aug;27(4):219-23
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  • [Title] Analysis of UbcH10 expression represents a useful tool for the diagnosis and therapy of astrocytic tumors.
  • Therefore, to look for possible tools to be used as diagnostic markers in astrocytic neoplasias, we investigated UbcH10 expression in normal brain, gliosis and low-grade and high-grade astrocytic tumors by immunohistochemistry.
  • UbcH10 expression was observed in low-grade astrocytoma and in glioblastoma.
  • Our data indicate a clear correlation between UbcH10 expression and the histological grade of the astrocytic tumors.
  • Moreover, the analysis of UbcH10 expression allows the differentiation between gliotic and malignant tissues.
  • Finally, since proteasome inhibitors have recently been considered as possible drugs in the chemotherapy of various tumors, our results would suggest new perspectives for the treatment of brain malignancies based on the suppression of the UbcH10 function.
  • [MeSH-major] Astrocytoma / diagnosis. Astrocytoma / metabolism. Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Ubiquitin-Conjugating Enzymes / biosynthesis

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  • (PMID = 18666437.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
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87. Murakami R, Hirai T, Sugahara T, Fukuoka H, Toya R, Nishimura S, Kitajima M, Okuda T, Nakamura H, Oya N, Kuratsu J, Yamashita Y: Grading astrocytic tumors by using apparent diffusion coefficient parameters: superiority of a one- versus two-parameter pilot method. Radiology; 2009 Jun;251(3):838-45
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  • [Title] Grading astrocytic tumors by using apparent diffusion coefficient parameters: superiority of a one- versus two-parameter pilot method.
  • PURPOSE: To assess the utility of both minimum apparent diffusion coefficients (ADCs) and ADC difference values for grading astrocytic tumors at magnetic resonance imaging.
  • Fifty patients (23 male patients, 27 female patients; median age, 53 years) with newly diagnosed astrocytic tumors were evaluated.
  • Two observers blinded to clinical information independently measured the ADCs by manually placing three to five regions of interest (40-60 mm(2)) within the solid tumor either with or without contrast material-enhanced components and calculated the average ADC.
  • These ADC values were used as the parameters for tumor grading and were compared by using the Kruskal-Wallis test and receiver operating characteristic (ROC) curve analysis.
  • RESULTS: According to ROC analyses for distinguishing tumor grade, minimum ADCs showed the largest areas under the ROC curve.
  • CONCLUSION: Using a combination of minimum ADCs and ADC difference values (the two-parameter method) facilitates the accurate grading of astrocytic tumors.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Contrast Media. Female. Gadolinium DTPA. Humans. Image Interpretation, Computer-Assisted. Male. Middle Aged. Neoplasm Staging. Pilot Projects. ROC Curve. Retrospective Studies

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  • (PMID = 19318585.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; K2I13DR72L / Gadolinium DTPA
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88. Mishima K, Kato Y, Kaneko MK, Nishikawa R, Hirose T, Matsutani M: Increased expression of podoplanin in malignant astrocytic tumors as a novel molecular marker of malignant progression. Acta Neuropathol; 2006 May;111(5):483-8
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  • [Title] Increased expression of podoplanin in malignant astrocytic tumors as a novel molecular marker of malignant progression.
  • Podoplanin is putatively involved in cancer cell migration, invasion, metastasis, and malignant progression and may be involved in platelet aggregation.
  • However, little information exists about its role in CNS astrocytic tumors.
  • In this study, 188 astrocytic tumors (30 diffuse astrocytomas, 43 anaplastic astrocytomas, and 115 glioblastomas) were investigated using immunohistochemistry with an anti-podoplanin antibody, YM-1.
  • In 11 of 43 anaplastic astrocytomas (25.6%) and in 54 of 115 glioblastomas (47.0%), podoplanin was expressed on the surface of anaplastic astrocytoma cells and glioblastoma cells, especially around necrotic areas and proliferating endothelial cells.
  • However, the surrounding brain parenchyma was not stained by YM-1.
  • On the other hand, podoplanin expression was not observed in diffuse astrocytoma (0/30: 0%).
  • Furthermore, we investigated the expression of podoplanin using quantitative real-time PCR and Western blot analysis in 54 frozen astrocytic tumors (6 diffuse astrocytomas, 14 anaplastic astrocytomas, and 34 glioblastomas).
  • These data suggest that podoplanin expression might be associated with malignancy of astrocytic tumors.
  • [MeSH-major] Astrocytoma / metabolism. Central Nervous System Neoplasms / metabolism. Glioblastoma / metabolism. Membrane Glycoproteins / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Blotting, Western. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16596424.001).
  • [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 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / PDPN protein, human; 0 / RNA, Messenger
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89. Santel T, Pflug G, Hemdan NY, Schäfer A, Hollenbach M, Buchold M, Hintersdorf A, Lindner I, Otto A, Bigl M, Oerlecke I, Hutschenreuther A, Sack U, Huse K, Groth M, Birkemeyer C, Schellenberger W, Gebhardt R, Platzer M, Weiss T, Vijayalakshmi MA, Krüger M, Birkenmeier G: Curcumin inhibits glyoxalase 1: a possible link to its anti-inflammatory and anti-tumor activity. PLoS One; 2008;3(10):e3508
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  • [Title] Curcumin inhibits glyoxalase 1: a possible link to its anti-inflammatory and anti-tumor activity.
  • METHODOLOGY/PRINCIPAL FINDINGS: Cultures of whole blood cells and tumor cell lines (PC-3, JIM-1, MDA-MD 231 and 1321N1) were set up to investigate the effect of selected polyphenols, including curcumin, on the LPS-induced cytokine production (cytometric bead-based array), cell proliferation (WST-1 assay), cytosolic Glo1 and Glo2 enzymatic activity, apoptosis/necrosis (annexin V-FITC/propidium iodide staining; flow cytometric analysis) as well as GSH and ATP content.
  • Moreover, whereas curcumin was found to hamper the growth of breast cancer (JIMT-1, MDA-MB-231), prostate cancer PC-3 and brain astrocytoma 1321N1 cells, no effect on growth or vitality of human primary hepatocytes was elucidated.
  • Curcumin decreased D-lactate release by tumor cells, another clue for inhibition of intracellular Glo1.
  • This may account for curcumin's potency as an anti-inflammatory and anti-tumor agent.

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  • [ErratumIn] PLoS One. 2011;6(7). doi:10.1371/annotation/0eb2b9f3-1006-4dcd-ad61-367310a2686a. Hutschenreuter, Antje [corrected to Hutschenreuther, Antje]
  • (PMID = 18946510.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Phenols; 0 / Polyphenols; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 4.4.1.5 / Lactoylglutathione Lyase; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2567432
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90. Das A, Banik NL, Ray SK: Retinoids induced astrocytic differentiation with down regulation of telomerase activity and enhanced sensitivity to taxol for apoptosis in human glioblastoma T98G and U87MG cells. J Neurooncol; 2008 Mar;87(1):9-22
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  • [Title] Retinoids induced astrocytic differentiation with down regulation of telomerase activity and enhanced sensitivity to taxol for apoptosis in human glioblastoma T98G and U87MG cells.
  • Treatment of cells with 1 microM all-trans retinoic acid (ATRA) or 1 microM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation, overexpression of glial fibrillary acidic protein (GFAP), and also down regulated telomerase expression and activity, thereby increased sensitivity to TXL for apoptosis.
  • Taken together, our results suggested that retinoid (ATRA or 13-CRA) induced astrocytic differentiation with down regulation of telomerase activity to increase sensitivity to TXL to enhance apoptosis in glioblastoma cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Astrocytes / drug effects. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Telomerase / drug effects
  • [MeSH-minor] Blotting, Western. Cell Differentiation. Cell Line, Tumor. Down-Regulation. Humans. Isotretinoin / administration & dosage. Paclitaxel / administration & dosage. RNA, Messenger / analysis. Reactive Oxygen Species. Retinoids / administration & dosage. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Tretinoin / administration & dosage


91. Tsunoda K, Kitange G, Anda T, Shabani HK, Kaminogo M, Shibata S, Nagata I: Expression of the constitutively activated RelA/NF-kappaB in human astrocytic tumors and the in vitro implication in the regulation of urokinase-type plasminogen activator, migration, and invasion. Brain Tumor Pathol; 2005;22(2):79-87
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  • [Title] Expression of the constitutively activated RelA/NF-kappaB in human astrocytic tumors and the in vitro implication in the regulation of urokinase-type plasminogen activator, migration, and invasion.
  • Although malignant gliomas are highly invasive tumors, a characteristic that contributes to the commonly observed therapeutic failures and local disease recurrences, the molecular events that regulate invasion in these tumors remain poorly understood.
  • Because the transcription factor RelA/NF-kappaB has been shown to regulate invasion during several cellular processes, we have examined immunohistochemically expression of the constitutively activated RelA/NF-kappaB in tissues obtained from 49 astrocytic tumors [8 diffuse astrocytomas, 9 anaplastic astrocytomas (AAs) and 32 glioblastomas (GBMs)].
  • This expression was significantly correlated with the malignant potential in astrocytic tumors (P < 0.001).
  • Thus, the expression of constitutively activated RelA/NF-kappaB is associated with malignancy potential in astrocytic tumors and may play a critical role in the regulation of u-PA expression and invasiveness in gliomas.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. NF-kappa B / biosynthesis. Neoplasm Proteins / biosynthesis. Transcription Factor RelA / biosynthesis. Urokinase-Type Plasminogen Activator / biosynthesis
  • [MeSH-minor] Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Movement / drug effects. Cell Nucleus / metabolism. Culture Media, Conditioned. Curcumin / pharmacology. Enzyme Induction / genetics. Humans. Neoplasm Invasiveness. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Retrospective Studies. Single-Blind Method. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 18095109.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Oligonucleotides, Antisense; 0 / RELA protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factor RelA; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; IT942ZTH98 / Curcumin; NI40JAQ945 / Tetradecanoylphorbol Acetate
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92. Lefranc F, Rynkowski M, DeWitte O, Kiss R: Present and potential future adjuvant issues in high-grade astrocytic glioma treatment. Adv Tech Stand Neurosurg; 2009;34:3-35
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  • [Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.
  • Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.
  • Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.
  • Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.
  • Components of these pathways are mutated or aberrantly expressed in human cancer, notably glioblastomas.
  • Monoclonal antibodies and low molecular-weight kinase inhibitors of these pathways are the most common classes of agents in targeted cancer treatment.
  • Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.
  • Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.
  • Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells.
  • The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.
  • [MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy


93. Wilms H, Sievers J, Rickert U, Rostami-Yazdi M, Mrowietz U, Lucius R: Dimethylfumarate inhibits microglial and astrocytic inflammation by suppressing the synthesis of nitric oxide, IL-1beta, TNF-alpha and IL-6 in an in-vitro model of brain inflammation. J Neuroinflammation; 2010;7:30
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  • [Title] Dimethylfumarate inhibits microglial and astrocytic inflammation by suppressing the synthesis of nitric oxide, IL-1beta, TNF-alpha and IL-6 in an in-vitro model of brain inflammation.
  • BACKGROUND: Brain inflammation plays a central role in multiple sclerosis (MS).
  • The purpose of this study was to use an established in vitro model of brain inflammation to determine if DMF modulates the release of neurotoxic molecules from microglia and astrocytes, thus inhibiting glial inflammation.
  • METHODS: Primary microglial and astrocytic cell cultures were prepared from cerebral cortices of neonatal rats.
  • After 6 hours of treatment RT-PCR was used to determine transcription levels of iNOS, IL-1beta, IL-6 and TNF-alpha mRNA in microglial and astrocytic cell cultures initially treated with DMF, followed after 30 min by LPS treatment.
  • CONCLUSIONS: Collectively, these results suggest that the neuroprotective effects of DMF may be in part functionally attributable to the compound's ability to inhibit expression of multiple neuroinflammatory mediators in brain of MS patients.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Astrocytes / drug effects. Encephalomyelitis, Autoimmune, Experimental / pathology. Fumarates / pharmacology. Inflammation / prevention & control. Interleukin-1beta / antagonists & inhibitors. Interleukin-6 / antagonists & inhibitors. Microglia / drug effects. Nitric Oxide / biosynthesis. Nitric Oxide Synthase Type II / antagonists & inhibitors. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Animals. Blotting, Western. Brain / pathology. Dimethyl Fumarate. Extracellular Signal-Regulated MAP Kinases / metabolism. GA-Binding Protein Transcription Factor / biosynthesis. GA-Binding Protein Transcription Factor / genetics. Nitrites / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] J Neurosci Res. 1994 Jul 1;38(4):433-43 [7932874.001]
  • (PMID = 20482831.001).
  • [ISSN] 1742-2094
  • [Journal-full-title] Journal of neuroinflammation
  • [ISO-abbreviation] J Neuroinflammation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Fumarates; 0 / GA-Binding Protein Transcription Factor; 0 / Gabpa protein, rat; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Nitrites; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; FO2303MNI2 / Dimethyl Fumarate
  • [Other-IDs] NLM/ PMC2880998
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94. Järvelä S, Helin H, Haapasalo J, Järvelä T, Junttila TT, Elenius K, Tanner M, Haapasalo H, Isola J: Amplification of the epidermal growth factor receptor in astrocytic tumours by chromogenic in situ hybridization: association with clinicopathological features and patient survival. Neuropathol Appl Neurobiol; 2006 Aug;32(4):441-50
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  • [Title] Amplification of the epidermal growth factor receptor in astrocytic tumours by chromogenic in situ hybridization: association with clinicopathological features and patient survival.
  • Our data verify the central role of EGFR in the pathobiology of astrocytic tumours, and highlight the advantages of CISH as a simple and practical assay to screen for EGFR gene amplification in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Apoptosis / physiology. Child. Child, Preschool. Chromogenic Compounds. Female. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Protein Array Analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Survival Rate. Tumor Suppressor Protein p53

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  • [ErratumIn] Neuropathol Appl Neurobiol. 2006 Oct;32(5):568. Järvellä, S [corrected to Järvelä, Sally]; Järvellä, T [corrected to Järvelä, Timo]
  • (PMID = 16866989.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromogenic Compounds; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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95. Liu M, Hurn PD, Roselli CE, Alkayed NJ: Role of P450 aromatase in sex-specific astrocytic cell death. J Cereb Blood Flow Metab; 2007 Jan;27(1):135-41
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  • [Title] Role of P450 aromatase in sex-specific astrocytic cell death.
  • Female animals are protected from ischemic brain damage relative to age-matched males, in part through protection provided by endogenous estradiol.
  • In brain, estradiol is produced from testosterone by cytochrome P450 aromatase (cyp 19), a steroid synthetic enzyme present in astrocytes.
  • We tested the hypothesis that astrocytes derived from neonatal female rat brain are less susceptible than male cells to oxygen-glucose deprivation (OGD), and that this endogenous protection is associated with enhanced aromatase activity.
  • [MeSH-minor] Animals. Blotting, Western. Cell Death / drug effects. Cell Death / physiology. Cell Hypoxia / physiology. Cells, Cultured. Female. Glucose / deficiency. Hydrogen Peroxide / toxicity. Interleukin-1beta / toxicity. Lipopolysaccharides / toxicity. Male. Nitric Oxide / toxicity. Oxidative Stress / drug effects. RNA / biosynthesis. RNA / isolation & purification. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. Sex Characteristics. Tumor Necrosis Factor-alpha / toxicity

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  • (PMID = 16736049.001).
  • [ISSN] 0271-678X
  • [Journal-full-title] Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • [ISO-abbreviation] J. Cereb. Blood Flow Metab.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS049210; United States / NINDS NIH HHS / NS / NS20020; United States / NINDS NIH HHS / NS / NS33668; United States / NINDS NIH HHS / NS / NS44313
  • [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 / Interleukin-1beta; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 63231-63-0 / RNA; BBX060AN9V / Hydrogen Peroxide; EC 1.14.14.1 / Aromatase; IY9XDZ35W2 / Glucose
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96. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Alterations in dipeptidyl peptidase-IV (DPP-IV) enzymatic activity are characteristic of malignant transformation.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • This is the first report showing that non-malignant brain tissue contains a DPP-IV-like enzymatic activity attributable mostly to DPP-8/9, while the substantial part of the activity in glioma is due to increased DPP-IV/CD26, localized in both the vascular and parenchymal compartments.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-major] Astrocytoma / enzymology. Astrocytoma / genetics. Dipeptidyl Peptidase 4 / genetics. Dipeptidyl Peptidase 4 / metabolism. Gene Expression Regulation, Enzymologic / physiology
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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97. Eddaoudi A, Townsend-Nicholson A, Timms JF, Schorge S, Jayasinghe SN: Molecular characterisation of post-bio-electrosprayed human brain astrocytoma cells. Analyst; 2010 Oct;135(10):2600-12
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  • [Title] Molecular characterisation of post-bio-electrosprayed human brain astrocytoma cells.
  • [MeSH-minor] Astrocytoma. Brain Neoplasms. Calcium / metabolism. Cell Survival. Electrophoresis, Gel, Two-Dimensional. Humans. Indoles / pharmacology. Maleimides / pharmacology. Potassium Channels / metabolism. Receptor, Muscarinic M3 / genetics. Receptor, Muscarinic M3 / metabolism. Transfection. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 20694206.001).
  • [ISSN] 1364-5528
  • [Journal-full-title] The Analyst
  • [ISO-abbreviation] Analyst
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0601440; United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indoles; 0 / Maleimides; 0 / Potassium Channels; 0 / Receptor, Muscarinic M3; 0 / Tumor Necrosis Factor-alpha; 0 / bisindolylmaleimide VIII; SY7Q814VUP / Calcium
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98. Fountzilas G, Karkavelas G, Kalogera-Fountzila A, Karina M, Ignatiadis M, Koukoulis G, Plataniotis G, Misailidou D, Bobos M, Pectasides D, Razis E, Karavelis A, Selviaridis P: Post-operative combined radiation and chemotherapy with temozolomide and irinotecan in patients with high-grade astrocytic tumors. A phase II study with biomarker evaluation. Anticancer Res; 2006 Nov-Dec;26(6C):4675-86
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  • [Title] Post-operative combined radiation and chemotherapy with temozolomide and irinotecan in patients with high-grade astrocytic tumors. A phase II study with biomarker evaluation.
  • BACKGROUND: Clinical studies have shown that temozolomide (TMZ) and irinotecan demonstrate activity in high grade astrocytic tumors (HGAT).
  • PATIENTS AND METHODS: In the present study, a total of 45 HGAT patients, 38 with glioblastoma multiforme (GBM) and 7 with anaplastic astrocytoma (AA), were treated with TMZ, 150 mg/m(2) on days 1-5, followed by irinotecan, 150 mg/m(2) on days 6 and 17, every 4 weeks for 6 cycles or until the occurrence of unacceptable toxicity or disease progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / metabolism. Astrocytoma / therapy. Biomarkers, Tumor / biosynthesis. Brain Neoplasms / metabolism. Brain Neoplasms / therapy. Glioblastoma / metabolism. Glioblastoma / therapy

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  • (PMID = 17214326.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Vascular Endothelial Growth Factor C; 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; XT3Z54Z28A / Camptothecin
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99. 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
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  • [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-major] Apoptosis Regulatory Proteins / biosynthesis. Brain Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Glioblastoma / pathology. Membrane Proteins / biosynthesis. Microtubule-Associated Proteins / biosynthesis
  • [MeSH-minor] Adult. Astrocytoma / metabolism. Astrocytoma / pathology. Autophagy. Blotting, Western. Disease Progression. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged

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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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100. Varan A, Akyüz C, Akalan N, Atahan L, Söylemezoglu F, Selek U, Yalçin B, Kutluk T, Büyükpamukçu M: Astrocytic tumors in children: treatment results from a single institution. Childs Nerv Syst; 2007 Mar;23(3):315-9
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  • [Title] Astrocytic tumors in children: treatment results from a single institution.
  • PATIENTS AND METHODS: Five hundred fourteen patients diagnosed with brain tumor between 1972 and 2003 were retrospectively analyzed.
  • RESULTS: Ninety-eight (19%) out of 514 patients have astrocytic histopathology.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / therapy. Brain Neoplasms / therapy

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  • (PMID = 17058082.001).
  • [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] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7BRF0Z81KG / Lomustine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; COPP protocol
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