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1. Mortazavi H, Abedini R, Sadri F, Soori T, Vasheghani-Farahani A: Crusted scabies in a patient with brain astrocytoma: report of a case. Int J Infect Dis; 2010 Jun;14(6):e526-7
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  • [Title] Crusted scabies in a patient with brain astrocytoma: report of a case.
  • He suffered from a brain tumor (astrocytoma) and was immunosuppressed because he was receiving systemic steroids and chemo-radiation therapy.
  • He also had psychomotor retardation and behavior changes due to the pressure effect of his brain tumor.
  • The diagnosis of crusted scabies was established based on direct positive skin smears from the lesions.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Sarcoptes scabiei. Scabies / diagnosis
  • [MeSH-minor] Adult. Animals. Diagnosis, Differential. Fatal Outcome. Humans. Immunocompromised Host. Male. Pruritus / pathology

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  • [Copyright] Copyright 2009 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 19700360.001).
  • [ISSN] 1878-3511
  • [Journal-full-title] International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
  • [ISO-abbreviation] Int. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
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2. Allerstorfer S, Sonvilla G, Fischer H, Spiegl-Kreinecker S, Gauglhofer C, Setinek U, Czech T, Marosi C, Buchroithner J, Pichler J, Silye R, Mohr T, Holzmann K, Grasl-Kraupp B, Marian B, Grusch M, Fischer J, Micksche M, Berger W: FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities. Oncogene; 2008 Jul 10;27(30):4180-90
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  • Here we report simultaneous overexpression of FGF5 and its predominant high-affinity receptor (FGFR1 IIIc) in astrocytic brain tumour specimens (N=49) and cell cultures (N=49).
  • Moreover, tumour cell migration was distinctly stimulated by rFGF5 but attenuated by FGF5 siRNA.
  • In summary, we demonstrate for the first time that FGF5 contributes to the malignant progression of human astrocytic brain tumours by both autocrine and paracrine effects.
  • [MeSH-major] Autocrine Communication / physiology. Brain Neoplasms / genetics. Fibroblast Growth Factor 5 / physiology. Glioblastoma / genetics. Oncogenes. Paracrine Communication / physiology
  • [MeSH-minor] Cell Death / drug effects. Cell Movement / drug effects. Cell Proliferation / drug effects. Culture Media, Conditioned / pharmacology. Disease Progression. Genes, Dominant / physiology. Humans. Mutant Proteins / genetics. Mutant Proteins / physiology. Neovascularization, Pathologic / chemically induced. Neovascularization, Pathologic / genetics. Recombinant Proteins / pharmacology. Transfection. Tumor Cells, Cultured

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  • (PMID = 18362893.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 19920
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / FGF5 protein, human; 0 / Mutant Proteins; 0 / Recombinant Proteins; 129653-64-1 / Fibroblast Growth Factor 5
  • [Other-IDs] NLM/ PMC2879862; NLM/ UKMS30927
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3. 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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4. Stegh AH, Kim H, Bachoo RM, Forloney KL, Zhang J, Schulze H, Park K, Hannon GJ, Yuan J, Louis DN, DePinho RA, Chin L: Bcl2L12 inhibits post-mitochondrial apoptosis signaling in glioblastoma. Genes Dev; 2007 Jan 1;21(1):98-111
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  • Glioblastoma (GBM) is an astrocytic brain tumor characterized by an aggressive clinical course and intense resistance to all therapeutic modalities.
  • Enforced Bcl2L12 expression confers marked apoptosis resistance in primary cortical astrocytes, and, conversely, its RNA interference (RNAi)-mediated knockdown sensitizes human glioma cell lines toward apoptosis in vitro and impairs tumor growth with increased intratumoral apoptosis in vivo.
  • Thus, Bcl2L12 contributes to the classical tumor biological features of GBM such as intense apoptosis resistance and florid necrosis, and may provide a target for enhanced therapeutic responsiveness of this lethal cancer.

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  • (PMID = 17210792.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099041; United States / NCI NIH HHS / CA / P01 CA095616; United States / NINDS NIH HHS / NS / K08 NS042737; United States / NCI NIH HHS / CA / R01 CA57683; United States / NCI NIH HHS / CA / R01 CA057683; United States / NCI NIH HHS / CA / P01 CA95616; United States / NINDS NIH HHS / NS / K08NS42737
  • [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 / Apoptosomes; 0 / BCL2L12 protein, human; 0 / Bcl2l2 protein, mouse; 0 / Immunoglobulin G; 0 / Muscle Proteins; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ PMC1759904
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5. 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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6. 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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  • [ErratumIn] Proc Natl Acad Sci U S A. 2007 Sep 18;104(38):15168. Bock-Axelsen, Jacob [corrected to Bock, Jacob Bock]
  • (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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7. Kostic A, Mihailovic D, Veselinovic S, Tasic D, Stefanovic I, Novak V, Stojanovic N, Veselinovic D, Pavlovic S: Tumor size and karyometric variables in brain astrocytoma. J BUON; 2009 Jul-Sep;14(3):473-7
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  • [Title] Tumor size and karyometric variables in brain astrocytoma.
  • PURPOSE: To show any possible correlation of some karyometric variables with tumor size in patients with brain astrocytoma, in order to confirm karyometry as an objective histological method.
  • PATIENTS AND METHODS: The study included 63 patients of different ages and both genders with brain astrocytoma histologically confirmed on the surgically removed material.
  • In all patients maximal tumor excision was done, and all were postoperatively treated according to different therapeutic protocols.
  • Tumor size (preoperative CT scan) was correlated with the duration of survival and the values of some karyometric tumor variables: area, density, maximal axis, mean axis, minimal axis, circumference, roundness, integrated optical density (IOD) and number of nuclei.
  • RESULTS: Patients were separated into 3 groups according to the average tumor diameter.
  • Seven out of 9 examined karyometric variables were significantly related (p<0.05) to the tumor size: area, maximal axis, mean axis, minimal axis, circumference, roundness and IOD.
  • The results of our morphometric analysis of the tumor cell nuclei, after correlation with CT findings, revealed that nuclear pleomorphism and larger nuclear size are associated with larger brain astrocytomas.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Nucleus / pathology

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  • (PMID = 19810141.001).
  • [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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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. 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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10. 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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11. 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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12. 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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13. 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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14. Banerjee HN, Zhang L: Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy. Mol Cell Biochem; 2007 Jan;295(1-2):237-40
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  • [Title] Deciphering the finger prints of brain cancer astrocytoma in comparison to astrocytes by using near infrared Raman spectroscopy.
  • To explore the biochemical differences between brain cancer cells Astrocytoma and normal cells Astrocyte, we investigated the Raman spectra of single cell from these two cell types and analyzed the difference in spectra and intensity.
  • The Raman spectra of brain cancer cells was similar to those of normal cells, but the Raman intensity of cancer cells was much higher than that of normal cells.
  • The Raman spectra of brain cancer Astrocytoma shows that the structural changes of cancer cells happen so that many biological functions of these cells are lost.
  • The results indicate that Raman spectra can offer the experimental basis for the cancer diagnosis and treatment.
  • [MeSH-major] Astrocytes / chemistry. Astrocytoma / chemistry. Brain Neoplasms / chemistry. Spectroscopy, Near-Infrared. Spectrum Analysis, Raman

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  • (PMID = 16924417.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / G11HD 34280-05
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
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15. 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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16. 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] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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17. Zeltner L, Schittenhelm J, Mittelbronn M, Roser F, Tatagiba M, Mawrin C, Kim YJ, Bornemann A: The astrocytic response towards invasive meningiomas. Neuropathol Appl Neurobiol; 2007 Apr;33(2):163-8
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  • [Title] The astrocytic response towards invasive meningiomas.
  • The fate of subpial astrocytes during the course of brain invasion by meningiomas is not known.
  • In the present study we immunolabelled sections of 35 brain-invasive meningiomas (14 meningothelial meningiomas WHO grade I, 11 atypical WHO grade II and 10 anaplastic WHO grade III) using anti-collagen IV to label basement membrane material, and antibodies against astrocytic markers CD44, SPARC (secreted protein, acidic and rich in cysteine) and glial fibrillary acidic protein (GFAP).
  • Astrocytes were present at the tumour-brain interface of 14/14 WHO grade I meningiomas, 9/11 WHO grade II tumours and 9/10 WHO grade III tumours.
  • However, tumour embedded in deep brain parenchyma lacked both an astrocytic reaction and basement membrane material.
  • In conclusion, astrocytes eventually disappear from the tumour-brain interface during the course of meningioma infiltration.
  • [MeSH-minor] Aged. Antigens, CD44 / metabolism. Basement Membrane / metabolism. Basement Membrane / pathology. Cell Movement. Collagen Type IV / metabolism. Humans. Middle Aged. Neoplasm Invasiveness. Osteonectin / metabolism. Pia Mater / pathology

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  • (PMID = 17359357.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / Collagen Type IV; 0 / Osteonectin
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18. 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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19. 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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20. 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


21. 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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22. 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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23. Capper D, Mittelbronn M, Goeppert B, Meyermann R, Schittenhelm J: Secreted protein, acidic and rich in cysteine (SPARC) expression in astrocytic tumour cells negatively correlates with proliferation, while vascular SPARC expression is associated with patient survival. Neuropathol Appl Neurobiol; 2010 Apr;36(3):183-97
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  • [Title] Secreted protein, acidic and rich in cysteine (SPARC) expression in astrocytic tumour cells negatively correlates with proliferation, while vascular SPARC expression is associated with patient survival.
  • AIMS: Secreted protein, acidic and rich in cysteine (SPARC) is a regulator of cell-matrix interaction and has been associated with tumour stage and patient survival in various malignancies.
  • As no large-scale study has yet been undertaken, we investigated human brain and astrocytomas for SPARC expression and associations with tumour grade, proliferation, vascular density and patient survival.
  • METHODS: A spectrum of 188 WHO grade I-IV astrocytic tumours and 24 autopsy cases were studied by immunohistochemistry for SPARC, MIB-1 proliferation index and CD31-positive vessels.
  • RESULTS: In normal brain, SPARC is expressed in cortical marginal glia, cerebellar Bergmann glia and focally in white matter but is absent in neurones or vessels.
  • High SPARC expression levels in the cytoplasm of astrocytic tumour cells decreased with the grade of malignancy but showed an increase with grade of malignancy in tumour vessels.
  • SPARC negatively correlated with tumour proliferation but not with vascular density.
  • CONCLUSIONS: SPARC is highly expressed in astrocytomas and decreases with tumour progression.
  • While there is no association between the level of SPARC in the tumour cells and patient survival, increased tumour vascular SPARC expression is associated with decreased patient survival.
  • [MeSH-major] Astrocytoma / metabolism. Blood Vessels / metabolism. Brain / metabolism. Brain Neoplasms / metabolism. Cell Proliferation. Osteonectin / metabolism

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  • (PMID = 20132490.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Osteonectin; 0 / RNA, Messenger
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24. 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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25. Tan G, Sun SQ, Yuan DL: Expression of the water channel protein aquaporin-9 in human astrocytic tumours: correlation with pathological grade. J Int Med Res; 2008 Jul-Aug;36(4):777-82
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  • [Title] Expression of the water channel protein aquaporin-9 in human astrocytic tumours: correlation with pathological grade.
  • This study investigated the expression of the water channel protein aquaporin-9 (AQP9) in 100 cases of human astrocytic tumour compared with normal brain tissue.
  • The expression of both AQP9 mRNA and protein in astrocytic tumours was significantly greater than in normal brain tissue and was positively correlated with pathological grade.
  • No significant correlations were found between the level of AQP9 mRNA or protein expression and gender, age, tumour size or tumour site.
  • This study indicates that AQP9 may play an important role in the malignant progression of brain astrocytic tumours and may, therefore, be useful as a biomarker in its diagnosis and as a new target for gene therapy.
  • The molecular mechanisms by which AQP9 affects the proliferation and apoptosis of astrocytic tumours need to be studied further.
  • [MeSH-major] Aquaporins / metabolism. Astrocytoma. Brain Neoplasms
  • [MeSH-minor] Adolescent. Adult. Aged. Brain / cytology. Brain / metabolism. Child. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 18652774.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AQP9 protein, human; 0 / Aquaporins
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26. 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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27. 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] United States
  • [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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28. Likavcanová K, Dobrota D, Liptaj T, Prónayová N, Mlynárik V, Belan V, Galanda M, Béres A, De Riggo J: In vitro study of astrocytic tumour metabolism by proton magnetic resonance spectroscopy. Gen Physiol Biophys; 2005 Sep;24(3):327-35
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  • [Title] In vitro study of astrocytic tumour metabolism by proton magnetic resonance spectroscopy.
  • In vivo magnetic resonance spectroscopy (MRS) studies of glial brain tumours reported that higher grade of astrocytoma is associated with increased level of choline-containing compounds (Cho) and decreased levels of N-acetylaspartate (NAA) and creatine and phosphocreatine (Cr).
  • 1H-MR spectra were recorded in vitro from perchloric acid extracts of astrocytoma (WHO II) and glioblastoma multiforme (WHO IV) samples.
  • We observed differences between astrocytoma and glioblastoma multiforme in the levels of Cho, alanine, lactate, NAA, and glutamate/glutamine.
  • In astrocytoma samples, we found higher MR signal of NAA and lower signal of Cho and alanine.
  • In contrast, levels of Cr were the same in both tumour types.
  • We also determined NAA/Cr and Cho/Cr ratios in the tumour samples.
  • The results indicate that MRS is a promising method for distinguishing pathologies in human brain and for pre-surgical grading of brain tumours.
  • [MeSH-major] Astrocytes / pathology. Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Spectroscopy / methods. Neoplasms / metabolism
  • [MeSH-minor] Aspartic Acid / analogs & derivatives. Aspartic Acid / therapeutic use. Brain / metabolism. Brain / pathology. Choline / chemistry. Choline / pharmacology. Chromium / chemistry. Creatine / chemistry. Glioblastoma / chemistry. Glioblastoma / metabolism. Glioma / pathology. Humans. In Vitro Techniques. Phosphocreatine / chemistry. Spectrophotometry

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  • (PMID = 16308427.001).
  • [ISSN] 0231-5882
  • [Journal-full-title] General physiology and biophysics
  • [ISO-abbreviation] Gen. Physiol. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 020IUV4N33 / Phosphocreatine; 0R0008Q3JB / Chromium; 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; MU72812GK0 / Creatine; N91BDP6H0X / Choline
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29. 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] United States
  • [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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30. 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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31. Shapiro WR, Carpenter SP, Roberts K, Shan JS: (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma. Expert Opin Biol Ther; 2006 May;6(5):539-45
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  • [Title] (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma.
  • Treatment of malignant glioma is therapeutically challenging.
  • Despite improvements in neurosurgery, radiotherapy and chemotherapy, few patients diagnosed with anaplastic astrocytoma (AA) or glioblastoma multiforme (GBM) (WHO grades 3 and 4, respectively) will live beyond 2 years.
  • Most malignant gliomas cannot be completely resected or irradiated due to their ability to infiltrate diffusely into normal brain tissue.
  • Brain tissue is protected from the systemic circulation via the blood-brain barrier (BBB), which impedes entry of water-soluble chemotherapeutic agents into the tumour at therapeutic concentrations. (131)I-chTNT-1/B mAb (Cotara) employs an innovative strategy to treat the invasive portion of the tumour and the core lesion. (131)I-chTNT-1/B mAb is a genetically engineered, radiolabelled, chimeric monoclonal antibody specific for a universal intracellular antigen (i.e., DNA/histone H1 complex) exposed in the necrotic core of malignant gliomas.
  • Once localised to necrotic regions of the tumour, (131)I-chTNT-1/B mAb delivers a cytotoxic dose of (131)I radiation to the core lesion. (131)I-chTNT-1/B mAb is delivered via convection-enhanced delivery in order to maximise coverage to the tumour and the invasive front of the glial tumour.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Astrocytoma / radiotherapy. Iodine Radioisotopes / therapeutic use

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  • (PMID = 16610983.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Histones; 0 / Iodine Radioisotopes; 9007-49-2 / DNA
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32. 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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33. 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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34. Ichimura K, Mungall AJ, Fiegler H, Pearson DM, Dunham I, Carter NP, Collins VP: Small regions of overlapping deletions on 6q26 in human astrocytic tumours identified using chromosome 6 tile path array-CGH. Oncogene; 2006 Feb 23;25(8):1261-71
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  • [Title] Small regions of overlapping deletions on 6q26 in human astrocytic tumours identified using chromosome 6 tile path array-CGH.
  • Deletions of chromosome 6 are a common abnormality in diverse human malignancies including astrocytic tumours, suggesting the presence of tumour suppressor genes (TSG).
  • A total of 104 adult astrocytic tumours (10 diffuse astrocytomas, 30 anaplastic astrocytomas (AA), 64 glioblastomas (GB)) were analysed using this array.
  • [MeSH-major] Astrocytoma / genetics. Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Glioblastoma / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Chromosomes, Artificial, Bacterial. DNA, Neoplasm / analysis. Gene Dosage. Humans. Microsatellite Repeats. Telomere / genetics

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  • [Copyright] Oncogene (2006) 25, 1261-1271. doi:10.1038/sj.onc.1209156; published online 3 October 2005.
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  • (PMID = 16205629.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Other-IDs] NLM/ PMC2760128; NLM/ UKMS2686
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35. 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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36. Magalhaes A, Godfrey W, Shen Y, Hu J, Smith W: Proton magnetic resonance spectroscopy of brain tumors correlated with pathology. Acad Radiol; 2005 Jan;12(1):51-7
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  • [Title] Proton magnetic resonance spectroscopy of brain tumors correlated with pathology.
  • RATIONALE AND OBJECTIVES: Evaluate proton magnetic resonance spectroscopy ((1)H-MRS) for assessing and grading brain tumors.
  • In 16 patients with brain astrocytoma of various grades, the pathology grading was correlated with Cho/NAA and Cho/Cr.
  • These values were 6.53 and 3.35 for nine patients with Grade 4 astrocytoma; 1.85 and 1.62 for three patients with Grade 3 astrocytoma; 2.21 and 1.50 for three patients with Grade 2 astrocytoma; and 1.45 and 1.49 for one patient with Grade 1 astrocytoma.
  • CONCLUSION: MRS ratios can be used to differentiate malignant and nonmalignant lesions from normal brain tissue.
  • In general, high-grade astrocytoma have higher Cho/NAA and Cho/Cr ratios compared with low-grade astrocytoma.
  • [MeSH-major] Aspartic Acid / analogs & derivatives. Brain Neoplasms / diagnosis. Magnetic Resonance Spectroscopy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Astrocytoma / diagnosis. Astrocytoma / pathology. Brain / pathology. Choline / analysis. Creatine / analysis. Female. Glioblastoma / diagnosis. Glioblastoma / pathology. Glioma / diagnosis. Glioma / pathology. Gliosarcoma / diagnosis. Gliosarcoma / pathology. Humans. Hydrogen. Image Processing, Computer-Assisted / methods. Male. Middle Aged. Oligodendroglioma / diagnosis. Oligodendroglioma / pathology. Protons

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  • (PMID = 15691725.001).
  • [ISSN] 1076-6332
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protons; 30KYC7MIAI / Aspartic Acid; 7YNJ3PO35Z / Hydrogen; 997-55-7 / N-acetylaspartate; MU72812GK0 / Creatine; N91BDP6H0X / Choline
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37. Moenninghoff C, Maderwald S, Theysohn JM, Kraff O, Ladd ME, El Hindy N, van de Nes J, Forsting M, Wanke I: Imaging of adult astrocytic brain tumours with 7 T MRI: preliminary results. Eur Radiol; 2010 Mar;20(3):704-13
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  • [Title] Imaging of adult astrocytic brain tumours with 7 T MRI: preliminary results.
  • PURPOSE: In this study tumour vascularity and necrosis of intracranial astrocytomas were compared using 7 T and 1.5 T magnetic resonance imaging (MRI).
  • Histological findings and T2*-w MR images at both field strengths were compared for the presence of assumed tumour microvascularity and necrosis.
  • RESULTS: T2*-w images depicted susceptibility patterns representing presumed tumour microvascularity in 8 out of 15 (53%) gliomas at 7 T compared with 5 out of 15 (33%) gliomas at 1.5 T.
  • Compared with 1.5 T MRI three additional necrotic tumour areas were depicted only on 7 T T2- and T2*-w images of one glioblastoma.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Magnetic Resonance Imaging / methods. Neovascularization, Pathologic / pathology

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  • (PMID = 19763581.001).
  • [ISSN] 1432-1084
  • [Journal-full-title] European radiology
  • [ISO-abbreviation] Eur Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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38. Beetz C, Bergner S, Brodoehl S, Brodhun M, Ewald C, Kalff R, Krüger J, Patt S, Kiehntopf M, Deufel T: Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology. Int J Oncol; 2006 Nov;29(5):1183-91
MedlinePlus Health Information. consumer health - Brain Tumors.

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  • [Title] Outcome-based profiling of astrocytic tumours identifies prognostic gene expression signatures which link molecular and morphology-based pathology.
  • Astrocytomas are intracranial malignancies for which invasive growth and high motility of tumour cells preclude total resection; the tumours usually recur in a more aggressive and, eventually, lethal form.
  • In order to identify novel molecular markers for prognosis we obtained expression profiles of: i) tumours associated with particularly long recurrence-free intervals, ii) tumours which led to rapid patient death, and iii) tumour-free control brain.
  • Our finding of cell-specificity for some of these outcome-determining genes relates global expression data to the presence of morphological correlates of tumour behaviour and, thus, provides a link between morphology-based and molecular pathology.
  • Our identification of expression signatures that are associated individually with clinical outcome confirms the prognostic relevance of gene expression data and, thus, represents a step towards eventually implementing molecular diagnosis into clinical practice in neuro-oncology.
  • [MeSH-major] Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / mortality. Gene Expression Profiling. Genes, Neoplasm / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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

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  • (PMID = 18729076.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLTSCR2 protein, human; 0 / Tumor Suppressor Proteins
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40. Andersson AK, Rönnbäck L, Hansson E: Lactate induces tumour necrosis factor-alpha, interleukin-6 and interleukin-1beta release in microglial- and astroglial-enriched primary cultures. J Neurochem; 2005 Jun;93(5):1327-33
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  • [Title] Lactate induces tumour necrosis factor-alpha, interleukin-6 and interleukin-1beta release in microglial- and astroglial-enriched primary cultures.
  • This study investigated how treatment with NH4Cl and lactate, which increase in the brain as a consequence of hyperammonaemia, affects cells in primary rat cultures enriched in either astrocytes or microglia.
  • Release of the proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-6 and IL-1beta was measured using ELISA.
  • Lactate treatment altered astrocytic appearance, resulting in increased space between individual cells.
  • [MeSH-major] Astrocytes / metabolism. Interleukin-1 / metabolism. Interleukin-6 / metabolism. Lactates / pharmacology. Microglia / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15934951.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-1; 0 / Interleukin-6; 0 / Lactates; 0 / Tumor Necrosis Factor-alpha; 01Q9PC255D / Ammonium Chloride
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41. McGirt MJ, Chaichana KL, Gathinji M, Attenello FJ, Than K, Olivi A, Weingart JD, Brem H, Quiñones-Hinojosa AR: Independent association of extent of resection with survival in patients with malignant brain astrocytoma. J Neurosurg; 2009 Jan;110(1):156-62
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  • [Title] Independent association of extent of resection with survival in patients with malignant brain astrocytoma.
  • OBJECT: With recent advances in the adjuvant treatment of malignant brain astrocytomas, it is increasingly debated whether extent of resection affects survival.
  • METHODS: The authors retrospectively reviewed the cases of 1215 patients who underwent surgery for malignant brain astrocytomas (World Health Organization [WHO] Grade III or IV) at a single institution from 1996 to 2006.
  • Surgery consisted of primary resection in 549 patients (58%) and revision resection for tumor recurrence in 400 patients (42%).
  • Adjusting for factors associated with survival for WHO Grade III astrocytoma (age, KPS score, and revision resection), GTR versus STR (p < 0.05) was associated with improved survival.
  • CONCLUSIONS: In the authors' experience with both primary and secondary resection of malignant brain astrocytomas, increasing extent of resection was associated with improved survival independent of age, degree of disability, WHO grade, or subsequent treatment modalities used.
  • [MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery

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  • (PMID = 18847342.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Decanoic Acids; 0 / Polyesters; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 90409-78-2 / decanedioic acid-4,4'-(1,3-propanediylbis(oxy))bis(benzoic acid) copolymer; U68WG3173Y / Carmustine
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42. Suzuki T, Izumoto S, Fujimoto Y, Maruno M, Ito Y, Yoshimine T: Clinicopathological study of cellular proliferation and invasion in gliomatosis cerebri: important role of neural cell adhesion molecule L1 in tumour invasion. J Clin Pathol; 2005 Feb;58(2):166-71
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  • [Title] Clinicopathological study of cellular proliferation and invasion in gliomatosis cerebri: important role of neural cell adhesion molecule L1 in tumour invasion.
  • BACKGROUND/AIMS: In patients with gliomatosis cerebri (GC), glial fibrillary acidic protein (GFAP) positive cells invade the entire brain, particularly the white matter.
  • METHODS: An immunohistochemical analysis of neoplastic cells from four patients with GC and 20 with astrocytic tumours using antibodies against Ki-67, GFAP, and L1, the last of which is a neural cell adhesion molecule putatively related to glioma invasion.
  • RESULTS: GC tumour cells can be divided into two types, those mainly composed of strongly GFAP and L1 positive gemistocytic cells, the other composed of small, GFAP and L1 negative spindle shaped cells.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasms, Neuroepithelial / pathology. Neural Cell Adhesion Molecule L1 / analysis
  • [MeSH-minor] Adult. Aged. Antibodies, Neoplasm / analysis. Astrocytoma / chemistry. Astrocytoma / pathology. Brain Chemistry. Cell Division / physiology. Female. Glial Fibrillary Acidic Protein / analysis. Glioblastoma / chemistry. Glioblastoma / pathology. Humans. Immunohistochemistry / methods. Ki-67 Antigen / immunology. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness

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  • (PMID = 15677537.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Glial Fibrillary Acidic Protein; 0 / Ki-67 Antigen; 0 / Neural Cell Adhesion Molecule L1
  • [Other-IDs] NLM/ PMC1770574
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43. Birlik B, Canda S, Ozer E: Tumour vascularity is of prognostic significance in adult, but not paediatric astrocytomas. Neuropathol Appl Neurobiol; 2006 Oct;32(5):532-8
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  • [Title] Tumour vascularity is of prognostic significance in adult, but not paediatric astrocytomas.
  • Astrocytomas are the commonest type of brain tumours in adults and children.
  • Although the most reliable prognostic indicators have been shown consistently to be patient age and tumour histological grade, biological progression in these tumours is inevitable and the overall prognosis has remained poor.
  • Due to the evidence that vascular changes are important histological features of astrocytomas, the aim of this study was to investigate prognostic significance of tumour vascularity in paediatric and adult astrocytomas.
  • Study population consisted of 70 patients (45 adult and 25 children) with histologically proven diagnosis of astrocytoma with no history of previous therapy.
  • Histological quantification of tumour vascularity was performed using three different methods: microvessel density, vascular grading and Chalkley counting.
  • In contrast to the results in paediatric astrocytomas, tumour vascularity in adult tumours correlated significantly with postoperative survival by univariate analysis (P < 0.05).
  • Patient age and tumour histological grade were also correlated with survival.
  • We conclude that histological quantification of tumour vascularity is a significant prognosticator in adult astrocytomas, but not in children.
  • Our data do not support the validity of applications of antiangiogenic agents in paediatric astrocytic tumours, particularly pilocytic astrocytomas.
  • [MeSH-major] Aging / pathology. Astrocytoma / blood supply. Astrocytoma / pathology. Brain Neoplasms / blood supply. Brain Neoplasms / pathology

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  • (PMID = 16972887.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31
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44. Arjona D, Bello MJ, Alonso ME, Aminoso C, Isla A, De Campos JM, Sarasa JL, Gutierrez M, Villalobo A, Rey JA: Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations. Neuropathol Appl Neurobiol; 2005 Aug;31(4):384-94
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  • [Title] Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations.
  • For the 19 samples with sufficient available tumour tissue we found over-expression in 11, and no EGFR mRNA expression in three.
  • These findings corroborate that EGFR is non-randomly involved in malignant glioma development and that different mutant forms participate in aberrant activation of tyrosine kinase pathways.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Epidermal Growth Factor / genetics. Gene Amplification

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  • (PMID = 16008822.001).
  • [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 / RNA, Messenger; 62229-50-9 / Epidermal Growth Factor
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45. Jacques TS, Swales A, Brzozowski MJ, Henriquez NV, Linehan JM, Mirzadeh Z, O' Malley C, Naumann H, Alvarez-Buylla A, Brandner S: Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes. EMBO J; 2010 Jan 6;29(1):222-35
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  • [Title] Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes.
  • It has been suggested that intrinsic brain tumours originate from a neural stem/progenitor cell population in the subventricular zone of the post-natal brain.
  • However, the influence of the initial genetic mutation on the phenotype as well as the contribution of mature astrocytes to the formation of brain tumours is still not understood.
  • We found that only stem cells, but not astrocytes, gave rise to brain tumours, independent of their location.
  • This suggests a cell autonomous mechanism that enables stem cells to generate brain tumours, whereas mature astrocytes do not form brain tumours in adults.
  • Our study underlines an important role of stem cells and the relevance of initial genetic mutations in the pathogenesis and phenotype of brain tumours.

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  • (PMID = 19927122.001).
  • [ISSN] 1460-2075
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD032116; United States / NICHD NIH HHS / HD / R37 HD032116; United States / NICHD NIH HHS / HD / HD-32116
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / glial fibrillary astrocytic protein, mouse; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2808375
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46. Balkanov AS, Makarenko MF, Poliakov PIu, Kachkov IA: [Results of hyperfractionated radiation therapy used in combination with lomustin in malignant gliomas of the brain]. Zh Vopr Neirokhir Im N N Burdenko; 2005 Jul-Sep;(3):14-16; discussion 16-7
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  • [Title] [Results of hyperfractionated radiation therapy used in combination with lomustin in malignant gliomas of the brain].
  • The postoperative use of lomustin, a nitrosourea agent, was investigated for its impact on the efficiency of hyperfractionated radiation therapy performed in patients with glioblastoma and anaplastic astrocytoma of the brain.
  • A total of 35 patients (26 and 9 patients with glioblastoma and anaplastic astrocytoma, respectively) were followed up.
  • Lomustin in combination with hyperfractionated radiation therapy was found to have no effect on the survival of patients with glioblastoma and anaplastic astrocytoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Glioma / drug therapy. Glioma / radiotherapy. Lomustine / therapeutic use

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  • (PMID = 16485820.001).
  • [ISSN] 0042-8817
  • [Journal-full-title] Zhurnal voprosy neĭrokhirurgii imeni N. N. Burdenko
  • [ISO-abbreviation] Zh Vopr Neirokhir Im N N Burdenko
  • [Language] rus
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7BRF0Z81KG / Lomustine; 7S5I7G3JQL / Dexamethasone
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47. Beetz C, Brodoehl S, Patt S, Kalff R, Deufel T: Low expression but infrequent genomic loss of the putative tumour suppressor DBCCR1 in astrocytoma. Oncol Rep; 2005 Feb;13(2):335-40
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  • [Title] Low expression but infrequent genomic loss of the putative tumour suppressor DBCCR1 in astrocytoma.
  • DBCCR1 (deleted in bladder cancer chromosomal region 1) has been reported as the gene functionally affected by frequent loss of 9q32-33 in transitional cell carcinomas of the urinary bladder.
  • For these particular tumours, its proposed role in tumour suppression is supported both by the observation of methylation-based silencing of DBCCR1 in a large fraction of bladder cancers and by re-expression studies in bladder cancer-derived cell lines.
  • A more general involvement of DBCCR1 in tumour development might be inferred from recent chip-based expression studies in other tumours.
  • The present study addressed expression of DBCCR1 in gliomas, specifically in astrocytomas, using semi-quantitative RT-PCR on 25 tumours of different malignancy grade and on 5 control brain tissue samples.
  • Genomic deletion of the DBCCR1 locus at 9q32-33 was also investigated, together with the CDKN2A locus at 9p21, by loss of heterozygosity analysis in a second series of 26 astrocytic tumours.
  • We found that DBCCR1 mRNA expression is markedly reduced in the majority of tumour samples compared to controls, and that this reduction significantly correlates with tumour grade.
  • Genomic loss of the DBCCR1 region was found in only 5 of 24 (21%) informative samples, with no obvious correlation to tumour grade, while loss of the CDKN2A locus was observed in 13 of 21 (62%) informative samples with high-grade tumours being affected more often.
  • In contrast to the situation in bladder cancer, the prevalent inactivation of DBCCR1 seen at the expression level in astrocytomas is not primarily caused by genomic loss of the gene.
  • Our findings support a more general role for DBCCR1 in tumour suppression with mechanisms of inactivation differing between tumour types.
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, Tumor Suppressor. Tumor Suppressor Proteins / genetics

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  • (PMID = 15643521.001).
  • [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 / DBC1 protein, human; 0 / Tumor Suppressor Proteins
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48. Rashid MH, Ahmad SU, Rahman MH, Raihan MZ, Sayed MA: Surgical outcome of low grade astrocytoma of brain. Mymensingh Med J; 2010 Apr;19(2):185-90
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  • [Title] Surgical outcome of low grade astrocytoma of brain.
  • This study was carried out in the department of Neurosurgery, Dhaka Medical College Hospital, Dhaka, Bangladesh, during the period of January 2003 to December 2006 to elucidate the effectiveness of surgical treatment in the management of low grade astrocytoma of brain.
  • For this purpose, a total number of 50 cases admitted during the study period with low grade astrocytoma of brain supported by clinical features and radiological investigations (CT and MRI scan) were included in this study.
  • Out of 50 patients 60.0% had gross total removal of tumor and 40.0% sub total tumor resection.
  • Histopathological study was done in all cases after tumor resection.
  • Among the gross total tumor removal cases highest percentage had good recovery (93.4%) in the immediate post operative period.
  • Another 2(4.0%), those underwent subtotal tumor resection died during subsequent follow up period at 8th and 14th postoperative day.

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  • (PMID = 20395910.001).
  • [ISSN] 1022-4742
  • [Journal-full-title] Mymensingh medical journal : MMJ
  • [ISO-abbreviation] Mymensingh Med J
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Bangladesh
  • [Chemical-registry-number] 0 / Contrast Media
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49. Hlobilkova A, Ehrmann J, Knizetova P, Krejci V, Kalita O, Kolar Z: Analysis of VEGF, Flt-1, Flk-1, nestin and MMP-9 in relation to astrocytoma pathogenesis and progression. Neoplasma; 2009;56(4):284-90
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  • [Title] Analysis of VEGF, Flt-1, Flk-1, nestin and MMP-9 in relation to astrocytoma pathogenesis and progression.
  • Astrocytomas, particularly high grade astrocytoma, are brain tumors with potent angiogenic activity.
  • Our immnunohistochemical study assessed vascular endothelial growth factor (VEGF), VEGF receptors (Flk-1, and Flt-1), the intermediate filamental protein nestin which plays a role in central nervous system development, and MMP-9, which belongs the family of matrix metalloproteinases implicated in tumor invasion and angiogenesis regulation.
  • We investigated the expression of VEGF, its receptors, nestin and MMP-9 in astrocytomas and their correlation with tumor grade.
  • Expression of Flt-1 and Flk-1 showed no significant differences between low and high grade tumor groups.
  • Nestin expression in tumor astrocytes and endothelial cells increased in high grade group (p same 0.007 and 0.003).
  • Expression of nestin and MMP-9 also suggest their likely role in astrocytoma vascular development and proliferation.
  • [MeSH-major] Astrocytoma / etiology. Brain Neoplasms / etiology. Intermediate Filament Proteins / metabolism. Matrix Metalloproteinase 9 / metabolism. Nerve Tissue Proteins / metabolism. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-1 / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 19473053.001).
  • [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 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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50. Yamamoto S, Tetsuka K, Sato Y, Endo S: Unsuspected tracheal web inhibits endotracheal intubation: report of a case. J Anesth; 2010 Feb;24(1):132-3

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  • A 66-year-old woman was scheduled for resection of a recurrent brain astrocytoma.
  • [MeSH-major] Intraoperative Complications. Intubation, Intratracheal. Trachea / pathology. Tracheal Stenosis / diagnosis
  • [MeSH-minor] Aged. Astrocytoma / complications. Astrocytoma / surgery. Brain Neoplasms / complications. Brain Neoplasms / surgery. Bronchoscopy. Female. Humans. Lasers, Gas / therapeutic use. Neoplasm Recurrence, Local / complications. Neoplasm Recurrence, Local / surgery. Reoperation. Video-Assisted Surgery / instrumentation

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  • (PMID = 20052498.001).
  • [ISSN] 1438-8359
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51. Beaty O 3rd, Berg S, Blaney S, Malogolowkin M, Krailo M, Knight R, Schaiquevich P, Stewart C, Chen Z, Nelson M, Voss S, Ivy SP, Adamson PC: A phase II trial and pharmacokinetic study of oxaliplatin in children with refractory solid tumors: a Children's Oncology Group study. Pediatr Blood Cancer; 2010 Sep;55(3):440-5
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  • PATIENTS AND METHODS: Subjects, < or =21 years of age at original diagnosis, received oxaliplatin (130 mg/m(2)) intravenously every 21 days.
  • Histologies included: Ewing sarcoma/peripheral PNET, osteosarcoma, rhabdomyosarcoma, neuroblastoma, high and low grade astrocytoma, brain stem glioma, ependymoma, hepatoblastoma and selected rare tumors.

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20658614.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10CA98413; United States / NCI NIH HHS / CA / U10CA98543; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543-08; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA098413-08
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin
  • [Other-IDs] NLM/ NIHMS218622; NLM/ PMC4665115
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52. Tchaicha JH, Mobley AK, Hossain MG, Aldape KD, McCarty JH: A mosaic mouse model of astrocytoma identifies alphavbeta8 integrin as a negative regulator of tumor angiogenesis. Oncogene; 2010 Aug 5;29(31):4460-72
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  • [Title] A mosaic mouse model of astrocytoma identifies alphavbeta8 integrin as a negative regulator of tumor angiogenesis.
  • Furthermore, little is known about how cancer cells selectively circumvent the actions of these inhibitors to promote pathological angiogenesis, a requisite event for tumor progression.
  • Using mosaic mouse models of the malignant brain cancer, astrocytoma, we report that tumor cells induce pathological angiogenesis by suppressing expression of the ECM protein receptor alphavbeta8 integrin.
  • Diminished integrin expression in astrocytoma cells leads to reduced activation of latent TGFbetas, resulting in impaired TGFbeta receptor signaling in tumor-associated endothelial cells.
  • These data reveal that astrocytoma cells manipulate their angiogenic balance by selectively suppressing alphavbeta8 integrin expression and function.
  • Finally, these results show that an adhesion and signaling axis normally involved in developmental brain angiogenesis is pathologically exploited in adult brain tumors.

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  • (PMID = 20531304.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NINDS NIH HHS / NS / R01 NS059876-03; United States / NINDS NIH HHS / NS / R01NS059876; United States / NCI NIH HHS / CA / P50CA127001; United States / NINDS NIH HHS / NS / R01 NS059876-02S2; United States / NINDS NIH HHS / NS / R01 NS059876; United States / NCI NIH HHS / CA / P50 CA127001; United States / NINDS NIH HHS / NS / NS059876-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrins; 0 / integrin alphavbeta8
  • [Other-IDs] NLM/ NIHMS198457; NLM/ PMC3037767
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53. 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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54. Attenello FJ, Mukherjee D, Datoo G, McGirt MJ, Bohan E, Weingart JD, Olivi A, Quinones-Hinojosa A, Brem H: Use of Gliadel (BCNU) wafer in the surgical treatment of malignant glioma: a 10-year institutional experience. Ann Surg Oncol; 2008 Oct;15(10):2887-93
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  • [Title] Use of Gliadel (BCNU) wafer in the surgical treatment of malignant glioma: a 10-year institutional experience.
  • We set out to characterize Gliadel-associated morbidity in our 10-year experience with Gliadel wafers for treatment of malignant glioma.
  • METHODS: We retrospectively reviewed records of 1013 patients undergoing craniotomy for resection of malignant brain astrocytoma (World Health Organization grade III/IV disease).
  • RESULTS: A total of 1013 craniotomies were performed for malignant brain astrocytoma.
  • A total of 288 (28%) received Gliadel wafer (250 glioblastoma multiforme (GBM), 38 anaplastic astrocytoma/anaplastic oligodendroglioma (AA/AO), 166 primary resection, 122 revision resection).
  • Patients in Gliadel versus non-Gliadel cohorts had similar incidences of perioperative surgical site infection (2.8% vs. 1.8%, P = .33), cerebrospinal fluid leak (2.8% vs. 1.8%, P = .33), meninigitis (.3% vs. .3%, P = 1.00), incisional wound healing difficulty (.7% vs. .4%, P = .63), symptomatic malignant edema (2.1% vs. 2.3%, P = 1.00), 3-month seizure incidence (14.6% vs. 15.7%, P = .65), deep-vein thrombosis (6.3% vs. 5.2%, P = .53), and pulmonary embolism (PE) (4.9% vs. 3.7%, P = .41).
  • CONCLUSION: In our experience, use of Gliadel wafer was not associated with an increase in perioperative morbidity after surgical treatment of malignant astrocytoma.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Biocompatible Materials / therapeutic use. Brain Neoplasms / drug therapy. Brain Neoplasms / surgery. Carmustine / therapeutic use. Decanoic Acids / therapeutic use. Neurosurgical Procedures. Polyesters / therapeutic use

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  • (PMID = 18636295.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biocompatible Materials; 0 / Decanoic Acids; 0 / Drug Carriers; 0 / Polyesters; 90409-78-2 / decanedioic acid-4,4'-(1,3-propanediylbis(oxy))bis(benzoic acid) copolymer; U68WG3173Y / Carmustine
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55. Jayasinghe SN, Irvine S, McEwan JR: Cell electrospinning highly concentrated cellular suspensions containing primary living organisms into cell-bearing threads and scaffolds. Nanomedicine (Lond); 2007 Aug;2(4):555-67
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  • In that study, we demonstrated the process with an immortalized human brain astrocytoma (1321N1, European Collection of Cell Cultures) cell line at a cell concentration of 10(6) cells/ml.

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  • (PMID = 17716138.001).
  • [ISSN] 1748-6963
  • [Journal-full-title] Nanomedicine (London, England)
  • [ISO-abbreviation] Nanomedicine (Lond)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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56. Bach JP, Deuster O, Balzer-Geldsetzer M, Meyer B, Dodel R, Bacher M: The role of macrophage inhibitory factor in tumorigenesis and central nervous system tumors. Cancer; 2009 May 15;115(10):2031-40
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  • Vascular growth factor concentration raises because of increased levels of MIF in brain tumors.
  • Recently, the MIF receptor complex has been described, and it appears that this may be a suitable drug target for treatment of brain tumors.
  • In light of these findings, the authors chose to conduct a systematic search for information regarding MIF that has been published within the past 15 years using the terms "inflammation," "glioblastoma," "brain tumor," "astrocytoma," "microglia," "glioblastoma," "immune system and brain tumors," "glioblastoma and MIF," and "brain tumor and MIF."
  • The aim of this article was thus to present a detailed review of current knowledge regarding the role of MIF in CNS tumor pathophysiology.
  • [MeSH-minor] Brain Neoplasms / metabolism. Cell Transformation, Neoplastic. Drug Delivery Systems. Humans. Neovascularization, Pathologic / metabolism

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  • (PMID = 19326434.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Macrophage Migration-Inhibitory Factors
  • [Number-of-references] 67
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57. Xiang YY, Dong H, Wan Y, Li J, Yee A, Yang BB, Lu WY: Versican G3 domain regulates neurite growth and synaptic transmission of hippocampal neurons by activation of epidermal growth factor receptor. J Biol Chem; 2006 Jul 14;281(28):19358-68
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  • Versican is one of the major extracellular matrix (ECM) proteins in the brain.
  • Recent findings have revealed that peptide fragments containing the versican C terminus (G3 domain) are present in human brain astrocytoma.
  • [MeSH-major] Brain Neoplasms / metabolism. Chondroitin Sulfate Proteoglycans / physiology. Hippocampus / metabolism. Lectins, C-Type / physiology. Neurons / metabolism. Receptor, Epidermal Growth Factor / metabolism. Synaptic Transmission
  • [MeSH-minor] Animals. Astrocytoma / metabolism. Brain / metabolism. Brain / pathology. Cell Line, Tumor. Extracellular Matrix / metabolism. Humans. Protein Structure, Tertiary. Rats. Versicans

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  • (PMID = 16648628.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chondroitin Sulfate Proteoglycans; 0 / Cspg2 protein, rat; 0 / Lectins, C-Type; 0 / VCAN protein, human; 126968-45-4 / Versicans; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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58. Pantelis E, Papadakis N, Verigos K, Stathochristopoulou I, Antypas C, Lekas L, Tzouras A, Georgiou E, Salvaras N: Integration of functional MRI and white matter tractography in stereotactic radiosurgery clinical practice. Int J Radiat Oncol Biol Phys; 2010 Sep 1;78(1):257-67
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  • METHODS AND MATERIALS: fMRI and tractography data sets were acquired and fused with corresponding anatomical MR and computed tomography images of patients with arteriovenous malformation (AVM), astrocytoma, brain metastasis, or hemangioma and referred for stereotactic radiosurgery.
  • In the astrocytoma case, the dose to the motor cortex bordering the lesion was reduced to 1,900 cGy from 2,100 cGy, and therefore, the biologically equivalent dose in three fractions was delivered instead.
  • [MeSH-major] Brain Neoplasms. Intracranial Arteriovenous Malformations. Magnetic Resonance Imaging / methods. Radiation Injuries / prevention & control. Radiosurgery / methods
  • [MeSH-minor] Adult. Astrocytoma / pathology. Astrocytoma / radiography. Astrocytoma / surgery. Brain Stem Neoplasms / pathology. Brain Stem Neoplasms / radiography. Brain Stem Neoplasms / surgery. Carcinoma, Non-Small-Cell Lung / radiography. Carcinoma, Non-Small-Cell Lung / secondary. Carcinoma, Non-Small-Cell Lung / surgery. Diffusion Tensor Imaging / methods. Female. Hemangioma, Cavernous, Central Nervous System / pathology. Hemangioma, Cavernous, Central Nervous System / radiography. Hemangioma, Cavernous, Central Nervous System / surgery. Humans. Lung Neoplasms / pathology. Male. Middle Aged. Motor Cortex / anatomy & histology. Motor Cortex / radiation effects. Motor Cortex / radiography. Pyramidal Tracts / anatomy & histology. Pyramidal Tracts / radiation effects. Pyramidal Tracts / radiography. Radiotherapy Dosage. Radiotherapy Planning, Computer-Assisted / methods. Visual Pathways / anatomy & histology. Visual Pathways / radiation effects. Visual Pathways / radiography

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20421146.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article
  • [Publication-country] United States
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59. Weckesser M, Langen KJ, Rickert CH, Kloska S, Straeter R, Hamacher K, Kurlemann G, Wassmann H, Coenen HH, Schober O: O-(2-[18F]fluorethyl)-L-tyrosine PET in the clinical evaluation of primary brain tumours. Eur J Nucl Med Mol Imaging; 2005 Apr;32(4):422-9
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  • [Title] O-(2-[18F]fluorethyl)-L-tyrosine PET in the clinical evaluation of primary brain tumours.
  • PURPOSE: The aim of this study was to evaluate the differential uptake of O-(2-[18F]fluorethyl)-L-tyrosine (FET) in suspected primary brain tumours.
  • METHODS: Positron emission tomography (PET) was performed in 44 patients referred for the evaluation of a suspected brain tumour.
  • Tumour uptake was calculated as the ratio of maximal tumour intensity to mean activity within a reference region (FETmax).
  • No uptake was observed in nine lesions (one inflammatory lesion, one dysembryoplastic neuroepithelial tumour, one mature teratoma, six lesions without histological confirmation).
  • Similar results were obtained when the analysis was applied only to astrocytic tumours (2.0 vs 3.1 in the first frame; 2.4 vs 2.6 in the fourth frame).
  • CONCLUSION: These initial results indicate that FET PET is a useful method to identify malignant brain lesions.
  • It appears that high- and low-grade brain tumours exhibit a different uptake kinetics of FET.
  • A kinetic analysis of FET PET may provide additional information in the differentiation of suspected brain lesions.
  • [MeSH-major] Brain Neoplasms / diagnostic imaging. Brain Neoplasms / metabolism. Fluorine Radioisotopes / pharmacokinetics. Positron-Emission Tomography / methods. Tyrosine / analogs & derivatives. Tyrosine / pharmacokinetics

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  • (PMID = 15650870.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fluorine Radioisotopes; 0 / O-(2-fluoroethyl)tyrosine; 0 / Radiopharmaceuticals; 42HK56048U / Tyrosine
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60. Elgamal EA, Coakham HB: Hemifacial spasm caused by pontine glioma: case report and review of the literature. Neurosurg Rev; 2005 Oct;28(4):330-2
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  • Hemifacial spasm (HFS) is an involuntary paroxysmal contractions of the facial musculature, caused generally by vascular compression of the seventh cranial nerve at its root exit zone from the brain stem.
  • The case of an adult man harbouring brain stem glioma (BSG) whose only neurological signs were left HFS and mild facial weakness is reported.
  • No responsible vessel could be identified during surgery, but the causative lesion was found to be an astrocytic tumour encasing the facial nerve at its root exit zone from the brain stem.
  • [MeSH-major] Astrocytoma / complications. Brain Stem Neoplasms / complications. Hemifacial Spasm / etiology

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  • (PMID = 16001287.001).
  • [ISSN] 0344-5607
  • [Journal-full-title] Neurosurgical review
  • [ISO-abbreviation] Neurosurg Rev
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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61. Bajetto A, Barbieri F, Dorcaratto A, Barbero S, Daga A, Porcile C, Ravetti JL, Zona G, Spaziante R, Corte G, Schettini G, Florio T: Expression of CXC chemokine receptors 1-5 and their ligands in human glioma tissues: role of CXCR4 and SDF1 in glioma cell proliferation and migration. Neurochem Int; 2006 Oct;49(5):423-32
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  • Chemokines have been involved in cellular processes associated to malignant transformation such as proliferation, migration and angiogenesis.
  • The expression of five CXC chemokine receptors and their main ligands was analysed by RT-PCR in 31 human astrocytic neoplasms.
  • We show a marked co-localization of CXCR4 and SDF1 in tumour cells, mainly evident in psudolpalisade and microcystic degeneration areas and in the vascular endothelium.
  • These results provide evidence of the expression of multiple CXC chemokines and their receptors in brain tumours and that in particular CXCR4 and SDF1 sustain proliferation and migration of glioma cells to promote malignant progression.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Cell Proliferation. Chemokines, CXC / physiology. Glioma / metabolism. Receptors, Chemokine / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Tumor. DNA Primers. Humans. Immunohistochemistry. Ligands. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16621164.001).
  • [ISSN] 0197-0186
  • [Journal-full-title] Neurochemistry international
  • [ISO-abbreviation] Neurochem. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines, CXC; 0 / DNA Primers; 0 / Ligands; 0 / Receptors, Chemokine
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62. Miracco C, Cosci E, Oliveri G, Luzi P, Pacenti L, Monciatti I, Mannucci S, De Nisi MC, Toscano M, Malagnino V, Falzarano SM, Pirtoli L, Tosi P: Protein and mRNA expression of autophagy gene Beclin 1 in human brain tumours. Int J Oncol; 2007 Feb;30(2):429-36
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  • [Title] Protein and mRNA expression of autophagy gene Beclin 1 in human brain tumours.
  • Beclin 1 is is an autophagy gene, the role of which as a tumour suppressor has recently been recognized in a few studies.
  • We examined the expression of Beclin 1 protein in 212 primary human brain tumours, including 97 high-grade glial tumours, 29 low-grade glial tumours, 4 grade III meningiomas, 19 grade II meningiomas, 52 grade I meningiomas, and 11 medulloblastomas.
  • In most high-grade astrocytic, ependymal neoplasms and atypical meningiomas we found a decrease of cytoplasmic protein expression that was, instead, high in the majority of low-grade tumours and in medulloblastomas.
  • Our observations are in line with studies that demonstrated decreased expression of Beclin 1 in human breast, ovarian, prostate and ovarian cancer and furtherly support its involvement also in brain tumours, which had previously been demonstrated in a few experimental studies, both in spontaneous and in therapy-induced autophagy.
  • Furthermore, our study suggests possible differences of Beclin 1 involvement and its role among the different histotypes of brain neoplasms.
  • Further studies are needed to highlight Beclin 1 function in tumour suppression and/or in tumour survival through autophagy and other related programmed cell death processes in brain tumours.
  • [MeSH-major] Apoptosis Regulatory Proteins / biosynthesis. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Medulloblastoma / metabolism. Membrane Proteins / biosynthesis. Meningioma / metabolism. Oligodendroglioma / metabolism. RNA, Messenger / metabolism

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  • (PMID = 17203225.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / RNA, Messenger
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63. Servotte S, Camby I, Debeir O, Deroanne C, Lambert CA, Lapière CM, Kiss R, Nusgens B, Decaestecker C: The in vitro influences of neurotensin on the motility characteristics of human U373 glioblastoma cells. Neuropathol Appl Neurobiol; 2006 Dec;32(6):575-84
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  • Astrocytic tumours are associated with dismal prognoses due to their pronounced ability to diffusely invade the brain parenchyma.
  • Various neuropeptides, including gastrin, are able to modulate tumour astrocyte migration.
  • Treating U373 tumour cells with 10 nM neurotensin markedly modified the morphological patterns of these cells and also profoundly altered the organization of their actin cytoskeletons.
  • Our data thus strongly suggest that, in addition to gastrin, neurotensin is a neuropeptide capable of modulating tumour astrocyte migration into the brain parenchyma.
  • [MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Glioblastoma / metabolism. Neoplasm Invasiveness. Neurotensin / metabolism
  • [MeSH-minor] Actins / metabolism. Cell Line, Tumor. Cytoskeleton / metabolism. Enzyme Activation / physiology. Humans. In Vitro Techniques. Microscopy, Phase-Contrast. Microscopy, Video. RNA, Messenger / analysis. Receptors, Neurotensin / biosynthesis. cdc42 GTP-Binding Protein / metabolism. rac1 GTP-Binding Protein / metabolism. rhoA GTP-Binding Protein / metabolism

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  • (PMID = 17083472.001).
  • [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 / Actins; 0 / RNA, Messenger; 0 / Receptors, Neurotensin; 39379-15-2 / Neurotensin; EC 3.6.5.2 / cdc42 GTP-Binding Protein; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / rhoA GTP-Binding Protein
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64. Niedzielska G, Niedzielski A, Kotowski M: Nasal ganglioglioma--difficulties in radiological imaging. Int J Pediatr Otorhinolaryngol; 2008 Feb;72(2):285-7
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  • Ganglioglioma is a tumour containing both astrocytic and neuronal components.
  • Most gangliogliomas are observed in the brain, but may also manifest as a nasal glioma.

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  • (PMID = 18093665.001).
  • [ISSN] 0165-5876
  • [Journal-full-title] International journal of pediatric otorhinolaryngology
  • [ISO-abbreviation] Int. J. Pediatr. Otorhinolaryngol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Ireland
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65. Takaya S, Hashikawa K, Turkheimer FE, Mottram N, Deprez M, Ishizu K, Kawashima H, Akiyama H, Fukuyama H, Banati RB, Roncaroli F: The lack of expression of the peripheral benzodiazepine receptor characterises microglial response in anaplastic astrocytomas. J Neurooncol; 2007 Oct;85(1):95-103
ORBi (University of Liege). Free full Text at ORBi .

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  • We examined two anaplastic astrocytomas showing minimal contrast-enhancement and therefore little damage of the blood brain barrier to minimise the presence of blood borne macrophages within tumour tissue.
  • The two lesions were studied in vivo using positron emission tomography (PET) with the specific PBR ligand [(11)C](R)-PK11195 and the corresponding tumour tissue was investigated with an anti-PBR antibody.
  • Our results demonstrated PBR suppression in glioma-infiltrating microglia and suggested that PBR may have a relevant role in modulating the anti-tumour inflammatory response in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Microglia / metabolism. Microglia / pathology. Receptors, GABA-A / biosynthesis

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  • (PMID = 17520179.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U120085814
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Isoquinolines; 0 / RNA, Messenger; 0 / Radiopharmaceuticals; 0 / Receptors, GABA-A; YNF83VN1RL / PK 11195
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66. O'Sullivan JB, Ryan KM, Curtin NM, Harkin A, Connor TJ: Noradrenaline reuptake inhibitors limit neuroinflammation in rat cortex following a systemic inflammatory challenge: implications for depression and neurodegeneration. Int J Neuropsychopharmacol; 2009 Jun;12(5):687-99
Hazardous Substances Data Bank. Norepinephrine .

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  • Evidence suggests that noradrenaline has a tonic anti-inflammatory action in the central nervous system (CNS) via its ability to suppress microglial and astrocytic activation, and inhibit production of inflammatory mediators.
  • This was characterized by a reduction in cortical gene expression of the pro-inflammatory cytokines interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha), the enzyme inducible nitric oxide synthase (iNOS), and the microglial activation markers CD11b and CD40.
  • These results suggest that in vivo administration of NRIs limit inflammatory events in the brain, probably by increasing noradrenaline availability.

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  • (PMID = 19046481.001).
  • [ISSN] 1469-5111
  • [Journal-full-title] The international journal of neuropsychopharmacology
  • [ISO-abbreviation] Int. J. Neuropsychopharmacol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenergic Uptake Inhibitors; 0 / Inflammation Mediators; 0 / Lipopolysaccharides; X4W3ENH1CV / Norepinephrine
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67. El Ayachi I, Baeza N, Fernandez C, Colin C, Scavarda D, Pesheva P, Figarella-Branger D: KIAA0510, the 3'-untranslated region of the tenascin-R gene, and tenascin-R are overexpressed in pilocytic astrocytomas. Neuropathol Appl Neurobiol; 2010 Aug;36(5):399-410

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  • We took advantage of our previous study focused on genes that were critical in tumour invasion to further study here an unknown sequence, referred to as KIAA0510, the chromosomal location of which was 1q25, described as a 5596-bp long mRNA and that we found to be significantly overexpressed in pilocytic astrocytomas compared with glioblastomas.
  • We also analysed a large series of various brain tumours and found that in the group of astrocytic tumours, tenascin-R expression decreased with malignancy, whereas oligodendrogliomas sometimes retained a high level of tenascin-R even in high-grade tumours.
  • In normal brain, tenascin-R was exclusively expressed by normal oligodendrocytes and subsets of neurones during post-natal development and in adulthood, where it could differentially affect cellular adhesiveness and/or differentiation.
  • Whether tenascin-R overexpression negatively influences brain invasion remains to be determined.
  • [MeSH-major] Astrocytoma / genetics. Cerebellar Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Tenascin / genetics

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  • (PMID = 20202125.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / Tenascin; 147604-77-1 / tenascin R
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68. Walmsley GL, Chandler K, Davies ES, Lamb CR, Smyth B, Summers BA: Multi-focal cerebral oligoastrocytoma in a puppy. J Small Anim Pract; 2009 Aug;50(8):435-9
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  • [Title] Multi-focal cerebral oligoastrocytoma in a puppy.
  • Magnetic resonance imaging identified multiple, large lesions involving both cerebral hemispheres.
  • Histopathology following post-mortem examination found a mixed glial cell tumour with discrete areas where neoplastic cells appeared oligodendroglial or astrocytic.
  • Primary intracranial neoplasia is a rare cause of neurological disease in young dogs.
  • Moreover, this case is unusual in terms of both the mixed glial nature of the neoplasm and also its multi-focal distribution.
  • [MeSH-major] Astrocytoma / veterinary. Brain Neoplasms / veterinary. Neoplasms, Multiple Primary / veterinary

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  • (PMID = 19689673.001).
  • [ISSN] 1748-5827
  • [Journal-full-title] The Journal of small animal practice
  • [ISO-abbreviation] J Small Anim Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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69. Felsberg J, Yan PS, Huang TH, Milde U, Schramm J, Wiestler OD, Reifenberger G, Pietsch T, Waha A: DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours. Neuropathol Appl Neurobiol; 2006 Oct;32(5):517-24
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  • Using differential methylation hybridization as a genome-wide screening approach to determine DNA methylation patterns in gliomas, we recently identified two DNA fragments in 14q23.1 (CGI-clone musical sharp396) and 14q32.12 (CGI-clone musical sharp519) that were differentially methylated between astrocytic gliomas and mixed oligoastrocytomas.
  • To validate this observation, we examined these 14q32.12 locus for methylation in an extended series of 43 astrocytic and oligodendroglial gliomas.
  • Microsatellite analysis showed LOH in seven of 28 (25%) oligodendroglial tumours and three of 15 (20%) astrocytic tumours.
  • Taken together, our data lend further support for the location of one or more yet to be identified glioma-associated tumour suppressor gene(s) on 14q.
  • [MeSH-major] Brain Neoplasms / pathology. Chromosomes, Human, Pair 14 / genetics. DNA Methylation. Oligodendroglia / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Alleles. Child. Child, Preschool. DNA, Neoplasm / drug effects. Female. Humans. Male. Microsatellite Repeats / genetics. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Sulfites / pharmacology

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  • (PMID = 16972885.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Sulfites; TZX5469Z6I / sodium bisulfite
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70. Rose SR, Danish RK, Kearney NS, Schreiber RE, Lustig RH, Burghen GA, Hudson MM: ACTH deficiency in childhood cancer survivors. Pediatr Blood Cancer; 2005 Nov;45(6):808-13
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  • [Title] ACTH deficiency in childhood cancer survivors.
  • We assessed the prevalence of ACTHD in survivors of childhood cancer according to tumor diagnosis/therapy.
  • PROCEDURE: Chart review of endocrine/oncology history was performed in 310 childhood cancer survivors.
  • Of the 56 with ACTHD, 53 (95%) had received cranial irradiation (mean 45.5 Gy, range 14-70 Gy); three had not: one each with craniopharyngioma, hypothalamic astrocytoma, and brain stem glioma.
  • CONCLUSIONS: Childhood cancer survivors with greatest risk for ACTHD had craniopharyngioma, other suprasellar tumor, or medulloblastoma or > or =24 Gy cranial irradiation.
  • We recommend annual testing for ACTHD for 10-15 years and continued lifelong surveillance after CNS tumor or cranial irradiation, in patients with other hypothalamic-pituitary deficiencies or symptoms of ACTHD.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15700255.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R25 CA023944
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 9002-60-2 / Adrenocorticotropic Hormone
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71. Figarella-Branger D, Bouvier C: [Histological classification of human gliomas: state of art and controversies]. Bull Cancer; 2005 Apr;92(4):301-9
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  • The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.
  • In particular this classification does not take into account the intrinsic morphological heterogeneity of infiltrative gliomas and does not discriminate the tumour cells from the residual brain parenchyma.
  • According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).
  • In contrast, the Sainte Anne classification takes into account the macroscopic informations provided by imaging techniques and the tumour growth patterns.
  • Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.
  • According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).
  • [MeSH-major] Brain Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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  • (PMID = 15888386.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
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72. Tanaka KF, Ochi N, Hayashi T, Ikeda E, Ikenaka K: Fluoro-Jade: new fluorescent marker of Rosenthal fibers. Neurosci Lett; 2006 Oct 23;407(2):127-30

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  • Fluoro Jade-positive masses were seen in samples of Alexander disease brain, pilocytic astrocytoma, and in brain tissue from a mouse model of Alexander disease.
  • [MeSH-minor] Animals. Astrocytoma / pathology. Brain / pathology. Brain Diseases / pathology. Fluoresceins. Fluorescent Antibody Technique. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Mice. Mice, Transgenic. Microscopy, Confocal. Organic Chemicals. Tissue Embedding. Tissue Fixation

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  • (PMID = 16949206.001).
  • [ISSN] 0304-3940
  • [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 / Fluoresceins; 0 / Fluorescent Dyes; 0 / Glial Fibrillary Acidic Protein; 0 / Organic Chemicals; 0 / fluoro jade
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73. Laczko R, Szauter KM, Jansen MK, Hollosi P, Muranyi M, Molnar J, Fong KS, Hinek A, Csiszar K: Active lysyl oxidase (LOX) correlates with focal adhesion kinase (FAK)/paxillin activation and migration in invasive astrocytes. Neuropathol Appl Neurobiol; 2007 Dec;33(6):631-43
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  • The extracellular matrix (ECM) plays a critical role during the development and invasion of primary brain tumours.
  • We have recently reported the ECM enzyme, lysyl oxidase (LOX), in the central nervous system and observed up-regulation of LOX in anaplastic astrocytoma cells.
  • While the catalytic function of LOX is essential for cross-linking of ECM proteins, we also reported that LOX induced invasive and metastatic properties in breast tumour epithelial cells through hydrogen peroxide-mediated FAK/Src activation.
  • Results demonstrate that increased expression and activity of LOX positively correlated with invasive phenotype of malignant astrocytoma cell lines.
  • Immunohistochemistry detected increased LOX within tumour cells and ECM in grade I-IV astrocytic neoplasm compared with normal brain and coincidence of increased LOX with the loss of glial fibrillary acidic protein in higher-grade tumours.
  • These results demonstrate an important LOX-mediated mechanism that promotes migratory/invasive behaviour of malignant astrocytes.
  • [MeSH-major] Astrocytes / enzymology. Brain Neoplasms / enzymology. Enzyme Activation / physiology. Focal Adhesion Protein-Tyrosine Kinases / metabolism. Paxillin / metabolism. Protein-Lysine 6-Oxidase / metabolism
  • [MeSH-minor] Astrocytoma / enzymology. Blotting, Western. Cell Line, Tumor. Cell Movement / physiology. Humans. Immunohistochemistry. Neoplasm Invasiveness. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17931358.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR47713; United States / NCRR NIH HHS / RR / G12RR003096
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Paxillin; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
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74. Bäcklund LM, Nilsson BR, Liu L, Ichimura K, Collins VP: Mutations in Rb1 pathway-related genes are associated with poor prognosis in anaplastic astrocytomas. Br J Cancer; 2005 Jul 11;93(1):124-30
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  • Anaplastic astrocytoma (AA, WHO grade III) is, second to Glioblastoma, the most common and most malignant type of adult CNS tumour.
  • The survival data on 37 carefully sampled AA was correlated with the results of a detailed analysis of the status of nine genes known to be involved in the development of astrocytic tumours.
  • We found that loss of both wild-type copies of any of the three tumour suppressor genes CDKN2A, CDKN2B and RB1 or gene amplification of CDK4, disrupting the Rb1 pathway, were associated with shorter survival (P=0.009).
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Genes, Retinoblastoma. Mutation


75. Reyaz N, Tayyab M, Khan SA, Siddique T: Correlation of glial fibrillary acidic protein (GFAP) with grading of the neuroglial tumours. J Coll Physicians Surg Pak; 2005 Aug;15(8):472-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The non-neoplastic brain tissue was used as positive control, while cases reported medulloblastoma tumour was used as negative control.
  • We applied a scoring scale 0 to 3+, to evaluate its correlation with the grade of tumour.
  • The 35 cases of various grade astrocytoma showed a varying intensity of GFAP staining.
  • Similarly, 3 cases of glioblastoma multiforme, 2 cases of sub-ependymal giant cell astrocytoma, 2 cases of pleomorphic xanthoastrocytoma, 2 out of 4 cases of ependymoma and the case of oligoastrocytoma showed a positive reaction.
  • Comparison of the histological grade with GFAP score was significantly higher in high grade tumour when compared with tumour of grade I (p<0.001).
  • In astrocytic neoplasms the number of GFAP positive cells and the intensity of the stain were directly proportional to the degree of malignancy.
  • Only astrocytic component was positive which are poorly visualize by H&E stain.
  • [MeSH-major] Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Glial Fibrillary Acidic Protein / metabolism. Glioma / metabolism. Glioma / pathology
  • [MeSH-minor] Astrocytoma / metabolism. Astrocytoma / pathology. Child. Female. Humans. Immunoenzyme Techniques. Immunohistochemistry. Male. Neuroglia / metabolism. Oligodendroglioma / metabolism

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  • (PMID = 16202357.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein
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76. Ng WH, Lim T, Yeo TT: Pleomorphic xanthoastrocytoma in elderly patients may portend a poor prognosis. J Clin Neurosci; 2008 Apr;15(4):476-8
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  • Pleomorphic xanthoastrocytoma (PXA) is a rare primary astrocytic tumour of the nervous system usually involving the superficial temporal cortex of children and young adults.
  • Although the tumour may exhibit histological features of pleomorphism or cellular atypia, the overall prognosis is good compared with other glial tumours, with only 30% of PXA recurring and 20% undergoing anaplastic transformation.
  • Rarely, in older patients, PXA may have a poor prognosis as these patients tend to have intracranial hypertension and focal deficits, as well as histological features of mitosis, increased cellularity and necrosis.
  • Although a rare and benign tumour type, PXA in the elderly tend to be more malignant, may have the radiological appearance of a malignant tumour and have poor prognosis.
  • [MeSH-major] Astrocytoma / diagnosis. Brain Neoplasms / diagnosis
  • [MeSH-minor] Aged. Female. Glioblastoma / diagnosis. Humans. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging. Prognosis. Temporal Lobe / pathology

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  • (PMID = 18255294.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Ki-67 Antigen
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77. Loyant V, Jaffré A, Breton J, Baldi I, Vital A, Chapon F, Dutoit S, Lecluse Y, Loiseau H, Lebailly P, Gauduchon P: Screening of TP53 mutations by DHPLC and sequencing in brain tumours from patients with an occupational exposure to pesticides or organic solvents. Mutagenesis; 2005 Sep;20(5):365-73
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  • [Title] Screening of TP53 mutations by DHPLC and sequencing in brain tumours from patients with an occupational exposure to pesticides or organic solvents.
  • The aetiology of brain tumours remains unclear.
  • The case-control study CEREPHY (221 cases, 442 controls) carried in the Departement de la Gironde in France revealed a significantly increased risk of brain tumours for subjects most exposed to pesticides.
  • These mutations are present in approximately 30% of astrocytic brain tumours.
  • In a pilot study, we explored the hypothesis that pesticide or solvent exposure could raise the frequency of TP53 mutations in brain tumour cells.
  • We investigated TP53 mutations in exons 2-11 by denaturing high performance liquid chromatography (DHPLC) and sequencing, and p53 accumulation by immunohistochemistry in brain tumour of the 30 patients from CEREPHY study with a history of occupational exposure to pesticides (n = 21) and/or organic solvents (n = 14) for whom tumoral tissue was available.
  • These preliminary results, even if it was on a limited number of tumours, are not in favour of the role of pesticide or organic solvent exposure in the occurrence of TP53 mutations in brain tumours.
  • [MeSH-major] Brain Neoplasms / chemically induced. Mutagens / toxicity. Occupational Exposure. Pesticides / toxicity. Solvents / toxicity. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Case-Control Studies. Chromatography, High Pressure Liquid. DNA Mutational Analysis. DNA, Neoplasm / analysis. Exons / genetics. Female. Humans. Male. Mutation. Nucleic Acid Denaturation

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  • (PMID = 16105905.001).
  • [ISSN] 0267-8357
  • [Journal-full-title] Mutagenesis
  • [ISO-abbreviation] Mutagenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Mutagens; 0 / Pesticides; 0 / Solvents; 0 / Tumor Suppressor Protein p53
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78. Mondal S, Dirks P, Rutka JT: Immunolocalization of fascin, an actin-bundling protein and glial fibrillary acidic protein in human astrocytoma cells. Brain Pathol; 2010 Jan;20(1):190-9
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  • [Title] Immunolocalization of fascin, an actin-bundling protein and glial fibrillary acidic protein in human astrocytoma cells.
  • A role for fascin in cell migration has led to its study in many tumor types.
  • We show that fascin is expressed in astrocytes and in a panel of human astrocytoma cell lines.
  • Immunofluorescence analysis demonstrates that fascin and the intermediate filament protein, glial fibrillary acidic protein (GFAP), are both expressed in the perinuclear region and within cytoplasmic processes of astrocytes and astrocytoma cells.
  • These data show that fascin and GFAP are immunolocalized regionally within cells and tumors of astrocytic origin and suggest that their binding may occur during dynamic reorganization of intermediate filaments.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / ultrastructure. Carrier Proteins / metabolism. Glial Fibrillary Acidic Protein / metabolism. Microfilament Proteins / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Movement. Cytoskeletal Proteins / metabolism. Fluorescent Antibody Technique. Fluorescent Dyes. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Immunoprecipitation. Indoles. Microscopy, Confocal. Mitosis. Phosphorylation. Stem Cells / metabolism. Stem Cells / ultrastructure

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  • (PMID = 19170683.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / Fluorescent Dyes; 0 / Glial Fibrillary Acidic Protein; 0 / Indoles; 0 / Microfilament Proteins; 146808-54-0 / fascin; 47165-04-8 / DAPI
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79. Niizuma K, Fujimura M, Kumabe T, Tominaga T: Malignant transformation of high-grade astrocytoma associated with neurocysticercosis in a patient with Turcot syndrome. J Clin Neurosci; 2007 Jan;14(1):53-5
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  • [Title] Malignant transformation of high-grade astrocytoma associated with neurocysticercosis in a patient with Turcot syndrome.
  • A 45-year-old woman with anaplastic astrocytoma was clinically diagnosed with Turcot syndrome, and subsequently developed simultaneous neurocysticercosis and malignant transformation to glioblastoma.
  • Histological examination of surgical specimens revealed neurocysticercosis between the normal brain tissue and glioblastoma.
  • The clinical course and histological findings suggest that the parasitic infection and/or genetic changes contributed to the malignant transformation of the astrocytic tumour.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Cell Transformation, Neoplastic / pathology. Glioblastoma / pathology. Neurocysticercosis / pathology

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  • (PMID = 17138070.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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80. Bernreuther C, Salein N, Matschke J, Hagel C: Expression of doublecortin in tumours of the central and peripheral nervous system and in human non-neuronal tissues. Acta Neuropathol; 2006 Mar;111(3):247-54
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  • Glioneuronal tumours and oligodendrogliomas grade II and III uniformly showed a high intensity and frequency of doublecortin staining, whereas intermediate doublecortin expression was observed in astrocytic tumours of grade II-IV.
  • Double staining of tumour tissue revealed co-expression of doublecortin and neurofilament in cells of gangliocytomas and gangliogliomas and co-expression of doublecortin with S100 protein or GFAP in glial tumours, respectively.
  • Interestingly, doublecortin expression could not be shown in brain metastases of tumours originating from these tissues.
  • In conclusion, doublecortin can be regarded as specific neuronal marker only in normal developing brain, but lacks specificity in glioneuronal and glial tumours and other non-neuronal human tissues where it is expressed in a wide variety of tumours and tissues.
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Differentiation. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Humans. Nerve Sheath Neoplasms / metabolism. Nerve Sheath Neoplasms / pathology. Neurilemmoma / metabolism. Neurilemmoma / pathology. Neurofibroma / metabolism. Neurofibroma / pathology. Neurons / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Teratoma / metabolism. Teratoma / pathology

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  • (PMID = 16520969.001).
  • [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 / Biomarkers, Tumor; 0 / Microtubule-Associated Proteins; 0 / Neuropeptides; 0 / RNA, Messenger; 0 / doublecortin protein
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81. Schittenhelm J, Beschorner R, Simon P, Tabatabai G, Herrmann C, Schlaszus H, Capper D, Weller M, Meyermann R, Mittelbronn M: Diagnostic value of WT1 in neuroepithelial tumours. Neuropathol Appl Neurobiol; 2009 Feb;35(1):69-81
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  • AIMS: Currently, clinical trials using WT1 (Wilms tumour gene) peptide vaccines are conducted in haematopoietic malignancies and solid cancers.
  • Single reports showed that the Wilms tumour gene product WT1 is also expressed in astrocytic neoplasms.
  • Controlling for WHO grade, the comparison of oligodendrogliomas with ependymal and astrocytic tumours showed higher expression values for the latter.
  • These results suggest an important role of WT1 in tumourigenesis and progression in human brain tumours.
  • [MeSH-major] Brain Neoplasms / diagnosis. Neoplasms, Neuroepithelial / diagnosis. WT1 Proteins / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Brain / metabolism. Child. Endothelial Cells / metabolism. Female. Humans. Immunohistochemistry. Logistic Models. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Array Analysis. Young Adult

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  • (PMID = 18466223.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / WT1 Proteins
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82. Joensuu H, Puputti M, Sihto H, Tynninen O, Nupponen NN: Amplification of genes encoding KIT, PDGFRalpha and VEGFR2 receptor tyrosine kinases is frequent in glioblastoma multiforme. J Pathol; 2005 Oct;207(2):224-31
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  • The frequency of KIT and VEGFR2 amplification in glioblastomas is not known, and few data are available in any other human tumour type.
  • The four secondary glioblastomas arising from pre-existing lower grade astrocytic tumours investigated had KIT amplification but none had EGFR amplification.
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Vascular Endothelial Growth Factor Receptor-2 / genetics

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16021678.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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83. Strojnik T, Kavalar R, Zajc I, Diamandis EP, Oikonomopoulou K, Lah TT: Prognostic impact of CD68 and kallikrein 6 in human glioma. Anticancer Res; 2009 Aug;29(8):3269-79
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  • AIMS: To evaluate the expression of CD68 and kallikrein 6 in human gliomas, and investigate their prognostic significance for survival of brain cancer patients in comparison to some known prognostic markers.
  • PATIENTS AND METHODS: Histological sections of 51 primary astrocytic tumours (11 benign, 40 malignant) were immunohistochemically stained for CD68, cathepsin B, kallikrein 6 and Ki-67.
  • CD68 and kallikrein 6 expressions were also analyzed by real-time PCR in nine brain tumour biopsies.
  • RESULTS: Both microglia and tumour cells expressed CD68.
  • High CD68 and cathepsin B staining scores were significantly, more frequent in the malignant than in the benign tumours (p=0.036 and p=0.014, respectively).
  • In contrast, the benign group presented a stronger immunoreactivity for kallikrein 6 compared with the malignant tumours (p=0.013).
  • A CD68 staining score of tumour cells higher than 3 was a significant predictor of shorter overall survival (p<0.01) in all patients and of borderline significance in the malignant group (p=0.057).
  • CONCLUSION: Kallikrein 6 was down-regulated in malignant glioma, but this differential expression did not have an impact on patient prognosis.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. Kallikreins / metabolism
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19661345.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / RNA, Messenger; EC 3.4.21.- / KLK6 protein, human; EC 3.4.21.- / Kallikreins
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84. Mokrý J, Ehrmann J, Karbanová J, Cízková D, Soukup T, Suchánek J, Filip S, Kolár Z: Expression of intermediate filament nestin in blood vessels of neural and non-neural tissues. Acta Medica (Hradec Kralove); 2008;51(3):173-9

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  • To reach this goal we performed double immunofluorescent study to co-localize nestin with endothelium-specific markers (CD31, CD34 II, vimentin) or markers of perivascular cells (GFAP, SMA) in paraffin-embedded sections of normal human brain tissue, low- and high-grade gliomas, postinfarcted heart and samples of non-neural tumours.
  • Double immunostaining provided unambiguous evidence that endothelial cells expressed nestin and allowed them to distinguish from other nestin+ elements (perivascular astrocytic endfeet, undifferentiated tumour cells, smooth muscle cells and pericytes).

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  • (PMID = 19271685.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / Vimentin
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85. Masi A, Becchetti A, Restano-Cassulini R, Polvani S, Hofmann G, Buccoliero AM, Paglierani M, Pollo B, Taddei GL, Gallina P, Di Lorenzo N, Franceschetti S, Wanke E, Arcangeli A: hERG1 channels are overexpressed in glioblastoma multiforme and modulate VEGF secretion in glioblastoma cell lines. Br J Cancer; 2005 Oct 3;93(7):781-92
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  • The expression pattern of these two channels was compared to that of the classical inward rectifying K(+) channels, IRK, that are widely expressed in astrocytic cells and classically considered a marker of astrocytic differentiation.
  • Our data provide important confirmation for studies proposing the hERG1 channel as a molecular marker of tumour progression and a possible target for novel anticancer therapies.
  • [MeSH-major] Brain Neoplasms / metabolism. Glioblastoma / metabolism. Potassium Channels, Voltage-Gated / metabolism. Vascular Endothelial Growth Factor A / secretion
  • [MeSH-minor] Adult. Aged. Base Sequence. Cell Line, Tumor. Child. DNA Primers. Ether-A-Go-Go Potassium Channels. Female. Humans. Immunohistochemistry. Male. Middle Aged. Patch-Clamp Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16175187.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / ERG1 potassium channel; 0 / Ether-A-Go-Go Potassium Channels; 0 / Potassium Channels, Voltage-Gated; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC2361632
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86. Zscharnack K, Kessler R, Bleichert F, Warnke JP, Eschrich K: The PFKFB3 splice variant UBI2K4 is downregulated in high-grade astrocytomas and impedes the growth of U87 glioblastoma cells. Neuropathol Appl Neurobiol; 2009 Dec;35(6):566-78
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  • Here, we studied the role of the PFKFB3 splice variants in human astrocytic gliomas.
  • METHODS: We analysed the PFKFB3 splice variants in 48 astrocytic gliomas by RT-PCR and real-time PCR.
  • RESULTS: UBI2K5 and UBI2K6 are the predominant splice variants in rapidly proliferating high-grade astrocytomas while the expression of UBI2K3 and UBI2K4 is mainly restricted to low-grade astrocytomas and nonneoplastic brain tissue.
  • The UBI2K4 mRNA level is downregulated in astrocytic gliomas with increasing malignancy grade.
  • Moreover, the UBI2K4 mRNA level correlates with growth rate of several human cancer cell lines derived from different tissue types.
  • CONCLUSIONS: Our results demonstrate that the splice variant UBI2K4 impedes the tumour cell growth and might serve as a tumour suppressor in astrocytic tumours.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Phosphofructokinase-2 / metabolism
  • [MeSH-minor] Brain / metabolism. Cell Count. Cell Line, Tumor. Cell Proliferation. Cell Survival. Down-Regulation. Humans. Neoplasm Staging. Polymerase Chain Reaction. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Transfection

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  • (PMID = 19490427.001).
  • [ISSN] 1365-2990
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; EC 2.7.1.105 / PFKFB3 protein, human; EC 2.7.1.105 / Phosphofructokinase-2
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87. Abdel-Fattah R, Xiao A, Bomgardner D, Pease CS, Lopes MB, Hussaini IM: Differential expression of HOX genes in neoplastic and non-neoplastic human astrocytes. J Pathol; 2006 May;209(1):15-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • HOX genes are involved in malignant transformation and progression of different types of tumour.
  • RT-PCR, quantitative real-time PCR, immunocytochemistry, and western blot analyses revealed differential expression of nine HOX genes (A6, A7, A9, A13, B13, D4, D9, D10, and D13) in normal human astrocytic cell lines and non-neoplastic temporal lobe specimens.
  • The differential expression of HOX genes in normal and neoplastic astrocytes suggests a role for these genes in brain tumourigenesis.
  • [MeSH-minor] Astrocytoma / genetics. Astrocytoma / metabolism. Blotting, Western. Cell Line. DNA, Complementary / genetics. DNA, Neoplasm / genetics. Gene Expression. Gene Expression Profiling / methods. Homeodomain Proteins / metabolism. Humans. Neoplasm Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Temporal Lobe / metabolism. Tumor Cells, Cultured

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16463268.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90851; United States / NINDS NIH HHS / NS / NS35122
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins
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