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Items 1 to 46 of about 46
1. Hiremath GK, Bingaman WE, Prayson RA, Nair D: Oligoastrocytoma presenting with intractable epilepsy. Epileptic Disord; 2007 Sep;9(3):315-22
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  • OBJECTIVE: Oligoastrocytomas (OA) are mixed gliomas with distinct oligodendroglial and astrocytic neoplastic components.
  • Median age at diagnosis was 25 years (range 19-44 years).
  • Tumors arose from the left side in all patients and from the temporal lobe in five patients.
  • Median length of refractory epilepsy prior to surgery was 10.5 years (range 1-28 years), and the median number of antiepileptic drugs used was 2 (range 1-10).
  • There were no surgical complications, clinical or radiographic tumor recurrence at a mean follow up period of 3.2 years (range 2-8).
  • CONCLUSION: As a result of our small sample size, general conclusions may be imprecise, but this review suggests that OA behave similar to other tumors related to intractable epilepsy: they usually have a preoperative seizure course of many years, an excellent rate of seizure-freedom following surgery, and are in general, low-grade tumors with an indolent course for which serial imaging is sufficient follow-up.
  • [MeSH-major] Astrocytoma / complications. Brain Neoplasms / complications. Epilepsy / drug therapy. Epilepsy / etiology
  • [MeSH-minor] Adolescent. Adult. Anticonvulsants / therapeutic use. Craniotomy. Drug Resistance. Epilepsy, Complex Partial / etiology. Epilepsy, Complex Partial / surgery. Female. Humans. Magnetic Resonance Imaging. Male. Memory / physiology. Neoplasm Recurrence, Local. Neurosurgical Procedures. Temporal Lobe / pathology. Temporal Lobe / surgery

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  • (PMID = 17884756.001).
  • [ISSN] 1294-9361
  • [Journal-full-title] Epileptic disorders : international epilepsy journal with videotape
  • [ISO-abbreviation] Epileptic Disord
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anticonvulsants
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2. Nakamura M, Watanabe T, Yonekawa Y, Kleihues P, Ohgaki H: Promoter methylation of the DNA repair gene MGMT in astrocytomas is frequently associated with G:C --> A:T mutations of the TP53 tumor suppressor gene. Carcinogenesis; 2001 Oct;22(10):1715-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter methylation of the DNA repair gene MGMT in astrocytomas is frequently associated with G:C --> A:T mutations of the TP53 tumor suppressor gene.
  • Repair of O(6)-alkylguanine adducts by tumour cells has been implicated in drug resistance since it reduces the cytotoxicity of alkylating chemotherapeutic agents.
  • We assessed promoter methylation of the MGMT gene in astrocytic brain tumours by methylation-specific PCR.
  • MGMT promoter methylation was detected in 26 of 54 (48%) low-grade diffuse astrocytomas (WHO grade II) and in 12 of 16 (75%) of secondary glioblastomas (WHO grade IV) that had progressed from low-grade astrocytomas.
  • The frequency of MGMT methylation was significantly lower in primary (de novo) glioblastomas (13 of 36, 36%, P = 0.0155).
  • [MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. DNA Methylation. Genes, p53 / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Point Mutation. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Adult. Aged. DNA Primers / chemistry. DNA Repair / genetics. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 11577014.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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3. Xu GW, Nutt CL, Zlatescu MC, Keeney M, Chin-Yee I, Cairncross JG: Inactivation of p53 sensitizes U87MG glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea. Cancer Res; 2001 May 15;61(10):4155-9
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  • These studies were motivated by three observations: (a) some human astrocytomas are sensitive to BCNU and some are resistant;.
  • (b) chemosensitive astrocytomas are more likely to be found in young adults whose tumors are more likely to harbor a p53 mutation; and (c) mouse astrocytes lacking the p53 gene are more sensitive to BCNU than wild-type cells.
  • The question arises of whether p53 dysfunction might be a chemosensitizing genetic alteration in human astrocytic gliomas.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Carmustine / pharmacology. Glioma / drug therapy. Glioma / genetics. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Survival / genetics. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Cyclins / genetics. DNA Repair / physiology. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Transfection. Tumor Cells, Cultured

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  • (PMID = 11358839.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Tumor Suppressor Protein p53; U68WG3173Y / Carmustine
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4. Bello MJ, Alonso ME, Amiñoso C, Anselmo NP, Arjona D, Gonzalez-Gomez P, Lopez-Marin I, de Campos JM, Gutierrez M, Isla A, Kusak ME, Lassaletta L, Sarasa JL, Vaquero J, Casartelli C, Rey JA: Hypermethylation of the DNA repair gene MGMT: association with TP53 G:C to A:T transitions in a series of 469 nervous system tumors. Mutat Res; 2004 Oct 4;554(1-2):23-32
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  • [Title] Hypermethylation of the DNA repair gene MGMT: association with TP53 G:C to A:T transitions in a series of 469 nervous system tumors.
  • O6-methylguanine-DNA methyltransferase (MGMT) plays a major role in repairing DNA damage from alkylating agents.
  • By removing alkyl groups from the O6-position in guanine, MGMT can prevent G:C to A:T transition mutations, a type of variation frequently involving TP53 mutations in brain tumors.
  • Promoter hypermethylation of CpG islands in tumor-related genes can lead to their transcriptional inactivation, and this epigenetic mechanism has been shown to participate in MGMT silencing in some cancers, including those affecting the nervous system.
  • Accordingly, a link between both genetic and epigenetic anomalies may exist in these neoplasms.
  • To determine the relevance of defective MGMT function due to aberrant methylation in relation to the presence of TP53 mutations, we studied 469 nervous system tumors (including all major histological subtypes) for MGMT promoter methylation and TP53 mutations at exons 5-8.
  • Overall, aberrant methylation occurred in 38% of the samples (180/469), with values higher than 50% in the more malignant forms such as glioblastomas and anaplastic gliomas including those with astrocytic, oligodendroglial and ependymal differentiation.
  • In contrast, the non-glial tumors displayed an overall aberrant MGMT promoter methylation of 26%, even though this group includes highly malignant tumors such as neuroblastomas, medulloblastomas and brain metastases.
  • Overall, TP53 mutations were found in 25% of the methylated MGMT tumors (45/180), whereas only 10% of the unmethylated MGMT tumors (30/289) showed TP53 changes (P < 0.001).
  • G:C to A:T changes occurred at CpG sites in 9% of methylated tumors, and in 0.7% of the unmethylated samples.
  • This type of transition at non-CpG dinucleotides was also more frequent in the tumors with aberrant MGMT methylation (5%) than the unmethylated tumors (0.7%).
  • These data suggest that MGMT silencing as a result of promoter hypermethylation may lead to G:C to A:T transition mutations in the TP53 gene of some histological nervous system tumor subtypes.
  • [MeSH-major] DNA Methylation. DNA Repair / genetics. Genes, p53. Nervous System Neoplasms / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Child. Child, Preschool. DNA Primers. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational

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  • (PMID = 15450401.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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5. Aronica E, Gorter JA, Jansen GH, van Veelen CW, van Rijen PC, Leenstra S, Ramkema M, Scheffer GL, Scheper RJ, Troost D: Expression and cellular distribution of multidrug transporter proteins in two major causes of medically intractable epilepsy: focal cortical dysplasia and glioneuronal tumors. Neuroscience; 2003;118(2):417-29
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  • [Title] Expression and cellular distribution of multidrug transporter proteins in two major causes of medically intractable epilepsy: focal cortical dysplasia and glioneuronal tumors.
  • The cell-specific distribution of multidrug resistance extrusion pumps was studied in developmental glioneuronal lesions, including focal cortical dysplasia (15 cases) and ganglioglioma (15 cases) from patients with medically intractable epilepsy.
  • MRP1 and P-gp immunoreactivity was observed in dysplastic neurons of 11/15 cases of focal cortical dysplasia, as well as in the neuronal component of 14/15 ganglioglioma.
  • Glial cells with astrocytic morphology within the lesion showed multidrug-resistant protein immunoreactivity (P-gp>MRP1).
  • Moderate to strong MRP1 and P-gp immunoreactivity was observed in a population of large ballooned neuroglial cells.
  • P-gp appeared to be most frequently expressed in glial fibrillary acidic protein-positive balloon cells (glial type), whereas MRP1 was more frequently expressed in microtubule-associated protein 2-positive balloon cells (neuronal type).
  • The predominant intralesional cell-specific distribution of multidrug transporter proteins supports the hypothesis of a constitutive overexpression as common mechanism underlying the intrinsic pharmaco-resistance to antiepileptic drugs of both malformative and neoplastic glioneuronal developmental lesions.
  • [MeSH-major] Cerebral Cortex / metabolism. Epilepsy / metabolism. Ganglioglioma / metabolism. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / metabolism
  • [MeSH-minor] Adolescent. Adult. Brain / metabolism. Brain / pathology. Child. Child, Preschool. Endothelium / metabolism. Endothelium / pathology. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Infant. Male. Microtubule-Associated Proteins / metabolism. Middle Aged. Nerve Tissue Proteins / metabolism. Neuroglia / metabolism. Neuroglia / pathology. Neurons / metabolism. Neurons / pathology. Nuclear Proteins / metabolism. Synaptophysin / metabolism. Vimentin / metabolism

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  • (PMID = 12699778.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Microtubule-Associated Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / P-Glycoprotein; 0 / Synaptophysin; 0 / Vimentin; 0 / multidrug resistance-associated protein 1; 0 / neugrin
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6. Lin JH, Takano T, Cotrina ML, Arcuino G, Kang J, Liu S, Gao Q, Jiang L, Li F, Lichtenberg-Frate H, Haubrich S, Willecke K, Goldman SA, Nedergaard M: Connexin 43 enhances the adhesivity and mediates the invasion of malignant glioma cells. J Neurosci; 2002 Jun 1;22(11):4302-11
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  • [Title] Connexin 43 enhances the adhesivity and mediates the invasion of malignant glioma cells.
  • A hallmark of astrocytic tumors is their infiltrative nature.
  • Although their aggressive and typically widespread dispersal in the adult brain differs fundamentally from that of other brain tumors, little is known about their cellular basis.
  • Astrocytic tumors express the gap junction protein connexin 43 (Cx43), and we show here that Cx43 expression induced the morphological transformation of glioma cells into an epithelial phenotype.
  • Apart from their role in gap junction formation, connexins may therefore be considered a distinct class of membrane proteins with adhesive properties.
  • Cx43 expression therefore may modulate not only the adhesion of astrocytes to one another, but the spread of glial tumor cells throughout astrocytic syncytia.
  • These observations widen our concept of the potential interactions between tumor cells and their surroundings and suggest that both connexin proteins and their derived gap junctions are critical determinants of the invasiveness of central gliomas.
  • [MeSH-major] Brain Neoplasms / metabolism. Connexin 43 / biosynthesis. Glioma / metabolism. Neoplasms, Experimental / metabolism
  • [MeSH-minor] Animals. Antibodies / pharmacology. Astrocytes / cytology. Cell Adhesion / genetics. Cell Aggregation / drug effects. Cells, Cultured. Connexins / biosynthesis. Connexins / genetics. Dose-Response Relationship, Drug. Fluorescent Dyes. Gap Junctions / metabolism. Gap Junctions / pathology. Immunohistochemistry. Male. Mutagenesis, Site-Directed. Neoplasm Invasiveness. Neoplasm Transplantation. Patch-Clamp Techniques. Permeability. Rats. Rats, Wistar. Structure-Activity Relationship. Transfection. Tumor Cells, Cultured

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  • (PMID = 12040035.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01NS29813; United States / NINDS NIH HHS / NS / R01NS30007; United States / NINDS NIH HHS / NS / R01NS33106; United States / NINDS NIH HHS / NS / R01NS38073
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Connexin 43; 0 / Connexins; 0 / Fluorescent Dyes; 0 / connexin 32
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7. Pallini R, Pierconti F, Falchetti ML, D'Arcangelo D, Fernandez E, Maira G, D'Ambrosio E, Larocca LM: Evidence for telomerase involvement in the angiogenesis of astrocytic tumors: expression of human telomerase reverse transcriptase messenger RNA by vascular endothelial cells. J Neurosurg; 2001 Jun;94(6):961-71
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  • [Title] Evidence for telomerase involvement in the angiogenesis of astrocytic tumors: expression of human telomerase reverse transcriptase messenger RNA by vascular endothelial cells.
  • OBJECT: Evidence from recent in vitro studies indicates that reactivation of telomerase, the enzyme that synthesizes the telomere ends of chromosomes, is a crucial event in the unlimited clonal expansion of endothelial cells that precedes the neoplastic conversion of these cells.
  • It is known that high-grade gliomas express telomerase and that, in these neoplasms, proliferating endothelial cells may undergo transformational changes with development of sarcomatous components within the primitive tumor.
  • To assess whether telomerase is involved in the endothelial cell proliferation that characterizes brain tumor angiogenesis, the authors investigated at the single-cell level the expression of messenger (m)RNA for the human telomerase catalytic subunit human telomerase reverse transcriptase (hTERT) by vascular cells of astrocytic tumors.
  • The expression of hTERT mRNA by vascular endothelial cells was related to the histological grade of the tumor because it was detected in five (29%) of 17 low-grade astrocytomas, nine (56%) of 16 anaplastic astrocytomas, and 19 (100%) of 19 glioblastomas multiforme (GBMs).
  • Data from an in vitro assay in which human umbilical vein endothelial cells were stimulated to proliferate by adding vascular endothelial growth factor and an ISH study of newly formed vessels surrounding brain infarcts confirmed that expression of hTERT mRNA does not merely reflect the proliferative status of endothelial cells but represents a specific feature of brain tumor neovascularization.
  • CONCLUSIONS: The results of this study are consistent with a role of telomerase in the angiogenesis of astrocytic tumors.
  • Expression of hTERT mRNA by tumor vascular cells is an early event during the progression of astrocytic tumors, which precedes endothelial cell proliferation and may represent a first sign of dedifferentiation.
  • Other than elucidating the mechanisms of tumor angiogenesis, these results encourage research on antitelomerase drugs for the treatment of malignant gliomas.
  • [MeSH-major] Astrocytoma / blood supply. Brain Neoplasms / blood supply. Glioblastoma / blood supply. Neovascularization, Pathologic / physiopathology. Telomerase / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cells, Cultured. Endothelium, Vascular / cytology. Endothelium, Vascular / metabolism. Endothelium, Vascular / pathology. Female. Humans. Hyperplasia. In Situ Hybridization. Male. Middle Aged. RNA, Messenger / metabolism. RNA-Directed DNA Polymerase / genetics. Umbilical Veins / cytology. Umbilical Veins / metabolism

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  • (PMID = 11409526.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.7.49 / RNA-Directed DNA Polymerase; EC 2.7.7.49 / Telomerase
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8. Barnett JA, Urbauer DL, Murray GI, Fuller GN, Heimberger AB: Cytochrome P450 1B1 expression in glial cell tumors: an immunotherapeutic target. Clin Cancer Res; 2007 Jun 15;13(12):3559-67
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  • [Title] Cytochrome P450 1B1 expression in glial cell tumors: an immunotherapeutic target.
  • An immunotherapeutic agent targeting this antigen was shown to safely stimulate a good immune response.
  • EXPERIMENTAL DESIGN: We studied the frequency and extent of CYP1B1 expression by immunohistochemical analysis in 269 glial tumors (including all major pathologic types) on a tissue microarray.
  • RESULTS: Overall, increased CYP1B1 expression in glial tumors was associated with decreased patient survival time (P < 0.0014 for both percentage and intensity of staining).
  • A significant difference existed in percentage and intensity of staining between astrocytic and oligodendroglial tumors (P = 0.0002 and 0.0003, respectively), between grades of tumors (P < 0.0001 and 0.0079), and between pathologic types of tumors (P < 0.0001 and 0.0339).
  • Paradoxically, within specific tumor pathologies, there was a trend toward increased survival as CYP1B1 expression increased.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Cytochrome P-450 Enzyme System / biosynthesis. Gene Expression. Glioma / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Aryl Hydrocarbon Hydroxylases. Child. Child, Preschool. Cytochrome P-450 CYP1B1. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Tissue Array Analysis

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  • (PMID = 17575219.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP1B1 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1B1
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9. Lang FF, Bruner JM, Fuller GN, Aldape K, Prados MD, Chang S, Berger MS, McDermott MW, Kunwar SM, Junck LR, Chandler W, Zwiebel JA, Kaplan RS, Yung WK: Phase I trial of adenovirus-mediated p53 gene therapy for recurrent glioma: biological and clinical results. J Clin Oncol; 2003 Jul 01;21(13):2508-18
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  • [Title] Phase I trial of adenovirus-mediated p53 gene therapy for recurrent glioma: biological and clinical results.
  • PURPOSE: Advances in brain tumor biology indicate that transfer of p53 is an alternative therapy for human gliomas.
  • In stage 2, the tumor-catheter was resected en bloc, and the postresection cavity was treated with Ad-p53.
  • This protocol provided intact Ad-p53-treated biologic specimens that could be analyzed for molecular end points, and because the resection cavity itself was injected with Ad-p53, patients could be observed for clinical toxicity.
  • In all patients, exogenous p53 protein was detected within the nuclei of astrocytic tumor cells.
  • Clinical toxicity was minimal and a maximum-tolerated dose was not reached.
  • Although anti-adenovirus type 5 (Ad5) titers increased in most patients, there was no evidence of systemic viral dissemination.
  • Although toxicity was minimal, widespread distribution of this agent remains a significant goal.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / therapy. Genes, p53 / genetics. Genetic Therapy. Glioma / genetics. Glioma / therapy
  • [MeSH-minor] Adenoviridae / genetics. Adult. Aged. Female. Genetic Vectors. Humans. Male. Middle Aged. Transduction, Genetic. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2004 Apr 1;22(7):1344-5; author reply 1345 [15051789.001]
  • (PMID = 12839017.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA62399; United States / NCI NIH HHS / CA / CA62412; United States / NCI NIH HHS / CA / CA62422; United States / NCRR NIH HHS / RR / M01-RR00042; United States / NCRR NIH HHS / RR / M01-RR00079
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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10. Ritch PS, Carroll SL, Sontheimer H: Neuregulin-1 enhances survival of human astrocytic glioma cells. Glia; 2005 Aug 15;51(3):217-28
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  • [Title] Neuregulin-1 enhances survival of human astrocytic glioma cells.
  • Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.
  • These tumors are characterized by unrelenting growth that is often resistant to chemotherapy and radiation therapy.
  • Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.
  • In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.
  • Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.
  • We then verify receptor expression in a panel of human glioma cell lines.
  • Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.
  • Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.
  • This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

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  • [Cites] Oncogene. 1992 Sep;7(9):1859-66 [1354348.001]
  • [Cites] Neurosurgery. 1993 Jul;33(1):106-15 [7689190.001]
  • [Cites] Mol Cell Biol. 1994 Jan;14(1):492-500 [8264617.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 1;91(3):1064-8 [8302832.001]
  • [Cites] Mol Cell Biol. 1994 Mar;14(3):1909-19 [7509448.001]
  • [Cites] Mol Cell Biol. 1994 Jun;14(6):3550-8 [7515147.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9387-91 [7937775.001]
  • [Cites] Biochim Biophys Acta. 1994 Dec 30;1198(2-3):165-84 [7819273.001]
  • [Cites] Oncogene. 1995 Apr 6;10(7):1403-11 [7731691.001]
  • [Cites] J Cell Biol. 1995 Jul;130(1):127-35 [7540614.001]
  • [Cites] J Biol Chem. 1995 Aug 11;270(32):19188-96 [7642587.001]
  • [Cites] Neuron. 1996 Aug;17(2):229-43 [8780647.001]
  • [Cites] Mol Cell Neurosci. 1996 Apr;7(4):247-62 [8793861.001]
  • [Cites] EMBO J. 1997 Apr 1;16(7):1647-55 [9130710.001]
  • [Cites] Nature. 1997 May 29;387(6632):509-12 [9168114.001]
  • [Cites] Nature. 1997 May 29;387(6632):512-6 [9168115.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):4007-14 [9199335.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9562-7 [9275162.001]
  • [Cites] J Neurochem. 1997 Nov;69(5):1859-63 [9349528.001]
  • [Cites] J Neurosci Res. 1997 Dec 1;50(5):755-68 [9418963.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):193-209 [9440020.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):223-48 [9440022.001]
  • [Cites] J Neurooncol. 1997 Dec;35(3):335-46 [9440030.001]
  • [Cites] Genes Dev. 1998 Jun 15;12(12):1825-36 [9637684.001]
  • [Cites] Biochem J. 1998 Aug 1;333 ( Pt 3):757-63 [9677338.001]
  • [Cites] Biochem J. 1998 Oct 1;335 ( Pt 1):1-13 [9742206.001]
  • [Cites] Can J Neurol Sci. 1998 Nov;25(4):267-81 [9827227.001]
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3675-85 [9851974.001]
  • [Cites] Eur J Neurosci. 1999 Mar;11(3):769-80 [10103071.001]
  • [Cites] Mol Cell Neurosci. 1999 Feb;13(2):79-94 [10192767.001]
  • [Cites] Oncogene. 1999 Apr 29;18(17):2681-9 [10348342.001]
  • [Cites] EMBO J. 1994 Jun 15;13(12):2831-41 [8026468.001]
  • [Cites] Adv Cancer Res. 2000;77:25-79 [10549355.001]
  • [Cites] Glia. 2000 Jan 15;29(2):104-11 [10625327.001]
  • [Cites] Toxicol Pathol. 2000 Jan-Feb;28(1):171-7 [10669005.001]
  • [Cites] Biochem J. 2000 Mar 15;346 Pt 3:561-76 [10698680.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3159-67 [10880430.001]
  • [Cites] J Neurosci. 2000 Oct 15;20(20):7622-30 [11027222.001]
  • [Cites] Bioessays. 2000 Nov;22(11):987-96 [11056475.001]
  • [Cites] Brain Res Dev Brain Res. 2000 Nov 30;124(1-2):93-9 [11113516.001]
  • [Cites] Annu Rev Neurosci. 2001;24:385-428 [11283316.001]
  • [Cites] Neuro Oncol. 2000 Apr;2(2):96-102 [11303626.001]
  • [Cites] Mol Cell Neurosci. 2001 Apr;17(4):761-7 [11312610.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2841-51 [11042203.001]
  • [Cites] J Biol Chem. 2001 Mar 9;276(10):7320-6 [11058599.001]
  • [Cites] Curr Opin Neurobiol. 2001 Jun;11(3):287-96 [11399426.001]
  • [Cites] J Neurooncol. 2001 Feb;51(3):245-64 [11407596.001]
  • [Cites] J Neurosci. 2001 Jul 1;21(13):4740-51 [11425901.001]
  • [Cites] Genes Dev. 2001 Aug 1;15(15):1913-25 [11485986.001]
  • [Cites] Curr Opin Neurol. 2001 Dec;14(6):683-8 [11723374.001]
  • [Cites] Fed Proc. 1983 Jun;42(9):2627-9 [6852276.001]
  • [Cites] Nature. 1985 Jan 10-18;313(5998):144-7 [2981413.001]
  • [Cites] Cell. 1985 Jul;41(3):697-706 [2860972.001]
  • [Cites] Science. 1985 Dec 6;230(4730):1132-9 [2999974.001]
  • [Cites] Cell. 1986 Jun 6;45(5):649-57 [2871941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6899-903 [3477813.001]
  • [Cites] Cancer Res. 1988 Jul 15;48(14):3910-8 [2454731.001]
  • [Cites] Science. 1989 May 12;244(4905):707-12 [2470152.001]
  • [Cites] Neurosurgery. 1989 Nov;25(5):681-94 [2685640.001]
  • [Cites] J Neurosurg. 1991 Aug;75(2):284-93 [1649272.001]
  • [Cites] Ann N Y Acad Sci. 1991;633:35-47 [1789559.001]
  • [Cites] Cell. 1992 Apr 3;69(1):205-16 [1348215.001]
  • [Cites] J Neurosci Res. 1992 Jan;31(1):175-87 [1377283.001]
  • (PMID = 15812817.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247-010003; United States / NINDS NIH HHS / NS / R01 NS036692-05A1; United States / NCI NIH HHS / CA / CA097247-010003; United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50CA97247; United States / NINDS NIH HHS / NS / NS036692-05A1; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01-NS36692; United States / NINDS NIH HHS / NS / R01 NS036692-06; United States / NINDS NIH HHS / NS / NS036692-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neuregulin-1; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS25075; NLM/ PMC2548407
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11. Robe PA, Martin DH, Nguyen-Khac MT, Artesi M, Deprez M, Albert A, Vanbelle S, Califice S, Bredel M, Bours V: Early termination of ISRCTN45828668, a phase 1/2 prospective, randomized study of sulfasalazine for the treatment of progressing malignant gliomas in adults. BMC Cancer; 2009;9:372
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  • [Title] Early termination of ISRCTN45828668, a phase 1/2 prospective, randomized study of sulfasalazine for the treatment of progressing malignant gliomas in adults.
  • BACKGROUND: Sulfasalazine, a NF-kappaB and x(c)-cystine/glutamate antiport inhibitor, has demonstrated a strong antitumoral potential in preclinical models of malignant gliomas.
  • As it presents an excellent safety profile, we initiated a phase 1/2 clinical study of this anti-inflammatory drug for the treatment of recurrent WHO grade 3 and 4 astrocytic gliomas in adults.
  • METHODS: 10 patients with advanced recurrent anaplastic astrocytoma (n = 2) or glioblastoma (n = 8) aged 32-62 years were recruited prior to the planned interim analysis of the study.
  • Subjects were randomly assigned to daily doses of 1.5, 3, 4.5, or 6 grams of oral sulfasalazine, and treated until clinical or radiological evidence of disease progression or the development of serious or unbearable side effects.
  • Primary endpoints were the evaluation of toxicities according to the CTCAE v.3.0, and the observation of radiological tumor responses based on MacDonald criteria.
  • One tumor remained stable for 2 months with sulfasalazine treatment, at the lowest daily dose of the drug.
  • CONCLUSION: Although the proper influence of sulfasalazine treatment on patient outcome was difficult to ascertain in these debilitated patients with a large tumor burden (median KPS = 50), ISRCTN45828668 was terminated after its interim analysis.
  • This study urges to exert cautiousness in future trials of Sulfasalazine for the treatment of malignant gliomas.
  • [MeSH-major] Early Termination of Clinical Trials. Glioma / drug therapy. Sulfasalazine / administration & dosage
  • [MeSH-minor] Adult. Disease Progression. Female. Humans. Male. Middle Aged. Prospective Studies. Treatment Failure

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  • [Cites] J Neurooncol. 2005 Sep;74(2):105-11 [16193380.001]
  • [Cites] J Neurosci. 2005 Aug 3;25(31):7101-10 [16079392.001]
  • [Cites] Physiol Rev. 2006 Jan;86(1):279-367 [16371600.001]
  • [Cites] J Clin Oncol. 2006 Jan 10;24(2):274-87 [16365179.001]
  • [Cites] BMC Cancer. 2006;6:29 [16448552.001]
  • [Cites] Intern Med. 2006;45(15):927-9 [16946577.001]
  • [Cites] Biochem Pharmacol. 2006 Oct 30;72(9):1054-68 [16973133.001]
  • [Cites] Int J Oncol. 2007 Jan;30(1):283-90 [17143539.001]
  • [Cites] Brain Tumor Pathol. 2005;22(2):79-87 [18095109.001]
  • [Cites] Headache. 2008 Feb;48(2):296-8 [18070060.001]
  • [Cites] Mol Cancer Res. 2008 Jan;6(1):21-30 [18184972.001]
  • [Cites] J Cell Physiol. 2008 Jun;215(3):593-602 [18181196.001]
  • [Cites] J Mol Diagn. 2008 Jul;10(4):332-7 [18556773.001]
  • [Cites] Clin Neuropharmacol. 2008 Nov-Dec;31(6):368-71 [19050416.001]
  • [Cites] Biochem Pharmacol. 2000 Oct 15;60(8):1085-9 [11007945.001]
  • [Cites] Neurol Med Chir (Tokyo). 2001 Apr;41(4):187-95 [11381677.001]
  • [Cites] J Neurosurg. 2002 May;96(5):909-17 [12005399.001]
  • [Cites] Lab Invest. 2004 Aug;84(8):941-51 [15184909.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5595-603 [15328202.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] J Neuroimmunol. 1991 Nov;34(2-3):109-20 [1680877.001]
  • [Cites] Neurosci Res. 1992 Feb;13(1):1-17 [1314349.001]
  • [Cites] Am J Gastroenterol. 1993 Oct;88(10):1759-63 [8105680.001]
  • [Cites] Drugs. 1995 Jul;50(1):137-56 [7588084.001]
  • [Cites] J Clin Invest. 1998 Jan 15;101(2):295-300 [9435300.001]
  • [Cites] J Clin Invest. 1998 Mar 1;101(5):1163-74 [9486988.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Jun 9;247(1):79-83 [9636658.001]
  • [Cites] J Immunol. 1998 Sep 15;161(6):2873-80 [9743348.001]
  • [Cites] Brain Res. 1998 Aug 17;802(1-2):232-40 [9748597.001]
  • [Cites] Oncogene. 1999 Apr 1;18(13):2261-71 [10327072.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • [Cites] Neuro Oncol. 2005 Oct;7(4):425-34 [16212807.001]
  • (PMID = 19840379.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN45828668
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 3XC8GUZ6CB / Sulfasalazine
  • [Other-IDs] NLM/ PMC2771045
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12. Dobbertin A, Rhodes KE, Garwood J, Properzi F, Heck N, Rogers JH, Fawcett JW, Faissner A: Regulation of RPTPbeta/phosphacan expression and glycosaminoglycan epitopes in injured brain and cytokine-treated glia. Mol Cell Neurosci; 2003 Dec;24(4):951-71
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  • Several chondroitin sulfate proteoglycans (CSPGs) are upregulated after CNS injury and are thought to limit axonal regeneration in the adult mammalian CNS.
  • Epidermal growth factor/transforming growth factor alpha strongly increased the astrocytic expression of long RPTPbeta and phosphacan and slightly the short RPTPbeta protein levels, while interferon gamma and tumor necrosis factor alpha reduced astrocytic levels of phosphacan, but not of the receptor forms.
  • Examining the effects of phosphacan on axon growth from rat E17 cortical neurons, we found that phosphacan stimulates outgrowth in a largely CS dependent manner, while it blocks the outgrowth-promoting effects of laminin through an interaction that is not affected by removal of the CS chains.
  • [MeSH-major] Brain Injuries / enzymology. Chondroitin Sulfate Proteoglycans / biosynthesis. Glycosaminoglycans / biosynthesis. Nerve Tissue Proteins / biosynthesis. Neuroglia / enzymology. Protein Tyrosine Phosphatases / biosynthesis
  • [MeSH-minor] Animals. Cytokines / pharmacology. Epitopes / biosynthesis. Epitopes / genetics. Female. Gene Expression Regulation / drug effects. Gene Expression Regulation / physiology. Humans. Rats. Rats, Sprague-Dawley. Receptor-Like Protein Tyrosine Phosphatases, Class 5

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  • (PMID = 14697661.001).
  • [ISSN] 1044-7431
  • [Journal-full-title] Molecular and cellular neurosciences
  • [ISO-abbreviation] Mol. Cell. Neurosci.
  • [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 / Cytokines; 0 / Epitopes; 0 / Glycosaminoglycans; 0 / Nerve Tissue Proteins; EC 3.1.3.48 / PTPRZ1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Ptprz1 protein, rat; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
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13. Gologorsky Y, DeLaMora P, Souweidane MM, Greenfield JP: Cerebellar cryptococcoma in an immunocompetent child. Case report. J Neurosurg; 2007 Oct;107(4 Suppl):314-7
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  • Isolated cryptococcomas of the central nervous system (CNS) have been previously described in immunocompetent adults; however, this is the first report of a cryptococcoma in a child.
  • The patient underwent excision of the mass, and analysis of frozen sections suggested the presence of an astrocytic tumor with pilocytic features; therefore gross-total resection was performed.
  • Once the definitive diagnosis of a cryptococcal abscess was obtained, medical treatment with antifungal medications led to the resolution of all symptoms and the normalization of serum titers.
  • [MeSH-minor] Antifungal Agents / therapeutic use. Child. HIV Seronegativity. Humans. Male. Treatment Outcome

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  • (PMID = 17941497.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents
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14. Hwang SL, Lieu AS, Kuo TH, Lin CL, Chang CZ, Huang TY, Howng SL: Preoperative and postoperative seizures in patients with astrocytic tumours: analysis of incidence and influencing factors. J Clin Neurosci; 2001 Sep;8(5):426-9
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  • [Title] Preoperative and postoperative seizures in patients with astrocytic tumours: analysis of incidence and influencing factors.
  • To evaluate the incidence and influencing factors related to preoperative and postoperative seizures, a retrospective analysis was performed in 190 patients with astrocytic tumours.
  • Seizures at presentation were significantly correlated with age at diagnosis (P=0.0204) and pathological grade of tumour (P=0.0040).
  • The patients aged less than 40 years had a high risk of seizures at presentation (odds ratio=3.076, P=0.0134).
  • Postoperative seizures were significantly associated with the presence of preoperative seizures (P<0.0001), type or duration of preoperative seizures (P<0.0001, P<0.0001, respectively) and serum level of anticonvulsant drug (P=0.0068).
  • Despite therapeutic anticonvulsant levels, most postoperative seizures were associated with tumour recurrence or haemorrhage.
  • In patients with postoperative seizures, particularly in the presence of therapeutic anticonvulsant level, brain computed tomography should be performed to exclude tumour recurrence or haemorrhage.
  • [MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Epilepsy / epidemiology. Postoperative Complications / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Craniotomy. Female. Humans. Incidence. Infant. Logistic Models. Male. Middle Aged. Retrospective Studies


15. Hwang SL, Lin CL, Lee KS, Lieu AS, Kuo TH, Chang CZ, Yen CP, Lin CK, Loh JK, Huang TY, Howng SL: Factors influencing seizures in adult patients with supratentorial astrocytic tumors. Acta Neurochir (Wien); 2004 Jun;146(6):589-94: discussion 594
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  • [Title] Factors influencing seizures in adult patients with supratentorial astrocytic tumors.
  • Seizures and epilepsy in adults are important and increasingly common clinical problems.
  • Despite this, the investigation of seizures in adults with astrocytic tumors remains a grey area.
  • The incidence and influencing factors of preoperative and postoperative seizures were evaluated in 101 patients of 45 years or older with supratentorial astrocytic tumors.
  • Seizures at presentation were significantly correlated with pathological grades of astrocytic tumors (p = 0.0318).
  • There was no association of preoperative seizures with age, sex, location or site of the tumors.
  • Postoperative seizures occurred in 18 (18%) patients, including 8 (8/14, 57%) recurrent seizures and 10 (10/87, 12%) late-onset seizures.
  • Thirteen (72%) of 18 patients with postoperative seizures were associated with tumor recurrence in 7 cases, hemorrhage in 3 cases and malignant progression in 3 cases.
  • There was no association of postoperative seizures with age, sex, location or site of the tumors, grades of tumors, type of preoperative seizures, duration of preoperative seizures, serum level of anticonvulsant drug, extent of surgery, postoperative radiation or chemotherapy.
  • Imaging examination of brain to exclude the possibilities of tumor recurrence or hemorrhage is warrantable in supratentorial astrocytoma patients with postoperative seizures.
  • [MeSH-major] Astrocytoma / surgery. Epilepsy / etiology. Glioblastoma / surgery. Postoperative Complications / etiology. Supratentorial Neoplasms / surgery
  • [MeSH-minor] Aged. Cerebral Hemorrhage / complications. Disease Progression. Female. Humans. Male. Middle Aged. Recurrence. Regression Analysis. Retrospective Studies. Risk Factors

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  • [Copyright] Copyright 2004 Springer-Verlag
  • (PMID = 15168227.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
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16. Sipos L, Vitanovics D, Afra D: Temozolomide chemotherapy of patients with recurrent anaplastic astrocytomas and glioblastomas. Ideggyogy Sz; 2004 Nov 20;57(11-12):394-9
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  • INTRODUCTION: Anaplastic astrocytomas and glioblastomas are the most frequent and most malignant hemispherial tumours.
  • Unfortunately, astrocytic tumours are of infiltrative character and radical removal is not possible.
  • Recurrent malignant gliomas are rarely suitable for reoperation.
  • PATIENTS AND METHOD: Seventy-five consecutive patients with recurrent malignant astrocytomas and glioblastomas had been treated at our institute with per os temozolomide for five days every month.
  • Among the patients treated with temozolomide in seven cases complete response, 17 partial response, 14 progressive disease were observed.
  • In 33 cases the disease stabilized and out of them in 27% a significant neurological improvement was detected.
  • The time to progression was 6.8 months and the median survival time 8.75 months for patients with glioblastoma and with malignant astrocytoma or malignant mixed oligoastrocytoma 9.45 and 11.15 months, respectively.
  • CONCLUSIONS: Temozolomide chemotherapy in patients with recurrent malignant astrocytoma and glioblastoma proved to be efficacious and similar good results were achieved as with a nitrosourea based combined chemotherapy.
  • Even in those patients who received previous chemotherapy temozolomide is well tolerated and a relatively long time to progression was achieved in cases of recurrent malignant gliomas.
  • In a few number of patients where BCNU had been previously failed with temozolomide stable disease was achieved.
  • Temozolomide seems to be a promising drug in the chemotherapy of malignant gliomas and can be applied as a second line chemotherapy, as well.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / diagnosis. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Disease Progression. Disease-Free Survival. Drug Administration Schedule. Female. Glioblastoma / drug therapy. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Survival Analysis. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 15662767.001).
  • [ISSN] 0019-1442
  • [Journal-full-title] Ideggyógyászati szemle
  • [ISO-abbreviation] Ideggyogy Sz
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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17. 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.
  • Poor survival is due to the highly invasive nature and protected location of these tumours.
  • 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.
  • This antigen provides an abundant, insoluble, non-diffusible anchor for the mAb.
  • Once localised to necrotic regions of the tumour, (131)I-chTNT-1/B mAb delivers a cytotoxic dose of (131)I radiation to the core lesion. (131)I-chTNT-1/B mAb is delivered via convection-enhanced delivery in order to maximise coverage to the tumour and the invasive front of the glial tumour.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Astrocytoma / radiotherapy. Iodine Radioisotopes / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Clinical Trials as Topic. DNA / immunology. DNA / metabolism. Female. Histones / immunology. Histones / metabolism. Humans. Male. Middle Aged. Radioimmunotherapy / methods

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  • (PMID = 16610983.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Histones; 0 / Iodine Radioisotopes; 9007-49-2 / DNA
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18. Capper D, Mittelbronn M, Meyermann R, Schittenhelm J: Pitfalls in the assessment of MGMT expression and in its correlation with survival in diffuse astrocytomas: proposal of a feasible immunohistochemical approach. Acta Neuropathol; 2008 Feb;115(2):249-59
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  • Immunohistochemical studies showed that O(6)-methylguanine-DNA methyltransferase (MGMT) protein expression is negatively associated with survival in glioblastomas treated with alkylating agents in accordance with previous results of methylation-specific PCR.
  • Implementation of this data in routine clinical diagnostics is limited due to often inappropriate study designs, e.g. pooling of tumor entities, WHO grades or primary and secondary glioblastomas, disregard concerning the infiltration zone or various epidemiological factors.
  • The aim of our study was to evaluate MGMT expression and its prognostic value taking into consideration the aforementioned deficiencies.
  • For this, 162 astrocytic tumors WHO II-IV (36 diffuse astrocytomas WHO II, 51 anaplastic astrocytomas, 75 primary glioblastomas) as well as 25 glioblastoma infiltration zones and 19 glioblastoma relapses were analyzed for immunohistochemical MGMT protein expression using tissue microarray technique.
  • Expression of MGMT significantly decreased from WHO grade II (25.6%) to glioblastoma (16.8%, p = 0.01) with lowest levels in grade III tumors (10.2%, II/III p < 0.0001).
  • Significant negative associations of MGMT and survival were detected for WHO grade II and IV (p = 0.003 and 0.013).
  • The optimal cut-off value of MGMT positive nuclei in primary glioblastomas discriminating patients with significantly different survival rates was at 15% (Log-Rank p = 0.0002).
  • Individual relapse tumors showed changes of MGMT expression to a varying degree.
  • We conclude that immunohistochemical MGMT assessment has potential as a powerful diagnostic tool but analysis should only be performed in a grade dependent manner, before radio-/chemotherapy and with special attention to the infiltration zone of diffuse astrocytomas.
  • [MeSH-major] Astrocytoma / metabolism. Astrocytoma / mortality. Biomarkers, Tumor / analysis. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neurosurgical Procedures. Prognosis. Radiotherapy. Tissue Array Analysis

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  • (PMID = 17965865.001).
  • [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 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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19. Ono A, Kanno H, Hayashi A, Nishimura S, Kyuma Y, Sato H, Ito S, Shimizu N, Chang CC, Gondo G, Yamamoto I, Sasaki T, Tanaka M: Collagen gel matrix assay as an in vitro chemosensitivity test for malignant astrocytic tumors. Int J Clin Oncol; 2007 Apr;12(2):125-30
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  • [Title] Collagen gel matrix assay as an in vitro chemosensitivity test for malignant astrocytic tumors.
  • METHODS: We examined the chemosensitivites for four anticancer agents - 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3 (2-chloroethyl)-3-nitrosourea hydrochloride (ACNU), carboplatin, cisplatin, and etoposide - of 43 malignant astrocytic tumors (21 anaplastic astrocytomas and 22 glioblastomas) by using a collagen gel matrix assay, and we also determined the survival periods of the tumor-bearing patients.
  • The chemosensitivity was evaluated in terms of the growth inhibition rate, using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) method.
  • RESULTS: For the anaplastic astrocytomas, the mean growth inhibitory rate was 33.2% with cisplatin, 37.2% with carboplatin, 28.0% with ACNU, and 24.8% with etoposide.
  • The median overall and progression-free survivals of anaplastic astrocytoma-bearing patients who had undergone chemotherapy with two anticancer drugs, both of which showed significant anticancer activity (growth inhibitory rate >30%) were significantly longer than those of the patients who had been treated with two drugs, one or both of which did not show significant anticancer activity.
  • Individual chemotherapy for malignant astrocytic tumors, based on chemosensitivity data, could contribute to longer survival, particularly in anaplastic astrocytoma-bearing patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / pathology. Carboplatin / therapeutic use. Cisplatin / therapeutic use. Collagen. Etoposide / therapeutic use. Nimustine / therapeutic use
  • [MeSH-minor] Adult. Aged. Central Nervous System Neoplasms / drug therapy. Disease Progression. Disease-Free Survival. Drug Screening Assays, Antitumor. Female. Fibrin Foam. Follow-Up Studies. Glioblastoma / drug therapy. Glioblastoma / pathology. Humans. Japan. Karnofsky Performance Status. Male. Middle Aged. Sensitivity and Specificity. Survival Analysis. Tissue Adhesives. Treatment Outcome. Tumor Burden / drug effects. Tumor Cells, Cultured / drug effects

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  • [Cites] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2694-8 [3458228.001]
  • [Cites] Prog Clin Biol Res. 1980;48:259-76 [7208520.001]
  • [Cites] J Neurooncol. 1983;1(2):149-66 [6088712.001]
  • [Cites] Int J Urol. 2005 Jan;12(1):67-72 [15661056.001]
  • [Cites] Lancet. 1982 Apr 17;1(8277):885-7 [6122104.001]
  • [Cites] Jpn J Cancer Res. 1991 May;82(5):607-12 [1648053.001]
  • [Cites] Eur J Cancer. 1996 Feb;32A(2):226-30 [8664032.001]
  • [Cites] Br J Cancer. 1983 Feb;47(2):205-14 [6297528.001]
  • [Cites] Urol Res. 1993 Mar;21(2):83-8 [8503152.001]
  • [Cites] Cancer Treat Rep. 1986 Dec;70(12):1379-82 [3791251.001]
  • [Cites] J Cancer Res Clin Oncol. 1999 Aug-Sep;125(8-9):481-6 [10480340.001]
  • [Cites] J Neurooncol. 1994;21(3):225-32 [7699417.001]
  • [Cites] Cancer Res. 1985 Sep;45(9):4200-5 [4028010.001]
  • [Cites] Cancer Res. 1982 Mar;42(3):992-8 [7199383.001]
  • (PMID = 17443280.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fibrin Foam; 0 / Tissue Adhesives; 0S726V972K / Nimustine; 6PLQ3CP4P3 / Etoposide; 9007-34-5 / Collagen; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
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20. 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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  • [Title] DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours.
  • Cytogenetic and molecular genetic studies have shown frequent losses on the long arm of chromosome 14 in different types of human gliomas.
  • 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.
  • All tumours were additionally investigated for loss of heterozygosity (LOH).
  • Microsatellite analysis showed LOH in seven of 28 (25%) oligodendroglial tumours and three of 15 (20%) astrocytic tumours.
  • Seven tumours demonstrated LOH at all informative 14q loci whereas three tumours carried partial deletions defining a commonly deleted region at 14q22.3-q32.1 between the microsatellite markers D14S282 and D14S995.
  • Hypermethylation was restricted to tumours with oligodendroglial differentiation (12 of 28 tumours, 43%).
  • However, none of the hypermethylated tumours demonstrated LOH on 14q and vice versa.
  • In total, 19 of 28 oligodendroglial tumours (68%) showed either hypermethylation at the 14q32.12 locus or LOH at 14q22.3-q32.2.
  • 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.
  • In addition, the restriction of 14q32.12 methylation to oligodendroglial tumours suggests a role for epigenetic DNA modifications in these particular gliomas.
  • [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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21. Bronger H, König J, Kopplow K, Steiner HH, Ahmadi R, Herold-Mende C, Keppler D, Nies AT: ABCC drug efflux pumps and organic anion uptake transporters in human gliomas and the blood-tumor barrier. Cancer Res; 2005 Dec 15;65(24):11419-28
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  • [Title] ABCC drug efflux pumps and organic anion uptake transporters in human gliomas and the blood-tumor barrier.
  • Delivery of therapeutic agents to the brain and its neoplasms depends on the presence of membrane transport proteins in the blood-brain barrier and in the target cells.
  • The cellular and subcellular localization of these membrane transporters determines the drug accessibility to the brain and its tumors.
  • We therefore analyzed the expression and localization of six members of the multidrug resistance protein family of ATP-dependent efflux pumps (ABCC1-ABCC6, formerly MRP1-MRP6) and of six organic anion uptake transporters (OATP1A2, OATP1B1, OATP1B3, OATP1C1, OATP2B1, and OATP4A1) in 61 human glioma specimens of different histologic subtypes.
  • At the protein level, however, only OATP1A2 and OATP2B1 were detectable by immunofluorescence microscopy in the luminal membrane of endothelial cells forming the blood-brain barrier and the blood-tumor barrier, but not in the glioma cells.
  • ABCC4 and ABCC5 proteins were the major ABCC subfamily members in gliomas, localized both at the luminal side of the endothelial cells and in the glioma cells of astrocytic tumors and in the astrocytic portions of oligoastrocytomas.
  • These results indicate that expression of ABCC4 and ABCC5 is associated with an astrocytic phenotype, in accordance with their expression in astrocytes and with the higher chemoresistance of astrocytic tumors as compared with oligodendrogliomas.
  • Our data provide a basis for the assessment of the role of uptake transporters and efflux pumps in the accessibility of human gliomas for chemotherapeutic agents.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Blood-Brain Barrier. Brain Neoplasms / metabolism. Multidrug Resistance-Associated Proteins / metabolism. Oligodendroglioma / metabolism. Organic Anion Transporters / metabolism
  • [MeSH-minor] Adult. Aged. Astrocytoma / drug therapy. Astrocytoma / metabolism. Astrocytoma / pathology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Endothelium, Vascular / metabolism. Endothelium, Vascular / pathology. Female. Humans. Male. Membrane Transport Proteins / metabolism. Microscopy, Fluorescence. Middle Aged. Subcellular Fractions

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  • (PMID = 16357150.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / Membrane Transport Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / Organic Anion Transporters
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22. Ding Q, Stewart J Jr, Prince CW, Chang PL, Trikha M, Han X, Grammer JR, Gladson CL: Promotion of malignant astrocytoma cell migration by osteopontin expressed in the normal brain: differences in integrin signaling during cell adhesion to osteopontin versus vitronectin. Cancer Res; 2002 Sep 15;62(18):5336-43
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  • [Title] Promotion of malignant astrocytoma cell migration by osteopontin expressed in the normal brain: differences in integrin signaling during cell adhesion to osteopontin versus vitronectin.
  • The extracellular matrix of the normal adult brain lacks expression of most of the adhesive glycoproteins that are known to promote cell attachment, and it has been thought that the malignant invasion of astrocytoma tumor is mediated primarily by remodeling of the matrix by the tumor cells.
  • Therefore, we explored the possibility that the cell attachment protein, osteopontin, is expressed in the normal human brain.
  • Here, we report that osteopontin is expressed in the cortical gray and white matter of normal adult brain, with the levels of osteopontin expression being equivalent to those in malignant astrocytic tumor biopsies as assessed by Western blot analysis.
  • Immunoblotting identified osteopontin polypeptides with relative molecular weights of 60- and 65-kDa in normal brain white matter and in astrocytic tumors, with an additional 70-kDa polypeptide being identified in normal cortical gray matter and in some astrocytic tumors.
  • Recombinant osteopontin was found to promote attachment of U-251MG human malignant astrocytoma cells in a process that was inhibited by anti-integrin monoclonal antibodies anti-alphavbeta3 (75%), anti-alphavbeta5 (80%), and anti-alpha5 (40%).
  • These data indicate that the cell attachment protein, osteopontin, is expressed in the normal adult brain and that it has the potential to promote malignant astrocytoma cell invasion.
  • [MeSH-major] Astrocytoma / pathology. Brain / metabolism. Brain Neoplasms / pathology. Cell Movement / physiology. Sialoglycoproteins / physiology. Vitronectin / physiology
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Adhesion / physiology. Enzyme Activation. Humans. Integrins / physiology. Mice. Monomeric GTP-Binding Proteins / metabolism. Osteopontin. Rats. Receptors, Vitronectin / physiology. Recombinant Proteins / pharmacology. rho GTP-Binding Proteins / metabolism

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  • (PMID = 12235004.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 59958; United States / NCI NIH HHS / CA / CA 75682
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrins; 0 / Receptors, Vitronectin; 0 / Recombinant Proteins; 0 / SPP1 protein, human; 0 / Sialoglycoproteins; 0 / Spp1 protein, mouse; 0 / Spp1 protein, rat; 0 / Vitronectin; 0 / integrin alphaVbeta5; 0 / integrin alphavbeta1; 106441-73-0 / Osteopontin; EC 3.6.5.2 / Monomeric GTP-Binding Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins
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23. 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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  • Recent studies have led to considerable advancement in our understanding of the molecular mechanisms that underlie the relentless cell growth and invasiveness of human gliomas.
  • We studied the expression and properties of K(+) channels in primary cultures obtained from surgical specimens: human ether a gò-gò related (hERG)1 voltage-dependent K(+) channels, which have been found to be overexpressed in various human cancers, and human ether a gò-gò-like 2 channels, that share many of hERG1's biophysical features.
  • 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.
  • In addition, we present evidence that, in GBM cell lines, hERG1 channel activity actively contributes to malignancy by promoting vascular endothelial growth factor secretion, thus stimulating the neoangiogenesis typical of high-grade gliomas.
  • 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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  • [Cites] Biochem Biophys Res Commun. 2001 Sep 7;286(5):857-62 [11527377.001]
  • [Cites] Mol Biol Cell. 2005 Jun;16(6):2972-83 [15800067.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6885-91 [11559565.001]
  • [Cites] Xenobiotica. 2001 Aug-Sep;31(8-9):633-50 [11569530.001]
  • [Cites] Pflugers Arch. 2002 May;444(1-2):186-92 [11976931.001]
  • [Cites] Eur J Neurosci. 2002 Aug;16(3):415-28 [12193184.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1791-8 [12200695.001]
  • [Cites] Nat Med. 2002 Sep;8(9):971-8 [12172541.001]
  • [Cites] Pathol Res Pract. 2002;198(9):627-33; discussion 635-8 [12440786.001]
  • [Cites] Br J Pharmacol. 2003 Jan;138(1):161-71 [12522086.001]
  • [Cites] J Biol Chem. 2003 Jan 31;278(5):2947-55 [12431979.001]
  • [Cites] FASEB J. 2003 Feb;17(2):330-2 [12490549.001]
  • [Cites] Pflugers Arch. 2003 Feb;445(5):589-600 [12634931.001]
  • [Cites] Cancer Res. 2003 Apr 1;63(7):1602-7 [12670911.001]
  • [Cites] Curr Opin Oncol. 2003 May;15(3):197-203 [12778011.001]
  • [Cites] J Neurosci. 2003 Jul 2;23(13):5572-82 [12843258.001]
  • [Cites] Drug News Perspect. 2003 Jun;16(5):291-8 [12942160.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6613-25 [14583454.001]
  • [Cites] Gene Expr Patterns. 2003 Dec;3(6):767-76 [14643686.001]
  • [Cites] J Clin Pathol. 2003 Dec;56(12):972-5 [14645363.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):606-11 [14744775.001]
  • [Cites] Glia. 2004 Apr 1;46(1):63-73 [14999814.001]
  • [Cites] J Neurooncol. 2004 Jan;66(1-2):129-38 [15015778.001]
  • [Cites] Mol Pharmacol. 2004 May;65(5):1120-9 [15102940.001]
  • [Cites] Cancer Cell. 2004 May;5(5):405-6 [15144945.001]
  • [Cites] Neurosci Lett. 2004 Sep 30;368(3):249-53 [15364405.001]
  • [Cites] J Exp Ther Oncol. 2004 Jul;4(2):161-6 [15500011.001]
  • [Cites] Crit Rev Neurobiol. 1991;6(2):119-47 [1934088.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3438-42 [8159766.001]
  • [Cites] J Physiol. 1995 Dec 1;489 ( Pt 2):455-71 [8847640.001]
  • [Cites] J Physiol. 1996 Oct 1;496 ( Pt 1):13-23 [8910192.001]
  • [Cites] J Neurophysiol. 1998 May;79(5):2782-93 [9582244.001]
  • [Cites] J Neurobiol. 1999 Mar;38(4):466-74 [10084682.001]
  • [Cites] FASEB J. 2000 Dec;14(15):2601-10 [11099479.001]
  • [Cites] Br J Cancer. 2000 Dec;83(12):1722-9 [11104572.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6868-74 [11156382.001]
  • [Cites] J Neurophysiol. 2001 Feb;85(2):790-803 [11160513.001]
  • [Cites] J Biol Chem. 2001 Feb 16;276(7):4923-31 [11080495.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1311-33 [11390353.001]
  • [Cites] J Neurosci. 2001 Jul 1;21(13):4609-24 [11425889.001]
  • [Cites] Eur J Neurosci. 1999 Mar;11(3):753-60 [10103069.001]
  • [Cites] Am J Physiol. 1999 Jun;276(6 Pt 1):C1405-10 [10362604.001]
  • [Cites] J Neurosci. 1999 Jul 15;19(14):5942-54 [10407033.001]
  • [Cites] Eur J Cancer. 1999 Mar;35(3):445-9 [10448297.001]
  • [Cites] J Biol Chem. 1999 Aug 27;274(35):25018-25 [10455180.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):779-86 [11549567.001]
  • (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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24. Schäfer C, Fels C, Brucke M, Holzhausen HJ, Bahn H, Wellman M, Visvikis A, Fischer P, Rainov NG: Gamma-glutamyl transferase expression in higher-grade astrocytic glioma. Acta Oncol; 2001;40(4):529-35
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  • [Title] Gamma-glutamyl transferase expression in higher-grade astrocytic glioma.
  • Increased expression of gamma-glutamyltransferase (GGT) has been detected in a range of human malignancies and is thought to be involved in neoplastic proliferation and treatment resistance.
  • Since GGT expression and its role in malignant glioma biology remain largely unknown, we investigated this phenomenon by immunostaining 26 higher-grade human astrocytic gliomas (WHO grades III and IV) with a monoclonal anti-GGT-antibody (138H11).
  • Further, human pancreatic GGT cDNA was used for liposome-mediated transfection of 9L gliosarcoma cells.
  • GGT-expressing and control 9L cells were cultured in media containing different amounts of essential amino acids and/or cytotoxic agents.
  • Immunohistochemical staining of tumor specimens demonstrated that GGT expression is a frequent feature of higher-grade human astrocytic gliomas, but not of normal brain tissue.
  • Human tumors were strongly GGT-positive in 6 of 7 cases of grade III astrocytoma, and in 12 of 19 grade IV astrocytoma (glioblastoma multiforme, GBM) cases.
  • In the cell culture model, 9L-GGT cells had a growth advantage over control cells in cysteine-deficient medium. but not in standard or glutamine-free medium.
  • No significant difference in numbers of viable cells of either clone was found in media containing the alkylating drug BCNU (5-200 microg/ml).
  • In conclusion, GGT is expressed in a high percentage of human WHO grade III astrocytomas and GBM, but not in normal brain tissue.
  • This molecule seems to give neoplastic cells a moderate growth advantage under in vivo conditions.
  • [MeSH-major] Glioblastoma / enzymology. Neoplasm Proteins / biosynthesis. Nerve Tissue Proteins / biosynthesis. gamma-Glutamyltransferase / biosynthesis
  • [MeSH-minor] Adult. Aged. Animals. Antibodies, Monoclonal / immunology. Antineoplastic Agents, Alkylating / pharmacology. Brain / enzymology. Carmustine / pharmacology. Cell Division. Clone Cells / drug effects. Clone Cells / metabolism. Clone Cells / pathology. Culture Media / pharmacology. Cysteine / pharmacology. DNA, Complementary / genetics. Drug Resistance, Neoplasm. Enzyme Induction. Female. Gliosarcoma / pathology. Glutamine / pharmacology. Humans. Liposomes. Male. Microscopy, Immunoelectron. Middle Aged. Rats. Recombinant Fusion Proteins / biosynthesis. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology

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  • (PMID = 11504314.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents, Alkylating; 0 / Culture Media; 0 / DNA, Complementary; 0 / Liposomes; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0RH81L854J / Glutamine; EC 2.3.2.2 / gamma-Glutamyltransferase; K848JZ4886 / Cysteine; U68WG3173Y / Carmustine
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25. Kokkinakis DM, Rushing EJ, Shareef MM, Ahmed MM, Yang S, Singha UK, Luo J: Physiology and gene expression characteristics of carcinogen-initiated and tumor-transformed glial progenitor cells derived from the CNS of methylnitrosourea (MNU)-treated Sprague-Dawley rats. J Neuropathol Exp Neurol; 2004 Nov;63(11):1182-99
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  • [Title] Physiology and gene expression characteristics of carcinogen-initiated and tumor-transformed glial progenitor cells derived from the CNS of methylnitrosourea (MNU)-treated Sprague-Dawley rats.
  • Glial progenitors from the brain of normal adult Sprague-Dawley rats were compared to their initiated and malignant counterparts that were isolated from apparently normal brains of animals exposed to methylnitrosourea (MNU).
  • Fibroblast growth factor-2 (FGF-2) or platelet-derived growth factor (PDGF)-A or -B induced differentiation of normal progenitors to a pro-astrocytic or oligodendrocytic morphology, respectively, whereas the combination of these factors resulted in their terminal differentiation to oligodendrocytes and senescence.
  • In contrast, initiated progenitors did not exit the cell cycle when stimulated with PDGF and/or FGF-2. cDNA oligoarray analysis and RT-PCR verification showed an early upregulation/ induction of growth factor/receptors, PDGF-A, PDGFR-beta, IGFR-1, IGF-1 and -2, IL-6, MEGF-5, FRAG-1, IRS-2, HSPG, and FGFR-1, followed by a late increase in the expression IGFBP-6, PDGF-alpha, FGFR-4A, c/ERB-A, and FGFR-4, 2, and 1 during the tumorigenic progression.
  • Double immunofluorescence labeling showed progressive increase in nuclear colocalization of FGFR1, 2, and 4, which peaked in malignant lines.
  • Malignant transformation is enhanced by near elimination of p21 and PC3, induction of AP-1 (upregulation of JUN-B, c-JUN, FRA-1), activation of the NF-kB pro-survival pathway, and inhibition of the TGF-beta pro-apoptotic pathway possibly in response to changes in the expression of nerve growth factor (NGF) I-A and NGFI-B.
  • [MeSH-major] Brain / cytology. Carcinogens / pharmacology. Gene Expression Regulation, Neoplastic. Neuroglia / physiology. Stem Cells / drug effects. Stem Cells / physiology
  • [MeSH-minor] Animals. Blotting, Western. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Differentiation. Cell Line, Tumor. Cell Transformation, Neoplastic. Fluorescent Antibody Technique. Growth Substances / metabolism. Growth Substances / pharmacology. Methylnitrosourea / pharmacology. Oligonucleotide Array Sequence Analysis. Rats. Rats, Sprague-Dawley. Receptors, Growth Factor / drug effects. Receptors, Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction


26. Robe PA, Martin D, Albert A, Deprez M, Chariot A, Bours V: A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668]. BMC Cancer; 2006;6:29
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  • [Title] A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668].
  • BACKGROUND: The prognosis of patients suffering from WHO grade 3 and 4 astrocytic glioma remains poor despite surgery, radiation therapy and the use of current chemotherapy regimen.
  • Indeed, the median survival of glioblastoma multiforme (WHO grade 4) patients is at best 14.6 month with only 26.5 percent of the patients still alive after 2 years and the median survival of anaplastic astrocytomas (WHO grade 3) is 19.2 month.
  • Recent evidence suggests that the transcription factor NF-kappaB is constitutively expressed in malignant gliomas and that its inhibition by drugs like Sulfasalazine may block the growth of astrocytic tumors in vitro and in experimental models of malignant gliomas.
  • A total of twenty patients with progressive malignant glioma despite surgery, radiation therapy and a first line of chemotherapy will be recruited and assigned to four dosage regimen of Sulfasalazine.
  • This medication will be taken orally t.i.d. at a daily dose of 1.5-3-4 or 6 g, continuously until complete remission, evidence of progression or drug intolerance.
  • Primary endpoints are drug safety in the setting of malignant gliomas and tumor response as measured according to MacDonald's criteria.
  • An interim analysis of drug safety will be conducted after the inclusion of ten patients.
  • The complete evaluation of primary endpoints will be conducted two years after the enrollment of the last patient or after the death of the last patient should this occur prematurely.
  • DISCUSSION: The aim of this study is to evaluate the safety and efficacy of Sulfasalazine as a treatment for recurring malignant gliomas.
  • The safety and efficacy of this drug are analyzed as primary endpoints.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Sulfasalazine / therapeutic use
  • [MeSH-minor] Administration, Oral. Adult. Aged. Brain Neoplasms. Disease Progression. Double-Blind Method. Female. Glioma. Humans. Male. Middle Aged. Prognosis. Prospective Studies. Survival Analysis. Treatment Outcome

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  • [Cites] Biochem Pharmacol. 2000 Oct 15;60(8):1085-9 [11007945.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6938-47 [10602468.001]
  • [Cites] Exp Cell Res. 2001 May 1;265(2):221-33 [11302687.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 17):17-20 [12520480.001]
  • [Cites] Oncogene. 2003 Jan 9;22(1):90-7 [12527911.001]
  • [Cites] Oncologist. 2003;8(6):508-13 [14657528.001]
  • [Cites] Lab Invest. 2004 Aug;84(8):941-51 [15184909.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5595-603 [15328202.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] Drugs. 1995 Jul;50(1):137-56 [7588084.001]
  • [Cites] J Clin Invest. 1998 Mar 1;101(5):1163-74 [9486988.001]
  • [Cites] J Neurosurg. 1999 Jan;90(1):72-7 [10413158.001]
  • [Cites] Neurosurgery. 1999 Sep;45(3):423-31; discussion 431-3 [10493363.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):344-54 [15531918.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Jun;64(6):479-89 [15977639.001]
  • [Cites] Gastroenterology. 2000 Nov;119(5):1209-18 [11054378.001]
  • (PMID = 16448552.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN45828668
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 3XC8GUZ6CB / Sulfasalazine
  • [Other-IDs] NLM/ PMC1368982
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27. Tanaka A: Imaging diagnosis and fundamental knowledge of common brain tumors in adults. Radiat Med; 2006 Jul;24(6):482-92
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  • [Title] Imaging diagnosis and fundamental knowledge of common brain tumors in adults.
  • The most common primary brain tumors in Japanese adults are meningiomas, gliomas, pituitary adenomas, and schwannomas, which together account for 84.0% of all primary brain tumors.
  • The typical imaging findings of these tumors are well known by radiologists; therefore, the clinical and pathological issues, including terminology, genetics, and relation to hormones are discussed in this article.
  • The molecular genetic analysis of brain tumors has recently become important.
  • For instance, genetic analysis is important for differentiating oligodendroglial tumors from astrocytic tumors, and the gene mutation predicts response to chemotherapy for anaplastic oligodendrogliomas.
  • Background factors such as hormones, history of cranial irradiation, and medications influence oncogenesis, tumor growth, and tumor appearances as seen by imaging modalities.
  • Pituitary adenomas may be confused with nonneoplastic conditions such as physiological hypertrophy and Rathke's cleft cyst.
  • Such conditions should be carefully distinguished from neoplasms.
  • [MeSH-major] Brain Neoplasms / diagnosis. Magnetic Resonance Imaging. Tomography, X-Ray Computed
  • [MeSH-minor] Adult. Glioma / diagnosis. Humans. Image Processing, Computer-Assisted. Japan / epidemiology. Meningioma / diagnosis. Neurilemmoma / diagnosis. Pituitary Neoplasms / diagnosis

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  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] AJNR Am J Neuroradiol. 1993 Sep-Oct;14(5):1241-7 [8237710.001]
  • [Cites] Neuromolecular Med. 2003;3(1):41-52 [12665675.001]
  • [Cites] AJNR Am J Neuroradiol. 1990 Sep-Oct;11(5):935-8 [2120998.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Nov;84(11):3972-82 [10566636.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Aug 1;48(1):65-73 [10924973.001]
  • [Cites] AJNR Am J Neuroradiol. 2001 Aug;22(7):1306-15 [11498419.001]
  • [Cites] Radiology. 1999 Nov;213(2):383-8 [10551216.001]
  • [Cites] AJNR Am J Neuroradiol. 1994 Mar;15(3):525-32 [8197952.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4144-52 [10435596.001]
  • [Cites] Int J Cancer. 2000 Jan 1;85(1):78-81 [10585587.001]
  • [Cites] J Neurosurg. 1998 Jul;89(1):69-73 [9647174.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Jun;64(6):479-89 [15977639.001]
  • [Cites] J Neuroimaging. 1996 Apr;6(2):104-7 [8634482.001]
  • [Cites] Radiology. 1990 Aug;176(2):447-50 [2367659.001]
  • [Cites] Neuroradiology. 1997 Aug;39(8):593-8 [9272499.001]
  • [Cites] Surg Neurol. 2002 Dec;58(6):395-402; discussion 402 [12517619.001]
  • [Cites] Radiology. 1997 Apr;203(1):263-7 [9122405.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Mar;21(3):485-8 [10730639.001]
  • [Cites] AJNR Am J Neuroradiol. 1992 Sep-Oct;13(5):1279-91 [1414816.001]
  • [Cites] Radiology. 1994 Apr;191(1):41-51 [8134596.001]
  • [Cites] Cancer. 1975 Jul;36(1):216-20 [1203849.001]
  • [Cites] Nihon Igaku Hoshasen Gakkai Zasshi. 1998 Jun;58(7):349-52 [9711074.001]
  • [Cites] AJNR Am J Neuroradiol. 1997 Mar;18(3):551-4 [9090422.001]
  • [Cites] Surg Neurol. 1994 Jun;41(6):486-9 [8059328.001]
  • [Cites] AJNR Am J Neuroradiol. 2001 Jun-Jul;22(6):1081-8 [11415902.001]
  • [Cites] Radiology. 2002 Jul;224(1):177-83 [12091680.001]
  • [Cites] Radiology. 2003 Aug;228(2):533-8 [12819334.001]
  • [Cites] Jpn J Clin Oncol. 2001 Oct;31(10):510-3 [11696622.001]
  • (PMID = 16958433.001).
  • [ISSN] 0288-2043
  • [Journal-full-title] Radiation medicine
  • [ISO-abbreviation] Radiat Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 31
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28. Castilla EA, Prayson RA, Kanner AA, Rybicki LA, Tubbs RR, Vogelbaum MA, Barnett GH: Cyclooxygenase-2 in oligodendroglial neoplasms. Cancer; 2003 Oct 1;98(7):1465-72
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  • [Title] Cyclooxygenase-2 in oligodendroglial neoplasms.
  • BACKGROUND: Although increased expression of cyclooxygenase-2 (COX-2) has been described in association with a variety of neoplasms, including tumors of astrocytic derivation, limited data are available on COX-2 expression in oligodendrogliomas.
  • RESULTS: Patients included 35 males and 25 females, with a mean age of 41 years (range, 12-73 years) at the time of surgery.
  • Forty-four tumor specimens were classified as World Health Organization (WHO) Grade II neoplasms and 16 as WHO Grade III tumors.
  • Twenty-eight tumor specimens demonstrated allelic loss on chromosome 1p.
  • Positive staining was observed in 17 tumor specimens with COX-2 antibody.
  • COX-2-positive tumor specimens were also evaluated with CD68 (macrophage/microglial cell marker) by coimmunolabeling to confirm that the observed COX-2 immunostaining was not due to immunoreactive macrophages or microglial cells.
  • COX-2 expression, lack of allelic loss at chromosome 1p, and high proliferation indices were associated with decreased survival (P = 0.002, P = 0.009, and P = 0.015, respectively).
  • Tumors with expression of COX-2 by immunohistochemistry may, in theory, benefit from treatment with therapeutic agents that inhibit COX-2.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / enzymology. Oligodendroglioma / enzymology. Prostaglandin-Endoperoxide Synthases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Analysis of Variance. Biopsy, Needle. Child. Cohort Studies. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Probability. Prognosis. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Analysis. Time Factors

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  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11632
  • (PMID = 14508834.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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29. Dimitriadi M, Poulogiannis G, Liu L, Bäcklund LM, Pearson DM, Ichimura K, Collins VP: p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumours. Br J Cancer; 2008 Oct 07;99(7):1144-52
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  • [Title] p53-independent mechanisms regulate the P2-MDM2 promoter in adult astrocytic tumours.
  • The MDM2 gene is amplified and/or overexpressed in about 10% of glioblastomas and constitutes one of a number of ways the p53 pathway is disrupted in these tumours.
  • MDM2 encodes a nuclear phosphoprotein that regulates several cell proteins by binding and/or ubiquitinating them, with p53 being a well-established partner.
  • Transcription from P2 is believed to be controlled by p53 and a single-nucleotide polymorphism (SNP309, T>G) in P2 is reported to be associated with increased risk for, and early development of, malignancies.
  • We used RT-PCR to study P1- and P2-MDM2 transcript expression in astrocytic tumours, xenografts and cell lines with known MDM2, TP53 and p14(ARF) gene status.
  • Both promoters were used in all genetic backgrounds including the use of the P2 promoter in TP53 null cells, indicating a p53-independent induction of transcription.
  • Transcripts from the P1 promoter formed a greater proportion of the total MDM2 transcripts in tumours with MDM2 amplification, despite these tumours having two wild-type TP53 alleles.
  • Examination of SNP309 in glioblastoma patients showed a borderline association with survival but no apparent correlation with age at diagnosis nor with TP53 and p14(ARF) status of their tumours.
  • Our findings also indicate that elevated MDM2 mRNA levels in tumours with MDM2 amplification are preferentially driven by the P1 promoter and that the P2 promoter is not only regulated by p53 but also by other transcription factor(s).
  • [MeSH-major] Brain Neoplasms / genetics. Glioblastoma / genetics. Promoter Regions, Genetic. Proto-Oncogene Proteins c-mdm2 / genetics. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Adult. Genotype. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] Eur J Cancer. 1999 Jul;35(7):1083-8 [10533452.001]
  • [Cites] Neurol Med Chir (Tokyo). 2007 May;47(5):203-8; discussion 208-9 [17527046.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14517-22 [10588737.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):417-24 [10667596.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(6):2023-30 [10688649.001]
  • [Cites] Oncogene. 2000 Feb 10;19(6):831-5 [10698502.001]
  • [Cites] Int J Cancer. 2000 May 20;89(3):265-70 [10861503.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):587-96 [10934161.001]
  • [Cites] Cell. 2000 Oct 13;103(2):321-30 [11057904.001]
  • [Cites] Cancer Lett. 2001 Mar 26;164(2):177-88 [11179833.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1598-603 [11245471.001]
  • [Cites] Oncogene. 2001 May 31;20(25):3193-205 [11423969.001]
  • [Cites] Oral Oncol. 2001 Dec;37(8):620-31 [11590071.001]
  • [Cites] Oncol Rep. 2002 May-Jun;9(3):557-63 [11956627.001]
  • [Cites] Oncogene. 2002 Mar 27;21(13):1955-62 [11960368.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2616-23 [12750288.001]
  • [Cites] J Biol Chem. 2003 Jul 11;278(28):25716-21 [12730202.001]
  • [Cites] Clin Cancer Res. 2003 Sep 15;9(11):4151-8 [14519639.001]
  • [Cites] Mol Cancer Res. 2003 Dec;1(14):1017-26 [14707285.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(8):3536-51 [15060172.001]
  • [Cites] J Biol Chem. 2004 Jul 9;279(28):29841-8 [15090541.001]
  • [Cites] Int Rev Exp Pathol. 1983;24:135-202 [6601641.001]
  • [Cites] Cell. 1992 Jun 26;69(7):1237-45 [1535557.001]
  • [Cites] Cancer Res. 1993 Jun 15;53(12):2736-9 [8504413.001]
  • [Cites] Genes Dev. 1994 Aug 1;8(15):1739-49 [7958853.001]
  • [Cites] Leuk Lymphoma. 1995 Mar;17(1-2):13-8 [7773150.001]
  • [Cites] Nucleic Acids Res. 1995 Jul 25;23(14):2584-92 [7651818.001]
  • [Cites] Oncogene. 1996 Sep 5;13(5):1065-72 [8806696.001]
  • [Cites] Nature. 1997 May 15;387(6630):296-9 [9153395.001]
  • [Cites] Nature. 1997 May 15;387(6630):299-303 [9153396.001]
  • [Cites] Cancer Res. 1997 Aug 15;57(16):3562-8 [9270029.001]
  • [Cites] Oncogene. 1998 Apr 30;16(17):2249-57 [9619834.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8292-7 [9653180.001]
  • [Cites] Nucleic Acids Res. 1998 Aug 1;26(15):3453-9 [9671804.001]
  • [Cites] Cancer Res. 1998 Nov 15;58(22):5061-5 [9823311.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):864-72 [9858609.001]
  • [Cites] Cell. 2004 Nov 24;119(5):591-602 [15550242.001]
  • [Cites] Clin Cancer Res. 2007 Jun 1;13(11):3215-20 [17545525.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Cancer Cell. 2007 Oct;12(4):303-12 [17936556.001]
  • [Cites] J Neurooncol. 2007 Dec;85(3):241-4 [17568997.001]
  • [Cites] Brain Res. 2008 Mar 10;1198:16-20 [18262501.001]
  • [Cites] Oncogene. 2008 Mar 27;27(14):2097-108 [17934521.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1119-28 [15709179.001]
  • [Cites] Curr Cancer Drug Targets. 2005 Feb;5(1):9-20 [15720185.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Jun;43(2):181-93 [15770670.001]
  • [Cites] J Biol Chem. 2005 Apr 29;280(17):16651-8 [15723837.001]
  • [Cites] Genes Dev. 2005 Sep 15;19(18):2122-37 [16131611.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9582-7 [16230424.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1996-8 [16167062.001]
  • [Cites] J Mol Med (Berl). 2005 Nov;83(11):917-26 [16133418.001]
  • [Cites] Oncogene. 2006 Jul 13;25(30):4183-93 [16501602.001]
  • [Cites] Cancer Lett. 2006 Aug 28;240(2):195-7 [16239061.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1559-61 [16896050.001]
  • [Cites] Int J Cancer. 2007 Feb 1;120(3):563-5 [17096342.001]
  • [Cites] Anticancer Res. 2006 Nov-Dec;26(6C):4975-7 [17214373.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1317-23 [17322917.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Nov;58(11):1170-83 [10560660.001]
  • (PMID = 18781178.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6618; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2567066
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30. Tanaka S, Kobayashi I, Oka H, Fujii K, Watanabe T, Nagashima T, Hori T: Drug-resistance gene expression and progression of astrocytic tumors. Brain Tumor Pathol; 2001;18(2):131-7
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  • [Title] Drug-resistance gene expression and progression of astrocytic tumors.
  • To clarify the influence of biochemotherapy on the progression of astrocytic tumors, the expression of O6-methylguanine DNA-methyltransferase (MGMT) mRNA, as well as of other drug-resistance- and drug-sensitivity-related genes such as multidrug resistance gene 1, multidrug resistance-associated protein, glutathione S-transferase-pi, DNA topoisomerase II, and interferon receptor mRNA, and the interferon regulatory factor (IRF)-1 and -2 ratios in gliomas were investigated by quantitative reverse transcription-polymerase chain reaction (RT-PCR).
  • The mean MGMT/beta2-microglobulin (beta2-MG) ratio for 130 neuroepithelial tumors was 8.2 +/- 17.8.
  • The mean ratio of 45 glioblastomas was significantly higher than that for the other 85 tumors.
  • In contrast, the mean of 26 low-grade gliomas was significantly lower than that of other tumors.
  • The mean IRF-1/IRF-2 ratio of 16 other brain tumors that mainly consisted of medulloblastomas was significantly greater than that of the other 114 tumors.
  • Almost no significant differences were observed between primary and recurrent tumors in the expression of any gene, and before and after therapy with corresponding drugs.
  • The mean MGMT/beta2-MG ratio in primary glioblastomas was significantly higher than that in secondary tumors.
  • These findings suggest that native drug resistance is more important than acquired resistance when glioma therapy is considered.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Drug Resistance, Multiple / genetics. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Base Sequence. Chemotherapy, Adjuvant. DNA Topoisomerases, Type I / biosynthesis. DNA Topoisomerases, Type I / genetics. DNA Topoisomerases, Type II / biosynthesis. DNA Topoisomerases, Type II / genetics. Disease Progression. Female. Glioblastoma / drug therapy. Glioblastoma / genetics. Glioblastoma / pathology. Humans. Male. Middle Aged. Molecular Sequence Data. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Nerve Tissue Proteins / biosynthesis. Nerve Tissue Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / biosynthesis. O(6)-Methylguanine-DNA Methyltransferase / genetics. P-Glycoprotein / biosynthesis. P-Glycoprotein / genetics. Receptors, Interferon / biosynthesis. Receptors, Interferon / genetics

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  • (PMID = 11908869.001).
  • [ISSN] 1433-7398
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / P-Glycoprotein; 0 / Receptors, Interferon; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 5.99.1.2 / DNA Topoisomerases, Type I; EC 5.99.1.3 / DNA Topoisomerases, Type II
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31. Burton EC, Prados MD: Malignant gliomas. Curr Treat Options Oncol; 2000 Dec;1(5):459-68
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  • [Title] Malignant gliomas.
  • Gliomas are a heterogeneous group of neoplasms that comprise the majority of tumors originating in the central nervous system (CNS).
  • In adults, the most frequently encountered of these are high-grade or malignant neoplasms of astrocytic and oligodendrocytic lineage, ie, anaplastic astrocytoma (AA), glioblastoma multiforme (GBM), and anaplastic oligodendroglioma (AO), respectively.
  • Tumors of mixed lineage are also seen, the most common of which is designated anaplastic oligoastrocytoma (AOA).
  • Standard treatment for these tumors is typically surgery, followed by radiation then chemotherapy.
  • Surgery is required for a definitive histopathologic diagnosis, which in turn will dictate subsequent therapy options.
  • Moreover, aggressive tumor resection improves survival outcomes, and in many cases, the patient's neurologic function.
  • We generally advocate the safest, maximal resection attainable for patients with these tumors as a way to improve prognosis.
  • There is also mounting evidence to suggest that additional radiation, given in the form of brachytherapy or radiosurgery, at initial diagnosis as a "boost" to standard radiation or at tumor recurrence, may provide added improvement in survival outcome.
  • Bischloroethylnitrosourea (BCNU) is the typical first-line agent used, but chemotherapy seems to be most beneficial in young patients, with little if any impact on survival for patients over 60 years old.
  • For anaplastic astrocytomas, oligodendrogliomas, and oligoastrocytomas, a commonly accepted standard is adjuvant chemotherapy following irradiation with the three-drug regimen--procarbazine, CCNU, and vincristine (PCV).
  • AOs are a unique case with respect to tumor chemosensitivity and patient survival.
  • Molecular studies have identified a subpopulation of patients with AO whose tumors have lost chromosomes 1p and 19q.
  • Currently, trials are being conducted to confirm this finding and to determine the best treatment regimen for these patients, with particular regard to the timing of radiation and chemotherapy.
  • [MeSH-major] Brain Neoplasms / therapy. Glioma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Female. Humans. Radiotherapy. Survival Rate

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  • [Cites] Neurosurgery. 1998 Apr;42(4):709-20; discussion 720-3 [9574634.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1379-85 [1325539.001]
  • [Cites] Brain Pathol. 1993 Jul;3(3):255-68 [8293185.001]
  • [Cites] J Natl Cancer Inst. 1993 May 5;85(9):704-10 [8478956.001]
  • [Cites] J Neurosurg. 1993 May;78(5):767-75 [8468607.001]
  • [Cites] Neurosurgery. 2000 Feb;46(2):319-26; discussion 326-8 [10690720.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3389-95 [10550132.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jul 15;41(5):1005-11 [9719109.001]
  • [Cites] AJNR Am J Neuroradiol. 1999 Oct;20(9):1642-6 [10543634.001]
  • [Cites] J Natl Cancer Inst. 1998 Oct 7;90(19):1473-9 [9776413.001]
  • [Cites] J Neurooncol. 1999 May;42(3):233-45 [10433107.001]
  • [Cites] J Clin Oncol. 1999 Sep;17 (9):2762-71 [10561351.001]
  • [Cites] Neurosurgery. 2000 May;46(5):1123-8; discussion 1128-30 [10807244.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Oct 1;45(3):687-92 [10524423.001]
  • [Cites] J Neurooncol. 1999 May;42(3):247-58 [10433108.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Feb;18(2):321-4 [2154418.001]
  • [Cites] Neurosurgery. 1997 Nov;41(5):1028-36; discussion 1036-8 [9361056.001]
  • [Cites] Neurosurgery. 1995 Feb;36(2):275-82; discussion 282-4 [7731507.001]
  • [Cites] Neurosurgery. 1999 Jul;45(1):17-22; discussion 22-3 [10414561.001]
  • [Cites] J Neurooncol. 1995 Nov;26(2):111-23 [8787853.001]
  • [Cites] Neurosurgery. 2000 Feb;46(2):306-18 [10690719.001]
  • [Cites] J Clin Oncol. 2000 Apr;18(7):1481-91 [10735896.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2585-97 [8453582.001]
  • [Cites] Radiology. 2000 Apr;215(1):221-8 [10751490.001]
  • [Cites] Ann Med. 2000 Feb;32(1):81-5 [10711581.001]
  • [Cites] Nat Med. 1996 Mar;2(3):323-5 [8612232.001]
  • [Cites] Neurosurgery. 2000 May;46(5):1112-20; discussion 1120-2 [10807243.001]
  • [Cites] J Neurosurg. 1999 Jan;90(1):72-7 [10413158.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(4):708-15 [10673511.001]
  • [Cites] J Natl Cancer Inst. 1990 Dec 19;82(24):1918-21 [2250312.001]
  • (PMID = 12057153.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09291; United States / NCI NIH HHS / CA / CA13525
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 31
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32. 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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  • [Title] FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities.
  • Fibroblast growth factor 5 (FGF5) is widely expressed in embryonic but scarcely in adult tissues.
  • Here we report simultaneous overexpression of FGF5 and its predominant high-affinity receptor (FGFR1 IIIc) in astrocytic brain tumour specimens (N=49) and cell cultures (N=49).
  • Moreover, tumour cell migration was distinctly stimulated by rFGF5 but attenuated by FGF5 siRNA.
  • Blockade of FGFR1-mediated signals by pharmacological FGFR inhibitors or a dominant-negative FGFR1 IIIc protein inhibited GBM cell proliferation and/or induced apoptotic cell death.
  • Moreover, rFGF5 and supernatants of highly FGF5-positive GBM cell lines specifically stimulated proliferation, migration and tube formation of human umbilical vein endothelial cells.
  • 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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  • [Cites] Brain Res Mol Brain Res. 1996 May;38(1):161-5 [8737680.001]
  • [Cites] J Biol Chem. 1996 Jun 21;271(25):15292-7 [8663044.001]
  • [Cites] Vet Pathol. 1997 May;34(3):171-9 [9163872.001]
  • [Cites] Oncogene. 1997 Sep 18;15(12):1417-24 [9333017.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1998;59:135-76 [9427842.001]
  • [Cites] Cancer Res. 1998 Jan 15;58(2):352-61 [9443417.001]
  • [Cites] Surg Neurol. 1998 Feb;49(2):189-95; discussion 196 [9457270.001]
  • [Cites] Biochem Cell Biol. 1997;75(6):669-85 [9599656.001]
  • [Cites] J Pharmacol Exp Ther. 1998 Jul;286(1):569-77 [9655904.001]
  • [Cites] Neurosurgery. 1998 Aug;43(2):337-46 [9696088.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):29262-71 [9786939.001]
  • [Cites] Cancer Res. 1998 Dec 1;58(23):5285-90 [9850049.001]
  • [Cites] J Invest Dermatol. 1998 Dec;111(6):963-72 [9856803.001]
  • [Cites] Int J Cancer. 1999 Oct 29;83(3):415-23 [10495436.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Jun;131(6):355-63 [15856298.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):139-49 [15863030.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):179-86 [15863033.001]
  • [Cites] Growth Factors. 2005 Jun;23(2):87-95 [16019430.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11011-6 [16046538.001]
  • [Cites] Biochem Pharmacol. 2006 Feb 14;71(4):426-40 [16343446.001]
  • [Cites] J Cell Sci. 2006 Feb 1;119(Pt 3):459-69 [16418217.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3584-92 [16585183.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):281-93 [16554966.001]
  • [Cites] Mol Cancer Res. 2006 Dec;4(12):927-34 [17189383.001]
  • [Cites] Br J Cancer. 2007 Mar 26;96(6):960-9 [17342095.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4055-63 [17720881.001]
  • [Cites] J Neurosci. 2003 Jul 23;23(16):6404-12 [12878680.001]
  • [Cites] Cell Tissue Res. 2003 Aug;313(2):139-57 [12845521.001]
  • [Cites] J Clin Invest. 1973 Nov;52(11):2745-56 [4355998.001]
  • [Cites] Mol Cell Biol. 1988 Aug;8(8):3487-95 [3211147.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(20):8022-6 [1700424.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):1840-5 [2005884.001]
  • [Cites] Development. 1991 Jun;112(2):397-406 [1794310.001]
  • [Cites] J Invest Dermatol. 2000 Mar;114(3):456-63 [10692103.001]
  • [Cites] Glia. 2000 May;30(3):231-41 [10756073.001]
  • [Cites] Nat Cell Biol. 2001 Jul;3(7):650-7 [11433297.001]
  • [Cites] Cancer Res. 2001 Jul 15;61(14):5511-6 [11454700.001]
  • [Cites] J Cell Sci. 2002 Jan 15;115(Pt 2):329-39 [11839785.001]
  • [Cites] Int J Pancreatol. 2001;29(2):85-92 [11876253.001]
  • [Cites] Neurol Res. 2002 Apr;24(3):244-8 [11958417.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Feb;88(2):773-80 [12574212.001]
  • [Cites] Int J Cancer. 1993 Jan 21;53(2):209-14 [8381111.001]
  • [Cites] Neuron. 1993 Mar;10(3):369-77 [8461132.001]
  • [Cites] Brain Res. 1993 Mar 19;606(1):79-86 [8462006.001]
  • [Cites] Eur J Neurosci. 1994 Feb 1;6(2):244-52 [8167846.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2794-9 [8168112.001]
  • [Cites] Cell. 1994 Sep 23;78(6):1017-25 [7923352.001]
  • [Cites] J Neurooncol. 1994;18(3):207-16 [7964981.001]
  • [Cites] Oncogene. 1997 Jan 16;14(2):171-83 [9010219.001]
  • (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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33. Tews DS, Nissen A, Külgen C, Gaumann AK: Drug resistance-associated factors in primary and secondary glioblastomas and their precursor tumors. J Neurooncol; 2000 Dec;50(3):227-37
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  • [Title] Drug resistance-associated factors in primary and secondary glioblastomas and their precursor tumors.
  • Malignant gliomas are largely resistant to current chemotherapeutic strategies often displaying a multidrug-resistant phenotype.
  • Mechanisms involved in drug resistance are reduced cellular drug accumulation through membrane efflux pumps, drug detoxification as well as alterations in drug target specificity.
  • In 27 primary and 17 secondary glioblastomas and their astrocytic precursor tumors, we studied the immunohistochemical expression profile of P-glycoprotein (P-gp), multidrug resistance-associated protein (MRP), lung resistance-related protein (LRP), metallothionein, and topoisomerase II alpha.
  • Glial tumor cells in all glioblastomas showed constant up-regulation of LRP, MRP, and topoisomerase II alpha.
  • In precursor tumors, these drug resistance-related factors were expressed in varying proportions.
  • Metallothionein, also found in normal and activated astrocytes, was retained in all neoplastic phenotypes.
  • Furthermore, metallothionein, P-gp, LRP, and topoisomerase II alpha were strongly expressed by normal and neoplastic vessels which may confer to impaired penetration of therapeutic agents through the blood-brain and blood-tumor barrier.
  • However, the expression profiles of drug resistance-related proteins neither differed between primary and secondary glioblastomas nor revealed any correlation to precursor or recurrent tumors.
  • Nevertheless, inhibition of these factors may be promising approaches to the management of malignant gliomas.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Brain Neoplasms / metabolism. DNA Topoisomerases, Type II / metabolism. Drug Resistance, Neoplasm. Glioblastoma / metabolism. Isoenzymes / metabolism. Neoplasm Proteins / metabolism. Vault Ribonucleoprotein Particles / metabolism
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal. Antigens, Neoplasm. Antineoplastic Agents / therapeutic use. Cell Membrane / chemistry. DNA-Binding Proteins. Humans. Immunoenzyme Techniques. Metallothionein / metabolism. Middle Aged. Multidrug Resistance-Associated Proteins

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  • [Cites] J Neurooncol. 1998 Jan;36(1):41-53 [9525824.001]
  • [Cites] Glia. 1993 May;8(1):62-70 [8509165.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;41(2):93-7 [9443620.001]
  • [Cites] Br J Cancer. 1997;76(4):445-50 [9275020.001]
  • [Cites] Am J Pathol. 1996 Sep;149(3):853-8 [8780389.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1237-47 [8644864.001]
  • [Cites] Cancer Res. 1997 Dec 1;57(23):5292-9 [9393752.001]
  • [Cites] Eur J Biochem. 1997 Apr 15;245(2):307-15 [9151958.001]
  • [Cites] Exp Cell Res. 1990 Oct;190(2):212-7 [2209724.001]
  • [Cites] Am J Pathol. 1996 Mar;148(3):877-87 [8774142.001]
  • [Cites] J Neurooncol. 1992 Sep;14(1):37-43 [1361524.001]
  • [Cites] Anticancer Drugs. 1992 Aug;3(4):323-30 [1330080.001]
  • [Cites] J Neurooncol. 1993 Aug;17(2):111-21 [8145054.001]
  • [Cites] Biochemistry. 1986 Apr 22;25(8):2248-56 [3011082.001]
  • [Cites] Curr Opin Oncol. 1998 May;10(3):194-200 [9619354.001]
  • [Cites] J Neuropathol Exp Neurol. 1997 Feb;56(2):180-5 [9034372.001]
  • [Cites] Cancer. 1998 Dec 1;83(11):2361-9 [9840536.001]
  • [Cites] Br J Cancer. 1996 Oct;74(8):1263-8 [8883415.001]
  • [Cites] Nat Med. 1995 Jun;1(6):578-82 [7585126.001]
  • [Cites] Acta Neuropathol. 1997 Dec;94(6):605-11 [9444363.001]
  • [Cites] J Neurosurg. 1991 Mar;74(3):460-6 [1671590.001]
  • [Cites] Important Adv Oncol. 1994;:21-36 [7911445.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):13033-7 [7809167.001]
  • [Cites] Mol Toxicol. 1989 Apr-Jun;2(2):67-74 [2702304.001]
  • [Cites] Virchows Arch. 1994;425(2):133-8 [7952498.001]
  • [Cites] Br J Cancer. 1998 Feb;77(4):547-51 [9484809.001]
  • [Cites] Neuropathol Appl Neurobiol. 1999 Aug;25(4):272-84 [10476044.001]
  • [Cites] Gen Pharmacol. 1994 Nov;25(7):1297-310 [7896039.001]
  • [Cites] Clin Neuropathol. 1997 Jan-Feb;16(1):34-6 [9020393.001]
  • [Cites] Cancer Res. 1993 Dec 1;53(23):5663-8 [8242621.001]
  • [Cites] Pathol Res Pract. 1998;194(3):149-55 [9587932.001]
  • [Cites] Neurochem Int. 1995 Jul;27(1):1-22 [7655341.001]
  • [Cites] J Histochem Cytochem. 1990 Sep;38(9):1277-87 [1974900.001]
  • [Cites] Int J Cancer. 1994 Sep 15;58(6):860-4 [7927879.001]
  • [Cites] Biochim Biophys Acta. 1985 Jan 21;827(1):36-44 [2981555.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8822-6 [7916458.001]
  • [Cites] Ther Drug Monit. 1998 Oct;20(5):588-90 [9780140.001]
  • [Cites] Acta Neuropathol. 1991;82(6):516-9 [1723831.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7668-71 [2823270.001]
  • [Cites] J Neurosci. 1991 Jan;11(1):256-68 [1986066.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Feb 24;243(3):816-20 [9500978.001]
  • [Cites] Annu Rev Biochem. 1989;58:137-71 [2570548.001]
  • [Cites] Neuropathol Appl Neurobiol. 1996 Jun;22(3):243-7 [8804026.001]
  • [Cites] J Neurooncol. 1998 Oct;40(1):11-8 [9874181.001]
  • [Cites] Pathol Int. 1994 Jan;44(1):20-6 [8025645.001]
  • [Cites] Acta Neuropathol. 1997 Dec;94(6):599-604 [9444362.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6969-75 [1360873.001]
  • [Cites] Mol Pharmacol. 1996 Jun;49(6):962-71 [8649356.001]
  • [Cites] Eur J Cancer. 1993;29A(5):753-9 [8385972.001]
  • [Cites] Cell. 1994 May 20;77(4):491-502 [7910522.001]
  • [Cites] Methods Enzymol. 1991;205:613-26 [1779825.001]
  • [Cites] Cancer Lett. 1997 Jan 15;112(1):23-31 [9029166.001]
  • [Cites] J Neurosurg. 1991 Dec;75(6):941-6 [1682428.001]
  • (PMID = 11263502.001).
  • [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 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Isoenzymes; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 9038-94-2 / Metallothionein; EC 5.99.1.3 / DNA Topoisomerases, Type II
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34. Sbalchiero E, Azzalin A, Palumbo S, Barbieri G, Arias A, Simonelli L, Ferretti L, Comincini S: Altered cellular distribution and sub-cellular sorting of doppel (Dpl) protein in human astrocytoma cell lines. Cell Oncol; 2008;30(4):337-47
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  • [Title] Altered cellular distribution and sub-cellular sorting of doppel (Dpl) protein in human astrocytoma cell lines.
  • Doppel, a prion-like protein, is a GPI-membrane anchored protein generally not expressed in the Central Nervous System (CNS) of different mammalian species, including human.
  • Nevertheless, in astrocytomas, a particular kind of glial tumors, the doppel encoding gene (PRND) is over-expressed and the corresponding protein product (Dpl) is ectopically localized in the cytoplasm of the tumor cells.
  • In this study we have analysed the sub-cellular localization of Dpl using double-immunofluorescence staining and confocal microscopy examinations in two astrocytoma-derived human cell lines (IPDDC-A2 and D384-MG).
  • Noticeably, none of the examined tumor cells showed a membrane-Dpl localization.
  • Additionally, Dpl showed altered expression and traffic using the acidotropic agent ammonium chloride, leading to the accumulation of Dpl in nascent exocytic vesicles.
  • Altogether, these results indicated that in the astrocytic tumor cells Dpl has an altered biosynthetic trafficking, likely derived from abnormal post-translational processes: these modifications do not permit the localization of Dpl in correspondence of the plasma membrane and lead to its intracellular accumulation in the lysosomes.
  • In these proteolytic compartments, the astrocytic tumor cells might provide to the degradation of the excess of a potentially cytotoxic Dpl product.
  • [MeSH-major] Astrocytes / metabolism. Brain Neoplasms / metabolism. Glioblastoma / metabolism. Oligodendroglioma / metabolism. Prions / metabolism
  • [MeSH-minor] Adult. Ammonium Chloride / pharmacology. Cell Compartmentation. Cell Culture Techniques. Cell Membrane / metabolism. Cell Membrane / ultrastructure. GPI-Linked Proteins. Gene Expression Regulation, Neoplastic. Glycosylation. Glycosylphosphatidylinositols / genetics. Glycosylphosphatidylinositols / metabolism. HeLa Cells. Humans. Lysosomes / metabolism. Lysosomes / ultrastructure. Male. Mutant Proteins / analysis. Mutant Proteins / genetics. Mutant Proteins / metabolism. Protein Transport. Recombinant Proteins / analysis. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 18607068.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Glycosylphosphatidylinositols; 0 / Mutant Proteins; 0 / PRND protein, human; 0 / Prions; 0 / Recombinant Proteins; 01Q9PC255D / Ammonium Chloride
  • [Other-IDs] NLM/ PMC4618817
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35. Lewandowicz GM, Harding B, Harkness W, Hayward R, Thomas DG, Darling JL: Chemosensitivity in childhood brain tumours in vitro: evidence of differential sensitivity to lomustine (CCNU) and vincristine. Eur J Cancer; 2000 Oct;36(15):1955-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemosensitivity in childhood brain tumours in vitro: evidence of differential sensitivity to lomustine (CCNU) and vincristine.
  • The aim of this study was to examine the range of sensitivity of a panel of short-term cultures derived from different types of malignant childhood brain tumours including medulloblastoma, ependymoma and glioblastoma multiforme to three cytotoxic drugs, lomustine (CCNU), vincristine (VCR) and procarbazine (PCB).
  • Short-term cell lines derived from ependymomas were considerably more resistant to VCR than other types of childhood brain tumours, while cultures derived from supratentorial primitive neuroectodermal tumour (PNET) displayed marked sensitivity to both lomustine and VCR.
  • Cultures from ependymomas, medulloblastoma and astrocytic gliomas had similar sensitivity to lomustine and PCB as cultures derived from adult malignant astrocytoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Adult. Astrocytoma / drug therapy. Child. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Ependymoma / drug therapy. Female. Glioblastoma / drug therapy. Humans. Lomustine / therapeutic use. Male. Medulloblastoma / drug therapy. Procarbazine / therapeutic use. Tumor Cells, Cultured / drug effects. Vincristine / therapeutic use

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  • (PMID = 11000577.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine
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36. Nishio S, Morioka T, Fujii K, Inamura T, Fukui M: Spinal cord gliomas: management and outcome with reference to adjuvant therapy. J Clin Neurosci; 2000 Jan;7(1):20-3
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  • [Title] Spinal cord gliomas: management and outcome with reference to adjuvant therapy.
  • The authors review their experience with 19 consecutive cases with either astrocytic tumour (glioblastoma multiforme one, anaplastic astrocytoma one, astrocytoma 4, pilocytic astrocytoma 4) or ependymoma (10 tumours in 9 patients) of the spinal cord who were treated during the period from 1982 to 1996.
  • The patients included 10 male and 9 female patients with a median age of 38 years.
  • The main tumour locations included the cervicomedullary region 5 the cervical cord (8), the thoracic cord (5) and one each in the thoracolumbar region and conus medullaris.
  • While a total removal of the tumour was achieved in 8 out of 10 ependymomas, the initial treatment for astrocytic tumours was a partial resection in 5, and biopsy in the remaining 5.
  • Two patients with an astrocytic tumour received chemotherapy only, while the remaining 9 received neither radiation therapy nor chemotherapy initially.
  • After these treatments, 6 out of the 8 patients with low grade astrocytoma have remained alive for 1.3-12.6 years, while 2 patients with high grade astrocytic tumours died within 15 months following surgery.
  • Eight out of 9 patients with an ependymoma have remained alive for 3.0-12.3 years, while one committed suicide 2 years after surgery.
  • The postoperative results and the rationale for surgery is discussed, and an approach for utilising adjuvant therapy for high grade tumours is also suggested.
  • [MeSH-major] Astrocytoma / surgery. Ependymoma / surgery. Spinal Cord Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Chemotherapy, Adjuvant. Child, Preschool. Female. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Glioblastoma / surgery. Humans. Infant. Male. Middle Aged. Postoperative Care. Radiotherapy, Adjuvant. Retrospective Studies

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  • (PMID = 10847645.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] SCOTLAND
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37. Benito R, Gil-Benso R, Quilis V, Perez M, Gregori-Romero M, Roldan P, Gonzalez-Darder J, Cerdá-Nicolas M, Lopez-Gines C: Primary glioblastomas with and without EGFR amplification: relationship to genetic alterations and clinicopathological features. Neuropathology; 2010 Aug;30(4):392-400
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  • Glioblastomas express a notable heterogeneity in both the histological and cell patterns with glial astrocytic differentiation.
  • Primary glioblastoma, which is the most frequent presentation (90-95%), occurs mainly in older patients and arises de novo, without any clinical or histological evidence of a less malignant precursor lesion.
  • EGFR amplification was observed in 24 cases (53%), while in the remaining 21 cases (47%) this alteration was not displayed.
  • The amplification of EGFR was associated with amplifications in MDM2 and CDK4 and a higher percentage of cases with promoter methylation of INK4a.
  • The genetic studies suggest the existence of molecular subtypes within primary glioblastoma that may, when fully defined, contribute toward the development of drugs that specifically target tumors with divergent genetic profiles.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / pathology. Genes, erbB-1 / genetics. Glioblastoma / genetics. Glioblastoma / pathology
  • [MeSH-minor] Adult. Aged. Cyclin-Dependent Kinase 4 / genetics. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Middle Aged. Polymerase Chain Reaction. Proto-Oncogene Proteins c-mdm2 / genetics. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 20051017.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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38. Birlik B, Canda S, Ozer E: Tumour vascularity is of prognostic significance in adult, but not paediatric astrocytomas. Neuropathol Appl Neurobiol; 2006 Oct;32(5):532-8
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  • [Title] Tumour vascularity is of prognostic significance in adult, but not paediatric astrocytomas.
  • Astrocytomas are the commonest type of brain tumours in adults and children.
  • Although the most reliable prognostic indicators have been shown consistently to be patient age and tumour histological grade, biological progression in these tumours is inevitable and the overall prognosis has remained poor.
  • Due to the evidence that vascular changes are important histological features of astrocytomas, the aim of this study was to investigate prognostic significance of tumour vascularity in paediatric and adult astrocytomas.
  • Study population consisted of 70 patients (45 adult and 25 children) with histologically proven diagnosis of astrocytoma with no history of previous therapy.
  • Histological quantification of tumour vascularity was performed using three different methods: microvessel density, vascular grading and Chalkley counting.
  • In contrast to the results in paediatric astrocytomas, tumour vascularity in adult tumours correlated significantly with postoperative survival by univariate analysis (P < 0.05).
  • Patient age and tumour histological grade were also correlated with survival.
  • We conclude that histological quantification of tumour vascularity is a significant prognosticator in adult astrocytomas, but not in children.
  • Our data do not support the validity of applications of antiangiogenic agents in paediatric astrocytic tumours, particularly pilocytic astrocytomas.
  • [MeSH-major] Aging / pathology. Astrocytoma / blood supply. Astrocytoma / pathology. Brain Neoplasms / blood supply. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Angiogenesis Inhibitors / therapeutic use. Antigens, CD31 / metabolism. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Prognosis. Regional Blood Flow / physiology. Retrospective Studies. Survival

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  • (PMID = 16972887.001).
  • [ISSN] 0305-1846
  • [Journal-full-title] Neuropathology and applied neurobiology
  • [ISO-abbreviation] Neuropathol. Appl. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31
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39. Kaloshi G, Psimaras D, Mokhtari K, Dehais C, Houillier C, Marie Y, Laigle-Donadey F, Taillibert S, Guillevin R, Martin-Duverneuil N, Sanson M, Hoang-Xuan K, Delattre JY: Supratentorial low-grade gliomas in older patients. Neurology; 2009 Dec 15;73(24):2093-8
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  • BACKGROUND: Low-grade gliomas (LGG) are thought to be very rare in elderly patients (>60 years) and have not been thoroughly studied.
  • METHODS: A series of 62 elderly (>or=60 years of age) LGG patients were identified in a department database collecting information on pathologically identified adult supratentorial LGG.
  • The clinical, radiologic, pathologic, and therapeutic data of these patients were analyzed and compared to those of 704 younger LGG patients (<60 years).
  • RESULTS: Comparisons between older and younger groups showed that elderly patients more often presented with a clinical deficit (p < 0.0001), a lower Karnofsky performance status (p = 0.0002), a larger tumor on MRI (p = 0.03), and a lower rate of tumor resection (p < 0.0001).
  • Among the patients who died of progressive disease, 55% of the elderly patients had not received radiotherapy compared to 11% in the younger group (p < 0.0001).
  • Survival was shorter in older patients (p < 0.0001), with a 5-year survival rate of 40%.
  • An astrocytic phenotype (p = 0.0097), increasing age (p = 0.0049), and a tumor crossing the midline (p = 0.028) were negative prognostic factors in the older group.
  • CONCLUSION: We found that 8% of low-grade gliomas (LGG) occur in older patients (>or=60 years of age).
  • [MeSH-major] Glioma / physiopathology. Glioma / therapy. Supratentorial Neoplasms / physiopathology. Supratentorial Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Disease-Free Survival. Drug Therapy / statistics & numerical data. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neurosurgical Procedures / statistics & numerical data. Prognosis. Radiotherapy / statistics & numerical data. Severity of Illness Index. Survival Rate. Young Adult

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  • [CommentIn] Neurology. 2009 Dec 15;73(24):2056-7 [19907010.001]
  • (PMID = 19907009.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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40. Kong GY, Kristensson K, Bentivoglio M: Reaction of mouse brain oligodendrocytes and their precursors, astrocytes and microglia, to proinflammatory mediators circulating in the cerebrospinal fluid. Glia; 2002 Mar 1;37(3):191-205
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  • The response of glial cells to the acute intracerebroventricular administration of interferon-gamma, and of this cytokine combined with the endotoxin lipopolysaccharide or with tumor necrosis factor-alpha, was investigated in the brain of adult mice over a time course of 1 week.
  • Such glial responses to interferon-gamma injections were especially marked in the periventricular brain parenchyma and were enhanced by coadministration of lipopolysaccharide or tumor necrosis factor-alpha.
  • The findings show that a pulse of proinflammatory mediators in the cerebrospinal fluid affects mature oligodendrocytes, concomitantly with the early appearance of activated microglia, and that such reactions are rapidly followed by an increase of oligodendrocyte precursors paralleled by astrocytic activation.
  • The data, which allowed dissecting the events elicited in glial cell populations by inflammatory mediators via the cerebrospinal fluid, indicate that these molecules elicit in vivo a toxic effect on mature oligodendrocytes and a stimulation of their precursors in the adult brain.
  • [MeSH-minor] 2',3'-Cyclic-Nucleotide Phosphodiesterases / metabolism. Animals. Antigens, Differentiation / metabolism. Brain / drug effects. Brain / immunology. Brain / pathology. Cell Count. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Interferon-gamma / cerebrospinal fluid. Interferon-gamma / immunology. Interferon-gamma / pharmacology. Lipopolysaccharides / cerebrospinal fluid. Lipopolysaccharides / immunology. Lipopolysaccharides / pharmacology. Mice. Mice, Inbred C57BL. Tumor Necrosis Factor-alpha / cerebrospinal fluid. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects. Up-Regulation / immunology

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 11857678.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Cytokines; 0 / Glial Fibrillary Acidic Protein; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 0 / oligodendrocyte O antigen, mouse; 82115-62-6 / Interferon-gamma; EC 3.1.4.- / 2',3'-Cyclic-Nucleotide Phosphodiesterases; EC 3.1.4.16 / 2',3'-cyclic nucleotide 2'-phosphodiesterase
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41. Sanson M, Cartalat-Carel S, Taillibert S, Napolitano M, Djafari L, Cougnard J, Gervais H, Laigle F, Carpentier A, Mokhtari K, Taillandier L, Chinot O, Duffau H, Honnorat J, Hoang-Xuan K, Delattre JY, ANOCEF group: Initial chemotherapy in gliomatosis cerebri. Neurology; 2004 Jul 27;63(2):270-5
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  • METHODS: The authors treated 63 consecutive patients with GC with initial chemotherapy consisting of either PCV (procarbazine, 60 mg/m2 on days 8 to 21; CCNU, 110 mg/m2 on day 1; and vincristine, 1.4 mg/m2 on days 8 and 29) or temozolomide (TMZ; 150 to 200 mg/m2 for 5 days every 4 weeks).
  • There were 40 men and 23 women, with a median age of 48 years (range, 17 to 74 years) and a median Karnofsky performance status of 90 (range, 50 to 100).
  • GC was initially present at diagnosis in 49 patients (primary GC), whereas 14 patients with a circumscribed glioma at onset developed secondary GC after a median follow-up period of 5.11 years.
  • GC was classified based on the predominant tumor cells as astrocytic, oligodendroglial, or mixed GC.
  • Clinical objective responses were observed in 21 of 63 (33%) patients, and radiologic responses were seen in 16 of 62 (26%), with no significant difference between the two regimens.
  • Regardless of the chemotherapeutic regimen, oligodendroglial GC had a better prognosis than astrocytic and oligoastrocytic GC in terms of PFS (p < 0.02) and OS (p < 0.0001).
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Neoplasms, Neuroepithelial / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Astrocytoma / drug therapy. Astrocytoma / radiotherapy. Combined Modality Therapy. Cranial Irradiation. Disease Progression. Disease-Free Survival. Drug Administration Schedule. Female. Hematologic Diseases / chemically induced. Humans. Karnofsky Performance Status. Lomustine / administration & dosage. Lomustine / adverse effects. Magnetic Resonance Imaging. Male. Middle Aged. Oligodendroglioma / drug therapy. Oligodendroglioma / radiotherapy. Procarbazine / administration & dosage. Procarbazine / adverse effects. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

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  • [CommentIn] Neurology. 2004 Jul 27;63(2):204-5 [15277608.001]
  • (PMID = 15277619.001).
  • [ISSN] 1526-632X
  • [Journal-full-title] Neurology
  • [ISO-abbreviation] Neurology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 7BRF0Z81KG / Lomustine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; PCV protocol
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42. Murakami H, Sawa H, Kamada H: [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors]. No To Shinkei; 2006 Jan;58(1):43-9
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  • [Title] [Expression of cyclooxygenase (COX)-2 in astrocytic tumors and anti-tumor effects of selective COX-2 inhibitors].
  • Cyclooxygenase (COX)-2 of astrocytic tumors was studied by immunohistochemistry.
  • COX-2 was detected by an immnoblotting in 2 of 9 human glioblastoma cell lines (KNS42 and U138).
  • The result showed that COX-2 expression may be related with histological grades and COX-2 inhibitors will be one of promising therapeutic tools in human astrocytic tumors.
  • [MeSH-minor] Adult. Aged. Etodolac / pharmacology. Female. Glioblastoma / drug therapy. Glioblastoma / enzymology. Humans. Immunoblotting. Immunohistochemistry. Male. Middle Aged. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured

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  • (PMID = 16482921.001).
  • [ISSN] 0006-8969
  • [Journal-full-title] Nō to shinkei = Brain and nerve
  • [ISO-abbreviation] No To Shinkei
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitrobenzenes; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 2M36281008 / Etodolac; EC 1.14.99.1 / Cyclooxygenase 2
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43. Keating AK, Kim GK, Jones AE, Donson AM, Ware K, Mulcahy JM, Salzberg DB, Foreman NK, Liang X, Thorburn A, Graham DK: Inhibition of Mer and Axl receptor tyrosine kinases in astrocytoma cells leads to increased apoptosis and improved chemosensitivity. Mol Cancer Ther; 2010 May;9(5):1298-307
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  • Astrocytomas account for the majority of malignant brain tumors diagnosed in both adult and pediatric patients.
  • The therapies available to treat these neoplasms are limited, and the prognosis associated with high-grade lesions is extremely poor.
  • In this study, we found that Mer and Axl mRNA transcript and protein expression were elevated in astrocytic patient samples and cell lines. shRNA-mediated knockdown of Mer and Axl RTK expression led to an increase in apoptosis in astrocytoma cells.
  • Apoptotic signaling pathways including Akt and extracellular signal-regulated kinase 1/2, which have been shown to be activated in resistant astrocytomas, were downregulated with Mer and Axl inhibition whereas poly(ADP-ribose) polymerase cleavage was increased.
  • Furthermore, Mer and Axl shRNA knockdown led to a profound decrease of astrocytoma cell proliferation in soft agar and a significant increase in chemosensitivity in response to temozolomide, carboplatin, and vincristine treatment.
  • Our results suggest Mer and Axl RTK inhibition as a novel method to improve apoptotic response and chemosensitivity in astrocytoma and provide support for these oncogenes as attractive biological targets for astrocytoma drug development.

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  • [Cites] Nature. 1999 Dec 9;402(6762):672-6 [10604474.001]
  • [Cites] N Engl J Med. 2009 Oct 15;361(16):1570-83 [19828534.001]
  • [Cites] Nat Med. 2001 Feb;7(2):215-21 [11175853.001]
  • [Cites] Science. 2001 Jul 13;293(5528):306-11 [11452127.001]
  • [Cites] Anticancer Res. 2002 Mar-Apr;22(2B):1071-8 [12168903.001]
  • [Cites] J Clin Oncol. 2002 Aug 15;20(16):3470-7 [12177108.001]
  • [Cites] Curr Opin Immunol. 2003 Feb;15(1):31-6 [12495730.001]
  • [Cites] J Neurosci. 2003 May 15;23(10):4208-18 [12764109.001]
  • [Cites] Clin Exp Metastasis. 2003;20(7):665-74 [14669798.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1952-6 [3279421.001]
  • [Cites] Cell Growth Differ. 1994 Jun;5(6):647-57 [8086340.001]
  • [Cites] Mol Cell Biol. 1995 Dec;15(12):6582-92 [8524223.001]
  • [Cites] J Neurosurg. 1999 Mar;90(3):533-6 [10067924.001]
  • [Cites] Leukemia. 1999 Sep;13(9):1352-8 [10482985.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):237-46 [15650770.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Neoplasia. 2005 Dec;7(12):1058-64 [16354588.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5799-804 [16585512.001]
  • [Cites] Clin Cancer Res. 2006 May 1;12(9):2662-9 [16675557.001]
  • [Cites] J Neurosci. 2006 May 24;26(21):5638-48 [16723520.001]
  • [Cites] Nat Immunol. 2006 Jul;7(7):747-54 [16751775.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Aug;65(8):769-75 [16896310.001]
  • [Cites] Oncogene. 2006 Oct 5;25(45):6092-100 [16652142.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Dec;65(12):1181-8 [17146292.001]
  • [Cites] Neoplasma. 2007;54(4):334-41 [17822324.001]
  • [Cites] Autophagy. 2007 Nov-Dec;3(6):542-5 [17611390.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):130-8 [18172262.001]
  • [Cites] J Neurosci. 2008 Jan 2;28(1):264-78 [18171944.001]
  • [Cites] Cell. 2008 Jan 11;132(1):27-42 [18191218.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):327-36 [18421305.001]
  • [Cites] Adv Cancer Res. 2008;100:35-83 [18620092.001]
  • [Cites] J Cell Physiol. 2008 Dec;217(3):584-9 [18651562.001]
  • [Cites] Mol Endocrinol. 2008 Nov;22(11):2481-95 [18787040.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4466-74 [18587011.001]
  • [Cites] Adv Tech Stand Neurosurg. 2009;34:3-35 [19368079.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):459-66 [19269895.001]
  • [Cites] Oncogene. 2009 Oct 1;28(39):3442-55 [19633687.001]
  • [Cites] J Comp Neurol. 2000 Sep 18;425(2):295-314 [10954847.001]
  • (PMID = 20423999.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA082086-10; United States / NCI NIH HHS / CA / T32 CA082086; United States / NCI NIH HHS / CA / T32 CA082086-10
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; EC 2.7.10.1 / MERTK protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / axl receptor tyrosine kinase
  • [Other-IDs] NLM/ NIHMS304681; NLM/ PMC3138539
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44. Nawashiro H, Otani N, Shinomiya N, Fukui S, Ooigawa H, Shima K, Matsuo H, Kanai Y, Endou H: L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors. Int J Cancer; 2006 Aug 1;119(3):484-92
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  • [Title] L-type amino acid transporter 1 as a potential molecular target in human astrocytic tumors.
  • L-type amino acid transporter 1 (LAT1) is a Na+-independent neutral amino acid transport agency and essential for the transport of large neutral amino acids.
  • We have investigated for the first time, the expression of the transporter in the human primary astrocytic tumor tissue from 60 patients.
  • BCH inhibited the growth of C6 glioma cells in vitro and in vivo in a dose-dependent manner.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Large Neutral Amino Acid-Transporter 1 / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acids, Cyclic / pharmacology. Animals. Antigens, CD98 Heavy Chain / analysis. Cell Line, Tumor. Cell Survival / drug effects. Child. Female. Glioma / drug therapy. Glioma / mortality. Glioma / pathology. Humans. Immunohistochemistry. Infant, Newborn. Male. Middle Aged. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / mortality. Neoplasms, Experimental / pathology. Rats. Rats, Wistar. Survival Analysis. Survival Rate

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  • [Copyright] Copyright (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16496379.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Cyclic; 0 / Antigens, CD98 Heavy Chain; 0 / Large Neutral Amino Acid-Transporter 1; 20448-79-7 / 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid
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45. Pittock SJ, Lennon VA: Aquaporin-4 autoantibodies in a paraneoplastic context. Arch Neurol; 2008 May;65(5):629-32
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  • Its antigen is the astrocytic water channel aquaporin-4; NMO-IgG has not been described in a cancer context.
  • SETTING: Neuroimmunology Laboratory and Neurology Clinical Practice, Mayo Clinic College of Medicine.
  • (1) 31 patients (88% female) identified incidentally among 180 000 patients evaluated for paraneoplastic autoantibodies and (2) 141 patients identified through physician-requested serological evaluation for a suspected NMO-spectrum disorder.
  • An NMO-spectrum disorder was diagnosed in 26 patients (93%), of whom 6 had a neoplasm (5 carcinomas [2 breast, 1 lung, 1 thymic, and 1 uterine cervical] and 1 B-cell lymphoma) and 1 had monoclonal gammopathy.
  • In 4 patients, NMO-related symptoms followed neoplasia detection (median, 14 [range 3-18] months), and in 2 patients, symptoms preceded neoplasia detection (by 5 and 3 months).
  • Two patients had carcinoma (1 breast and 1 lung) without neurological evidence of an NMO-spectrum disorder.
  • In the second group, neoplasms were recorded in 7 seropositive patients (5.0%) with a clinically diagnosed NMO-spectrum disorder: 3 carcinomas (all breast), 1 thyroid Hürthle cell, 1 carcinoid, 1 pituitary somatotropinoma, and 1 B-cell lymphoma.
  • [MeSH-major] Aquaporin 4 / immunology. Autoantibodies / immunology. Autoimmune Diseases of the Nervous System / immunology. Neoplasms / immunology. Paraneoplastic Syndromes, Nervous System / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers / analysis. Comorbidity. Female. Humans. Immunoglobulin G / blood. Immunoglobulin G / immunology. Male. Middle Aged. Neuromyelitis Optica / immunology. Paraproteinemias / epidemiology. Paraproteinemias / immunology. Paraproteinemias / physiopathology. Predictive Value of Tests. Retrospective Studies

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  • [ErratumIn] Arch Neurol. 2008 Oct;65(10):1394
  • (PMID = 18474738.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aquaporin 4; 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G
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46. Preusser M, Hoischen A, Novak K, Czech T, Prayer D, Hainfellner JA, Baumgartner C, Woermann FG, Tuxhorn IE, Pannek HW, Bergmann M, Radlwimmer B, Villagrán R, Weber RG, Hans VH: Angiocentric glioma: report of clinico-pathologic and genetic findings in 8 cases. Am J Surg Pathol; 2007 Nov;31(11):1709-18
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  • Angiocentric glioma has recently been described as a novel epilepsy associated tumor with distinct clinico-pathologic features.
  • We report the clinical and pathologic findings in 8 additional cases of this rare tumor type and extend its characterization by genomic profiling.
  • Almost all patients had a history of long-standing drug-resistant epilepsy.
  • Cortico-subcortical tumors were located in the temporal and parietal lobes.
  • Seizures began at 3 to 14 years of age and surgery was performed at 6 to 70 years.
  • Histologically, the tumors were characterized by diffuse growth and prominent perivascular tumor cell arrangements with features of astrocytic/ependymal differentiation, but lacking neoplastic neuronal features.
  • In 1 of 3 cases, a high-resolution screen by array-comparative genomic hybridization identified a copy number gain of 2 adjacent clones from chromosomal band 11p11.2 containing the protein-tyrosine phosphatase receptor type J (PTPRJ) gene.
  • All patients are seizure free and without evidence of tumor recurrence at follow-up times ranging from 1/2 to 6.9 years.
  • Our findings support 2 previous reports proposing that angiocentric glioma is a novel glial tumor entity of low-grade malignancy.
  • [MeSH-major] Brain Neoplasms / genetics. Brain Neoplasms / ultrastructure. Epilepsy / genetics. Gene Expression Regulation, Neoplastic. Glioma / genetics. Glioma / ultrastructure
  • [MeSH-minor] Adolescent. Adult. Aged. Astrocytes / pathology. Cell Differentiation. Cell Proliferation. Child. Child, Preschool. Chromosome Deletion. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 6. Ependyma / pathology. Europe. Female. Follow-Up Studies. Gene Dosage. Gene Expression Profiling / methods. Glial Fibrillary Acidic Protein / analysis. Humans. Magnetic Resonance Imaging. Male. Membrane Glycoproteins / analysis. Middle Aged. Mucin-1 / analysis. Nerve Growth Factors / analysis. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Receptor-Like Protein Tyrosine Phosphatases, Class 3 / genetics. S100 Calcium Binding Protein beta Subunit. S100 Proteins / analysis. Time Factors. Treatment Outcome. Vimentin / analysis

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  • (PMID = 18059228.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Membrane Glycoproteins; 0 / Mucin-1; 0 / Nerve Growth Factors; 0 / PDPN protein, human; 0 / S100 Calcium Binding Protein beta Subunit; 0 / S100 Proteins; 0 / S100B protein, human; 0 / Vimentin; EC 3.1.3.48 / PTPRJ protein, human; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 3
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