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1. Ren H, Boulikas T, Lundstrom K, Söling A, Warnke PC, Rainov NG: Immunogene therapy of recurrent glioblastoma multiforme with a liposomally encapsulated replication-incompetent Semliki forest virus vector carrying the human interleukin-12 gene--a phase I/II clinical protocol. J Neurooncol; 2003 Aug-Sep;64(1-2):147-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunogene therapy of recurrent glioblastoma multiforme with a liposomally encapsulated replication-incompetent Semliki forest virus vector carrying the human interleukin-12 gene--a phase I/II clinical protocol.
  • Glioblastoma multiforme (GBM) is an incurable brain tumor resistant to standard treatment modalities such as surgery, radiation, and chemotherapy.
  • Since recurrent GBM tends to develop predominantly within the infiltrative rim surrounding the primary tumor focus, novel therapy strategies need in addition to focal tumor destruction to target this somewhat diffuse area.
  • This is a phase I/II clinical study in adult patients with recurrent GBM which is aimed at evaluating biological safety, maximum tolerated dose, and antitumor efficacy of a genetically modified replication-disabled Semliki forest virus vector (SFV) carrying the human interleukin 12 (IL-12) gene and encapsulated in cationic liposomes (LSFV-IL12).
  • The vector will be administered in doses of 1 x 10(7)-1 x 10(9) infectious particles by continuous intratumoral infusion, thus exploiting the advantages of convection-enhanced drug delivery in the brain.
  • The present protocol is also designed to investigate systemic and local immune response and to identify factors predicting tumor response to LSFV-IL12 therapy, such as volume of extracellular space of the tumor, volume of contrast enhancing lesion, and immune status of the patients.
  • SFV, an insect alphavirus, infects mitotic and non-mitotic cells and triggers apoptosis in tumor cells within 48-72 h.
  • [MeSH-major] Cerebellar Neoplasms / therapy. Genetic Therapy / methods. Glioblastoma / therapy. Immunotherapy / methods. Interleukin-12 / genetics. Interleukin-12 / immunology. Neoplasm Recurrence, Local / therapy

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  • [ErratumIn] J Neurooncol. 2003 Nov;65(2):191
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  • (PMID = 12952295.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsules; 0 / Liposomes; 187348-17-0 / Interleukin-12
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2. Vlassenko AG, Thiessen B, Beattie BJ, Malkin MG, Blasberg RG: Evaluation of early response to SU101 target-based therapy in patients with recurrent supratentorial malignant gliomas using FDG PET and Gd-DTPA MRI. J Neurooncol; 2000;46(3):249-59
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  • Changes in [18F]-2-fluoro-2-deoxyglucose (FDG) uptake and gadopentetate dimeglumine (Gd-DTPA) enhancement before and after the first course of treatment with a cytostatic agent SU101 (N-[(4-trifluoromethyl)-phenyl]-5-methylisoxazole-4-carboxamide, SUGEN) were assessed using positron emission tomography (PET) and magnetic resonance imaging (MRI) in a pilot study of 8 patients with recurrent supratentorial malignant gliomas.
  • The ratios of mean tumor activity to mean contralateral white matter and ipsilateral cerebellar activity were calculated for tumor regions, and SUV values corrected to the subjects' body surface area and glucose level (SUVbsa*glu) were calculated for nontumor regions.
  • Five patients had a substantial increase of tumor volume on both PET and MRI during the first course of SU101.
  • Large tumor volume increases were associated with a short time to clinical progression.
  • The metabolic change in the tumor following the first course of SU101 varied from patient to patient, ranging from a 31% reduction to a 43% increase in FDG uptake ratio.
  • In 2 patients with marked clinical deterioration and rapid tumor growth, there were differences in localization of Gd-DTPA enhancement and FDG hypermetabolism suggesting that hypermetabolism beyond the area of contrast enhancement may be of value in predicting rapid progression of high-grade glioma.
  • SU101 did not induce any appreciable changes in SUVbsa*glu for non-tumor brain in 6 of 8 patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Fluorodeoxyglucose F18. Gadolinium DTPA. Glioblastoma / drug therapy. Isoxazoles / therapeutic use. Magnetic Resonance Imaging. Neoplasm Recurrence, Local / drug therapy. Supratentorial Neoplasms / drug therapy. Tomography, Emission-Computed
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biological Transport, Active / drug effects. Carmustine / administration & dosage. Chemotherapy, Adjuvant. Combined Modality Therapy. Cranial Irradiation. Disease Progression. Disease-Free Survival. Energy Metabolism / drug effects. Female. Glucose / metabolism. Humans. Male. Middle Aged. Platelet-Derived Growth Factor / physiology. Prognosis. Signal Transduction / drug effects. Treatment Outcome

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  • (PMID = 10902856.001).
  • [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 / Antineoplastic Agents; 0 / Isoxazoles; 0 / Platelet-Derived Growth Factor; 0Z5B2CJX4D / Fluorodeoxyglucose F18; G162GK9U4W / leflunomide; IY9XDZ35W2 / Glucose; K2I13DR72L / Gadolinium DTPA; U68WG3173Y / Carmustine
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3. Kast RE: Why cerebellar glioblastoma is rare and how that indicates adjunctive use of the FDA-approved anti-emetic aprepitant might retard cerebral glioblastoma growth: a new hypothesis to an old question. Clin Transl Oncol; 2009 Jul;11(7):408-10
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  • [Title] Why cerebellar glioblastoma is rare and how that indicates adjunctive use of the FDA-approved anti-emetic aprepitant might retard cerebral glioblastoma growth: a new hypothesis to an old question.
  • [MeSH-major] Antiemetics / therapeutic use. Cerebellar Diseases / drug therapy. Cerebellar Diseases / epidemiology. Cerebellar Neoplasms / drug therapy. Cerebellar Neoplasms / epidemiology. Glioblastoma / drug therapy. Glioblastoma / epidemiology. Morpholines / therapeutic use
  • [MeSH-minor] Humans. United States. United States Food and Drug Administration

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  • (PMID = 19574198.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antiemetics; 0 / Morpholines; 1NF15YR6UY / aprepitant
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4. Ong CH, Bateman A: Progranulin (granulin-epithelin precursor, PC-cell derived growth factor, acrogranin) in proliferation and tumorigenesis. Histol Histopathol; 2003 10;18(4):1275-88
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  • It is abundantly expressed in rapidly cycling epithelial cells, in the immune system and in neurons, such as cerebellar Purkinje cells.
  • Progranulin contributes to tumorigenesis in diverse cancers, including breast cancer, clear cell renal carcinoma, invasive ovarian carcinoma and glioblastoma.
  • The defined biological actions of progranulin probably represent a small fraction of its overall functions.
  • Transcriptome analyses show that the progranulin gene is induced in numerous situations that vary from obesity to the transcriptional response of cells to antineoplastic drugs.
  • Here, the biological roles of progranulin will be reviewed, with an emphasis on cancer and cell proliferation.
  • [MeSH-major] Cell Division / physiology. Intercellular Signaling Peptides and Proteins / metabolism. Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Nucleus / physiology. Gene Expression Regulation. Growth / physiology. Hematopoiesis / physiology. Humans. Tissue Distribution

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  • (PMID = 12973694.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / GRN protein, human; 0 / Intercellular Signaling Peptides and Proteins
  • [Number-of-references] 125
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5. Weber F, Asher A, Bucholz R, Berger M, Prados M, Chang S, Bruce J, Hall W, Rainov NG, Westphal M, Warnick RE, Rand RW, Floeth F, Rommel F, Pan H, Hingorani VN, Puri RK: Safety, tolerability, and tumor response of IL4-Pseudomonas exotoxin (NBI-3001) in patients with recurrent malignant glioma. J Neurooncol; 2003 Aug-Sep;64(1-2):125-37
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  • [Title] Safety, tolerability, and tumor response of IL4-Pseudomonas exotoxin (NBI-3001) in patients with recurrent malignant glioma.
  • Of these, 25 patients were diagnosed with glioblastoma multiforme (GBM) while six were diagnosed with anaplastic astrocytoma.
  • RESULTS: No drug-related systemic toxicity, as evident by lack of hematological or serum chemical changes, was apparent in any patients; treatment-related adverse effects were limited to the central nervous system.
  • Drug-related grade 3 or 4 toxicity was seen in 39% of patients in all dose groups and 22% of patients at the maximum tolerated dose of 6 microg/ml x 40 ml.
  • Gadolinium-enhanced magnetic resonance imaging of the brain showed areas of decreased signal intensity within the tumor consistent with tumor necrosis following treatment in many patients.
  • [MeSH-major] Astrocytoma / drug therapy. Bacterial Toxins / therapeutic use. Cerebellar Neoplasms / drug therapy. Exotoxins / therapeutic use. Glioblastoma / drug therapy. Interleukin-4 / therapeutic use. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies / analysis. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Safety. Survival Analysis. Treatment Outcome

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  • (PMID = 12952293.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / interleukin-4-Pseudomonas exotoxin; 207137-56-2 / Interleukin-4
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6. Cao X, Li XM, Mousseau DD: Calcium alters monoamine oxidase-A parameters in human cerebellar and rat glial C6 cell extracts: possible influence by distinct signalling pathways. Life Sci; 2009 Jul 31;85(5-6):262-8
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  • [Title] Calcium alters monoamine oxidase-A parameters in human cerebellar and rat glial C6 cell extracts: possible influence by distinct signalling pathways.
  • MAIN METHODS: We examined the effects of Ca(2+) on MAO-A activity and on [(3)H]Ro 41-1049 binding to MAO-A in human cerebellar extracts, and compared this to its effects on MAO-A activity in glial C6 cells following the targeting of signalling pathways using specific chemical inhibitors.
  • KEY FINDINGS: Ca(2+) enhances MAO-A activity as well as the association of [(3)H]Ro 41-1049 to MAO-A in human cerebellar extracts.
  • [MeSH-major] Calcium / pharmacology. Cerebellum / drug effects. Monoamine Oxidase / metabolism. Neuroglia / drug effects. Neurons / drug effects
  • [MeSH-minor] Aged. Animals. Binding Sites. Calcium Signaling / drug effects. Calcium Signaling / physiology. Cell Line, Tumor. Gene Expression / drug effects. Gene Expression / physiology. Glioblastoma. Humans. Male. Mice. Middle Aged. Monoamine Oxidase Inhibitors / metabolism. Protein Binding. RNA, Messenger / metabolism. Rats. Thiazoles / metabolism. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19539632.001).
  • [ISSN] 1879-0631
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Monoamine Oxidase Inhibitors; 0 / RNA, Messenger; 0 / Thiazoles; 127500-84-9 / Ro 41-1049; EC 1.4.3.4 / Monoamine Oxidase; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; SY7Q814VUP / Calcium
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7. Poelen J, Bernsen HJ, Prick MJ: Metastatic medulloblastoma in an adult; treatment with temozolomide. Acta Neurol Belg; 2007 Jun;107(2):51-4
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  • Treatment of this tumour type usually consists of surgery followed by radiotherapy.
  • Recently improvement of survival was reported in patients with glioblastoma treated with a combination of radiotherapy and concomitant temozolomide.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Cerebellar Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Medulloblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging. Spinal Cord Neoplasms / drug therapy. Spinal Cord Neoplasms / secondary

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  • (PMID = 17710841.001).
  • [ISSN] 0300-9009
  • [Journal-full-title] Acta neurologica Belgica
  • [ISO-abbreviation] Acta Neurol Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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8. Meley D, Spiller DG, White MR, McDowell H, Pizer B, Sée V: p53-mediated delayed NF-κB activity enhances etoposide-induced cell death in medulloblastoma. Cell Death Dis; 2010 May 13;1:e41
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  • Medulloblastoma (MB) is an embryonic brain tumour that arises in the cerebellum.
  • Using several MB cell lines, we have demonstrated that the chemotherapeutic drug etoposide induces a p53- and caspase-dependent cell death.
  • We further demonstrated that in both MB and glioblastoma (GM) cell lines, in which the p53 pathway was not functional, no p65 activation could be detected upon etoposide treatment.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Etoposide / pharmacology. Medulloblastoma / pathology. NF-kappa B / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Caspases / metabolism. Cell Death / drug effects. Cell Line, Tumor. Drug Screening Assays, Antitumor. Humans. Models, Biological. Phosphorylation / drug effects. Receptors, Death Domain / metabolism. Transcription Factor RelA / metabolism

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  • (PMID = 21364648.001).
  • [ISSN] 2041-4889
  • [Journal-full-title] Cell death & disease
  • [ISO-abbreviation] Cell Death Dis
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/C520471/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E012965/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/F005938/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / BBC5204711
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Receptors, Death Domain; 0 / Transcription Factor RelA; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC3032310
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9. Vassal G, Merlin JL, Terrier-Lacombe MJ, Grill J, Parker F, Sainte-Rose C, Aubert G, Morizet J, Sévenet N, Poullain MG, Lucas C, Kalifa C: In vivo antitumor activity of S16020, a topoisomerase II inhibitor, and doxorubicin against human brain tumor xenografts. Cancer Chemother Pharmacol; 2003 May;51(5):385-94
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  • [Title] In vivo antitumor activity of S16020, a topoisomerase II inhibitor, and doxorubicin against human brain tumor xenografts.
  • New active drugs are needed for the treatment of primary brain tumors in both children and adults.
  • The aim of the study was to determine its antitumor activity in athymic mice bearing subcutaneous medulloblastoma (IGRM33, 34, 57) and glioblastoma (IGRG88, 93, 121) xenografts treated at an advanced stage of tumor growth in comparison with that of doxorubicin.
  • Animals were randomly assigned to receive i.v.
  • IGRM57 xenografts were highly sensitive with 100% tumor regressions and a tumor growth delay (TGD) of 102 days, while one of eight IGRM34 xenografts showed a partial regression with a TGD of 16 days.
  • IGRM33, a model established from a tumor in relapse after chemotherapy and radiotherapy, was refractory to both drugs.
  • S16020 demonstrated a significant antitumor activity in the three glioblastoma xenografts evaluated.
  • The wild-type p53 IGRG93 xenograft was highly sensitive with 100% tumor regressions and a TGD of 54 days.
  • All six xenografts exhibited low expression of mdr1 as quantitated by RT-PCR, and no correlation was found with the activity of either drug.
  • Conversely, a low activity of the two drugs was significantly associated with a high expression of MRP1 in medulloblastomas.
  • Finally, no relationship was observed between drug sensitivity to either drug and expression of their target, topoisomerase IIalpha.
  • In conclusion, S16020 and doxorubicin showed significant antitumor activity in brain tumor xenografts treated at an advanced stage of tumor growth.
  • [MeSH-major] Carbazoles / pharmacology. Cerebellar Neoplasms / drug therapy. Doxorubicin / pharmacology. Glioblastoma / drug therapy. Medulloblastoma / drug therapy. Multidrug Resistance-Associated Proteins / biosynthesis. Pyridines / pharmacology. Topoisomerase II Inhibitors
  • [MeSH-minor] Animals. Drug Therapy, Combination. Female. Gene Expression Regulation. Mice. Mice, Nude. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous

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  • (PMID = 12736760.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Carbazoles; 0 / Multidrug Resistance-Associated Proteins; 0 / NSC 659687; 0 / Pyridines; 0 / Topoisomerase II Inhibitors; 0 / multidrug resistance-associated protein 1; 80168379AG / Doxorubicin
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10. Kaiser HE, Bodey B: The role of apoptosis in normal ontogenesis and solid human neoplasms. In Vivo; 2000 Nov-Dec;14(6):789-803
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  • During the intrauterine ontogenesis, in thymocytes or resting T lymphocytes, p53 tumor suppressor protein was identified to be a critical mediator of PCD in response to DNA damage.
  • T-lymphocytes which do not undergo positive selection are killed by apoptosis in response to a number of intrinsic and extrinsic factors, such as chemical toxins, viral infections, X- and UV irradiation, mild hyperthermia, the actions of various hormones, extracellular survival factors, calcium ionophores (such as A23187), various chemotherapeutic drugs (adriamycin, actinomycin D, etc) and antibodies directed to the CD3-TCR (T cell receptor) complex.
  • We also observed 42 childhood glial tumors, divided as follows: 6 pilocytic ASTRs; 14 low grade ASTRs; 16 anaplastic ASTRs; and 6 GBMs.
  • The GBMs represent an end-stage brain tumor IP dedifferentiation of glial origin.
  • FasR expression was rated high, 70% to 90% on the tumor cells in pylocytic ASTRs, lowered to 50% to 60% on the neoplastic cells in low grade ASTRs, even lower between 30% to 40% in anaplastic ASTRs and significantly lower, between 20% to 35% on the neoplastically transformed cells of GBM tissues.
  • The expression of apoptosis related cell surface molecules on the surface of both neoplastically transformed cells and on tumor cell specific, cytotoxic T lymphocyte (CTL) surfaces (FasR-FasL system) raises a distinct possibility of active PCD induction in CTL by tumor cells.
  • Juxtacrine interactions between CTL and neoplastically transformed cells, coupled with observations that tumor cells can modulate the intracellular, signaling domains of cell surface receptors to elicit responses quite often contrary to the expected, may even provide a way for CTL to enhance the proliferation and dedifferentiation of cancer cells.
  • [MeSH-major] Apoptosis / immunology. Bacterial Proteins. Brain Neoplasms / pathology. Cerebellar Neoplasms / pathology. Glioblastoma / pathology. Medulloblastoma / pathology. Neuroectodermal Tumors, Primitive / pathology
  • [MeSH-minor] Adult. Antigens, CD3 / analysis. Antigens, CD4 / analysis. Antigens, CD8 / analysis. Antigens, CD95 / physiology. Child. Fas Ligand Protein. Humans. Immunophenotyping. Melanoma / immunology. Melanoma / pathology. Membrane Glycoproteins / physiology. Thymus Gland / chemistry. Thymus Gland / immunology. Thymus Gland / pathology. Transcription Factors / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 11204498.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Antigens, CD95; 0 / Bacterial Proteins; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / FasR protein, Rhodococcus fascians; 0 / Membrane Glycoproteins; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
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11. Vatter S, Pahlke G, Deitmer JW, Eisenbrand G: Differential phosphodiesterase expression and cytosolic Ca2+ in human CNS tumour cells and in non-malignant and malignant cells of rat origin. J Neurochem; 2005 Apr;93(2):321-9
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  • The role of cyclic nucleotide phosphodiesterases (PDEs), key enzymes in cAMP/cGMP signal transduction, was investigated in two human CNS tumour cell lines as well as in the rat glioblastoma cell line C6 in comparison with rat cerebellar astrocytes with the emphasis on target evaluation.
  • In human glioblastoma cells, intracellular cAMP and Ca(2+) levels correlated well with the PDE expression pattern.
  • There were, however, marked differences in PDE expression and Ca(2+) kinetics between the human glioblastoma cell lines.
  • In contrast to human epithelial tumour cells, shown earlier by us to express significantly enhanced cAMP-specific PDE activity, this was not the case in rat glioblastoma cells compared with non-malignant rat astrocytes.
  • These in vitro data do not support the concept of PDE1C representing a target exploitable for drug treatment of malignant CNS tumours.
  • [MeSH-minor] Animals. Cells, Cultured. Humans. Rats. Rats, Wistar. Tumor Cells, Cultured

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  • (PMID = 15816855.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.4.- / Phosphoric Diester Hydrolases; SY7Q814VUP / Calcium
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12. Schraen-Maschke S, Zanetta JP: Role of oligomannosidic N-glycans in the proliferation, adhesion and signalling of C6 glioblastoma cells. Biochimie; 2003 Jan-Feb;85(1-2):219-29
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  • [Title] Role of oligomannosidic N-glycans in the proliferation, adhesion and signalling of C6 glioblastoma cells.
  • The potential role of glycoprotein N-glycans in the proliferation and adhesion of C6 glioblastoma cells was investigated using a set of N-glycosylation inhibitors (tunicamycin, deoxynojirimycin, castanospermine, deoxymannojirimycin, swainsonine), and traffic (monensin).
  • It was observed that both the proliferative and adhesive properties of C6 cells were dependent upon the expression at the cell surface of glycoproteins with oligomannosidic and hybrid type N-glycans, whereas the absence of N-glycans (tunicamycin) or the presence of glucosyl-oligomannosides (deoxynojirimycin and castanospermine) and the absence of glycoproteins at the cell surface (monensin) reduced both the proliferative and adhesive properties of C6 cells.
  • Studies of the classical elements of signalling pathways indicated that the different inhibitors have a low impact on tyrosine phosphorylations and oncogene product expression (except the ras oncogene product), except on phosphorylations on other residues.
  • 49 (1987) 1250), specific for oligomannosidic and hybrid type N-glycans, was present and externalised by the cells through a pinching-off of large intracellular vesicles, a mechanism that was not blocked by monensine; in contrast with the externalisation of its glycoprotein ligands.
  • A mechanism for the loss of contact inhibition is discussed based on the over-expression of CSL ligands in C6 glioblastoma cells relative to normal cells.
  • [MeSH-minor] Antibodies, Monoclonal / immunology. Cell Adhesion / drug effects. Cell Aggregation / drug effects. Cell Division / drug effects. Cell Line, Tumor / drug effects. Contact Inhibition. Glioblastoma. Glycoproteins / chemistry. Glycoproteins / metabolism. Glycosylation / drug effects. Humans. Immunoglobulin Fab Fragments / pharmacology. Indolizines / pharmacology. Lectins / metabolism. Ligands. Monensin / pharmacology. Tunicamycin / pharmacology

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  • (PMID = 12765791.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Immunoglobulin Fab Fragments; 0 / Indolizines; 0 / Lectins; 0 / Ligands; 0 / Oligosaccharides; 0 / Polysaccharides; 0 / cerebellar soluble lectin; 0 / oligomannoside; 11089-65-9 / Tunicamycin; 906O0YJ6ZP / Monensin; Q0I3184XM7 / castanospermine
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13. Kurtek RW, Lai KK, Tauxe WN, Eidelman BH, Fung JJ: Tc-99m hexamethylpropylene amine oxime scintigraphy in the diagnosis of brain death and its implications for the harvesting of organs used for transplantation. Clin Nucl Med; 2000 Jan;25(1):7-10
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  • The virtual immediate localization of Tc-99m HMPAO to cerebral and cerebellar tissue provides an index of blood perfusion, and its absence denotes brain death.
  • METHODS: Twenty-three patients, who presented with head trauma, prolonged anoxia or intrinsic brain disease (e.g., glioblastoma multiforme) and who were brain-dead by clinical examination criteria, were referred to the nuclear medicine division for verification of brain death.
  • RESULTS: We demonstrated (1) both cerebral and cerebellar perfusion, (2) neither cerebral nor cerebellar perfusion, (3) cerebral without cerebellar perfusion, and (4) cerebellar without cerebral perfusion.
  • The significance of a viable cerebellum in the absence of cerebral viability was not fully appreciated, although organs were harvested from such patients.

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  • (PMID = 10634522.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 3B744AG22N / Technetium Tc 99m Exametazime
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14. Li JY, Wang H, May S, Song X, Fueyo J, Fuller GN, Wang H: Constitutive activation of c-Jun N-terminal kinase correlates with histologic grade and EGFR expression in diffuse gliomas. J Neurooncol; 2008 May;88(1):11-7
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  • [Title] Constitutive activation of c-Jun N-terminal kinase correlates with histologic grade and EGFR expression in diffuse gliomas.
  • The results were correlated with grade and EGFR expression status.
  • Constitutively activated JNK (pJNK) was detected in 90.5%, 62.9% and 17.5% of WHO grade IV, III and II gliomas, respectively (p < 0.001).
  • pJNK expression was not detected in the astrocytes or oligodendrocytes of any of 10 normal cerebral and cerebellar brain tissue samples.
  • [MeSH-minor] Astrocytoma / drug therapy. Astrocytoma / pathology. Blotting, Western. Cells, Cultured. Enzyme Activation / physiology. Glioblastoma / drug therapy. Glioblastoma / pathology. Gliosarcoma / drug therapy. Gliosarcoma / pathology. Humans. Immunohistochemistry. Oligodendroglioma / drug therapy. Oligodendroglioma / pathology


15. Rider NL, Craig TJ: Liver enzyme elevation and normal pulmonary function in an adult with a declining forced expiratory volume in 1 second. Allergy Asthma Proc; 2008 May-Jun;29(3):345-8
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  • The following disorders should be considered in any patient with elevated transaminases without an apparent etiology: viral hepatitides, medication toxicity, autoimmune hepatitis, alcohol-induced hepatic injury, and alpha-1-antitrypsin deficiency.

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  • (PMID = 18534093.001).
  • [ISSN] 1088-5412
  • [Journal-full-title] Allergy and asthma proceedings
  • [ISO-abbreviation] Allergy Asthma Proc
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha 1-Antitrypsin; EC 2.6.1.2 / Alanine Transaminase
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16. Zheludkova OG, Tarasova IS, Gorbatykh SV, Belogurova MB, Kumirova EV, Borodina ID, Prityko AG, Melikian AG, Shcherbenko OI: [Treatment of anaplastic astrocytomas and glioblastomas in children by the use of temozolomide (TMZ)]. Vopr Onkol; 2002;48(3):356-60
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  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Glioblastoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Age Factors. Brain Stem Neoplasms / drug therapy. Brain Stem Neoplasms / mortality. Cerebellar Neoplasms / drug therapy. Cerebellar Neoplasms / mortality. Child. Child, Preschool. Data Interpretation, Statistical. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Time Factors

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  • (PMID = 12455362.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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17. Marchan EM, Sekula RF Jr, Jannetta PJ, Quigley MR: Long-term survival enhanced by cordectomy in a patient with a spinal glioblastoma multiforme and paraplegia. Case report. J Neurosurg Spine; 2007 Dec;7(6):656-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival enhanced by cordectomy in a patient with a spinal glioblastoma multiforme and paraplegia. Case report.
  • Spinal glioblastomas multiforme (GBMs) are rare lesions of the central nervous system with a prognosis as poor as that of their intracranial counterpart.
  • Six months after the start of interferon therapy, magnetic resonance imaging revealed a right cerebellar mass pathologically consistent with a GBM.
  • [MeSH-major] Glioblastoma / complications. Glioblastoma / surgery. Neurosurgical Procedures. Paraplegia / etiology. Spinal Cord Neoplasms / complications. Spinal Cord Neoplasms / surgery
  • [MeSH-minor] Antiviral Agents / therapeutic use. Cerebellar Neoplasms / secondary. Fatal Outcome. Hepatitis C / complications. Hepatitis C / drug therapy. Humans. Interferon-alpha / therapeutic use. Magnetic Resonance Imaging. Male. Middle Aged. Polyethylene Glycols. Recombinant Proteins. Spinal Cord / surgery. Survival Analysis

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  • (PMID = 18074692.001).
  • [ISSN] 1547-5654
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2b; 30IQX730WE / Polyethylene Glycols; 99210-65-8 / interferon alfa-2b
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18. Endo H, Kumabe T, Kon H, Yoshimoto T, Nakasato Y: [A case of primary cerebellar glioblastoma in childhood]. No Shinkei Geka; 2002 Dec;30(12):1325-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of primary cerebellar glioblastoma in childhood].
  • Primary cerebellar glioblastomas are exceedingly rare in childhood, with only 19 cases having been reported.
  • We treated a 7-year-old girl with primary cerebellar glioblastoma, who rapidly deteriorated due to cerebrospinal fluid dissemination.
  • On admission, increased intracranial pressure and left cerebellar signs were observed.
  • Magnetic resonance imaging (MRI) revealed a ring-enhanced mass in the left cerebellar hemisphere and a low intensity lesion in the pons.
  • The tumor had compressed the fourth ventricle and caused obstructive hydrocephalus.
  • Gross total resection of the left cerebellar tumor was performed.
  • Histological examination revealed nuclear atypia, mitoses, and necrosis, which satisfied the World Health Organizations histological criteria for grade IV astrocytoma.
  • However, the patient developed of anorexia and vomiting 4 months after surgery, and MRI disclosed local recurrence at the left middle cerebellar peduncle and diffuse dissemination along the lateral ventricle wall.
  • The patient was treated with three-drug chemotherapy using ifosfamide, cisplatin, and etoposide and 39.2 Gy of whole-brain irradiation.
  • However, her condition deteriorated gradually and she died 10 months after admission (6 months after the onset of tumor recurrence).
  • Primary cerebellar glioblastomas in children carry a very poor prognosis and tend to cause cerebrospinal fluid dissemination.
  • [MeSH-major] Cerebellar Neoplasms / surgery. Glioblastoma / surgery

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  • (PMID = 12491584.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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19. DeAngelis LM: Chemotherapy for brain tumors--a new beginning. N Engl J Med; 2005 Mar 10;352(10):1036-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Glioblastoma / drug therapy. Medulloblastoma / drug therapy. O(6)-Methylguanine-DNA Methyltransferase / genetics
  • [MeSH-minor] Adult. Cerebellar Neoplasms / drug therapy. Chemotherapy, Adjuvant. Child, Preschool. Gene Silencing. Humans. Survival Analysis

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  • [CommentIn] N Engl J Med. 2005 Jun 2;352(22):2350-3; author reply 2350-3 [15938011.001]
  • [CommentOn] N Engl J Med. 2005 Mar 10;352(10):978-86 [15758008.001]
  • [CommentOn] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [CommentOn] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010.001]
  • (PMID = 15758016.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
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