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[Title] Malignant astrocytic glioma: genetics, biology, and paths to treatment.

Malignant astrocytic gliomas such as glioblastoma are the most common and lethal intracranial tumors.

This progress is fueling new opportunities for understanding the fundamental basis for development of this devastating disease and also novel therapies that, for the first time, portend meaningful clinical responses.

[MeSH-major] Astrocytoma / genetics. Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Brain Neoplasms / therapy

[MeSH-minor] Animals. Animals, Genetically Modified. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Models, Animal. Gene Regulatory Networks. Humans. Models, Biological. Necrosis / chemically induced. Neoplasm Invasiveness. Neoplasm Staging. Neovascularization, Pathologic / drug therapy

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(PMID = 17974913.001).

[ISSN] 0890-9369

[Journal-full-title] Genes & development

[ISO-abbreviation] Genes Dev.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA099041; United States / NCI NIH HHS / CA / CA95616

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Number-of-references] 306

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] O6-methylguanine-DNA methyltransferase regulation by p53 in astrocytic cells.

In this study, we tested the hypothesis that MGMT is regulated by p53 in astrocytic cells, the precursors of which may give rise to glioblastoma. p53 is of interest because, in addition to often being mutated in glioblastoma, inactivation sensitizes some astrocytoma cell lines to temozolomide.

MGMT expression was examined in neonatal murine astrocytes and SF767 human astrocytic glioma cells following p53 inactivation by knockout (murine only) or RNAi methods.

In SF767 human astrocytic glioma cells, transient knockdown of p53 led to the down-regulation of MGMT gene expression.

[MeSH-minor] Animals. Cell Line, Tumor. DNA Methylation. Gene Silencing. Glioma / enzymology. Glioma / genetics. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. Promoter Regions, Genetic

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(PMID = 17234766.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Neuregulin-1 enhances survival of human astrocytic glioma cells.

Malignant astrocytic gliomas, referred to as astrocytomas, represent the most commonly diagnosed adult primary brain tumor.

Tumor expansion into the healthy surrounding brain tissue produces severe and often fatal consequences.

In this study, we examine the potential for the neuregulin-1/erbB receptor signaling cascade to contribute to this process by modulating glioma cell growth.

Using antibodies specific for the erbB receptors, we demonstrate the expression patterns for the erbB2, erbB3, and erbB4 receptors in human glioma biopsy samples.

We then verify receptor expression in a panel of human glioma cell lines.

Next, we investigate the status of the erbB2 and erbB3 receptors in the human glioma cell lines and find that they are constitutively tyrosine-phosphorylated and heterodimerized.

Furthermore, we show that exogenous activation of erbB2 and erbB3 receptors in U251 glioma cells by recombinant Nrg-1beta results in enhanced glioma cell growth under conditions of serum-deprivation.

Moreover, Nrg-1beta activates an inhibitor of apoptosis, Akt, implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas.

This data suggests that glioma cells may use autocrine or paracrine neuregulin-1/erbB receptor signaling to enhance cell survival under conditions where growth would otherwise be limited.

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(PMID = 15812817.001).

[ISSN] 0894-1491

[Journal-full-title] Glia

[ISO-abbreviation] Glia

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA097247-010003; United States / NINDS NIH HHS / NS / R01 NS036692-05A1; United States / NCI NIH HHS / CA / CA097247-010003; United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / P50CA97247; United States / NINDS NIH HHS / NS / NS036692-05A1; United States / NINDS NIH HHS / NS / R01 NS036692; United States / NINDS NIH HHS / NS / R01-NS36692; United States / NINDS NIH HHS / NS / R01 NS036692-06; United States / NINDS NIH HHS / NS / NS036692-06

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Neuregulin-1; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt

[Other-IDs] NLM/ NIHMS25075; NLM/ PMC2548407

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

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(PMID = 28184642.001).

[ISSN] 1524-4040

[Journal-full-title] Neurosurgery

[ISO-abbreviation] Neurosurgery

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genomic and expression profiling of glioblastoma stem cell-like spheroid cultures identifies novel tumor-relevant genes associated with survival.

PURPOSE: Glioblastoma spheroid cultures are enriched in tumor stem-like cells and therefore may be more representative of the respective primary tumors than conventional monolayer cultures.

We exploited the glioma spheroid culture model to find novel tumor-relevant genes.

Microarray-based gene expression analysis was applied to determine genes with differential expression compared with normal brain tissue and to nonneoplastic brain spheroids in glioma spheroid cultures.

Immunohistochemistry on tissue microarrays revealed that expression of AJAP1, EMP3, and PDPN was significantly associated with overall survival of astrocytic glioma patients.

CONCLUSION: We identified a set of novel candidate genes that likely play a role in glioblastoma pathogenesis and implicate AJAP1, EMP3, and PDPN as molecular markers associated with the clinical outcome of glioma patients.

[MeSH-minor] Biomarkers, Tumor. Brain / metabolism. Cell Culture Techniques. Humans. Oligonucleotide Array Sequence Analysis. Tumor Cells, Cultured

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(PMID = 19861460.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Present and potential future adjuvant issues in high-grade astrocytic glioma treatment.

Despite major advances in the management of malignant gliomas of which glioblastomas represent the ultimate grade of malignancy, they remain characterized by dismal prognoses.

Malignant gliomas are associated with such dismal prognoses because glioma cells can actively migrate through the narrow extra-cellular spaces in the brain, often travelling relatively long distances, making them elusive targets for effective surgical management.

Clinical and experimental data have demonstrated that invasive malignant glioma cells show a decrease in their proliferation rates and a relative resistance to apoptosis (type I programmed cell death) as compared to the highly cellular centre of the tumor, and this may contribute to their resistance to conventional pro-apoptotic chemotherapy and radiotherapy.

Despite resistance to apoptosis being closely linked to tumorigenesis, tumor cells can still be induced to die by non-apoptotic mechanisms such as necrosis, senescence, autophagy (type II programmed cell death) and mitotic catastrophe.

Another way to potentially overcome apoptosis resistance is to decrease the migration of malignant glioma cells in the brain, which then should restore a level of sensitivity to pro-apoptotic drugs.

Recent series of studies have supported the concept that malignant gliomas might be seen as an orchestration of cross-talks between cancer cells, microenvironment, vasculature and cancer stem cells.

The present chapter focuses on (i) the major signaling pathways making glioblastomas resistant to apoptosis, (ii) the signaling pathways distinctly activated by pro-autophagic drugs as compared to pro-apoptotic ones, (iii) autophagic cell death as an alternative to combat malignant gliomas, (iv) the major scientific data already obtained by researchers to prove that temozolomide is actually a pro-autophagic and pro-apoptotic drug, (v) the molecular and cellular therapies and local drug delivery which could be used to complement conventional treatments, and a review of some of the currently ongoing clinical trials, (vi) the fact that reducing the levels of malignant glioma cell motility can restore pro-apoptotic drug sensitivity, (vii) the observation that inhibiting the sodium pump activity reduces both glioma cell proliferation and migration, (viii) the brain tumor stem cells as a target to complement conventional treatment.

[MeSH-major] Astrocytoma / pathology. Astrocytoma / therapy. Brain Neoplasms / pathology. Brain Neoplasms / therapy

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(PMID = 19368079.001).

[ISSN] 0095-4829

[Journal-full-title] Advances and technical standards in neurosurgery

[ISO-abbreviation] Adv Tech Stand Neurosurg

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 136

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pharmaceutical-mediated inactivation of p53 sensitizes U87MG glioma cells to BCNU and temozolomide.

We examined the effect of PFTalpha on the chemosensitivity of a human cancer in which cell cycle arrest, not apoptosis, is the principle cellular consequence of p53 activation.

This was of interest because E6 silencing of p53 sensitizes U87MG astrocytic glioma cells to BCNU and temozolomide (TMZ), cytotoxic drugs that are modestly helpful in the treatment of aggressive astrocytic gliomas.

Our findings suggest that in addition to protecting normal cells from the toxic effects of radiation and chemotherapy, small molecule inhibitors of p53, like PFTalpha, might play a role in clinical oncology by sensitizing certain resistant cancers to cytotoxic chemotherapies.

[MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Brain Neoplasms / pathology. Carmustine / pharmacology. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Glioma / pathology. Thiazoles / pharmacology. Toluene / analogs & derivatives. Toluene / pharmacology. Tumor Suppressor Protein p53 / metabolism

[MeSH-minor] Benzothiazoles. DNA Damage. Drug Interactions. Humans. Tumor Cells, Cultured

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[Copyright] Copyright 2005 Wiley-Liss, Inc.

(PMID = 15800902.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Benzothiazoles; 0 / Thiazoles; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 3FPU23BG52 / Toluene; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; U68WG3173Y / Carmustine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin.

p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.

In this report, we examined the effect of p53 inactivation on the chemosensitivity of two additional human astrocytic glioma cell lines, D54 and A172, in order to assess whether sensitization is a general property of astrocytic tumor cells.

Sensitization to both BCNU and TMZ was associated with failure of p21(WAF1) induction, lack of a sustained G2 cell cycle arrest and significant tumor cell death.

These findings suggest that enhanced sensitivity to BCNU and TMZ is a general property of human astrocytic glioma cells in which p53 was disrupted.

In contrast, p53 inactivation rendered D54 and U87MG cells significantly more resistant to cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which high-grade astrocytomas sometimes respond.

These results indicate that p53 status influences the chemosensitivity of astrocytic glioma cells in a drug-type specific manner, a finding that may have implications for the selection of drug treatments for patients with astrocytic gliomas.

[MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Carmustine / therapeutic use. Cisplatin / therapeutic use. Dacarbazine / analogs & derivatives. Gene Silencing. Tumor Suppressor Protein p53 / physiology

[MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. Tumor Cells, Cultured. Tumor Stem Cell Assay

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(PMID = 16193384.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Tumor Suppressor Protein p53; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; Q20Q21Q62J / Cisplatin; U68WG3173Y / Carmustine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult patients with diffuse astrocytomas.

: Clarification of TP53 alterations is important to understand the mechanisms underlying the development of diffuse astrocytomas.

The aim of this study was to analyze the possible association of TP53 mutation, p53 overexpression, and p53 codon 72 polymorphism with susceptibility to apoptosis in adult Brazilian patients with diffuse astrocytomas.

We analyzed 56 surgical specimens of diffuse astrocytomas for alterations of TP53, using polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) direct sequencing. p53 and cleaved caspase 3 protein expression were assessed by immunohistochemistry.

We concluded that clarification of the TP53 alterations allows a better understanding of the mechanisms involved in the progression of diffuse astrocytomas, and the allele status at codon 72 was not associated with apoptosis in these tumors.

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(PMID = 28207094.001).

[ISSN] 1724-6008

[Journal-full-title] The International journal of biological markers

[ISO-abbreviation] Int. J. Biol. Markers

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Downregulation of Wnt2 and beta-catenin by siRNA suppresses malignant glioma cell growth.

Increasing evidence suggests that aberrant activation of Wnt signaling is involved in tumor development and progression.

Our earlier study on gene expression profile in human gliomas by microarray found that some members of Wnt family were overexpressed.

To further investigate the involvement of Wnt signaling in gliomas, the expression of core components of Wnt signaling cascade in 45 astrocytic glioma specimens with different tumor grades was examined by reverse transcription-PCR and immunohistochemistry.

Wnt2, Wnt5a, frizzled2 and beta-catenin were overexpressed in gliomas.

Knockdown of Wnt2 and its key mediator beta-catenin in the canonical Wnt pathway by siRNA in human U251 glioma cells inhibited cell proliferation and invasive ability, and induced apoptotic cell death.

Furthermore, treating the nude mice carrying established subcutaneous U251 gliomas with siRNA targeting Wnt2 and beta-catenin intratumorally also delayed the tumor growth.

In conclusion, the canonical Wnt pathway is of critical importance in the gliomagenesis and intervention of this pathway may provide a new therapeutic approach for malignant gliomas.

[MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Female. Humans. Mice. Neoplasm Invasiveness. Neoplasm Transplantation. RNA Interference. Signal Transduction / physiology

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(PMID = 18949017.001).

[ISSN] 1476-5500

[Journal-full-title] Cancer gene therapy

[ISO-abbreviation] Cancer Gene Ther.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Wnt2 Protein; 0 / beta Catenin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Glioma tumour-suppressor candidate region gene 2 (GLTSCR2/PICT-1) is localized within the well-known 1.4 Mb tumour-suppressive region of chromosome 19q, which is frequently altered in various human tumours, including diffuse gliomas.

Finally, our immunohistochemical study demonstrates that GLTSCR2 is sequentially down-regulated according to the histological malignant progression of the astrocytic glial tumour.

Taken together, our results suggest that GLTSCR2 is involved in astrocytic glioma progression.

[MeSH-major] Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Glioblastoma / genetics. Tumor Suppressor Proteins / genetics

[MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / pathology. Cell Line, Tumor. Chi-Square Distribution. Female. Gene Deletion. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18729076.001).

[ISSN] 1096-9896

[Journal-full-title] The Journal of pathology

[ISO-abbreviation] J. Pathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / GLTSCR2 protein, human; 0 / Tumor Suppressor Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Glial tumors of the brain: classification, present-day aspects of immunopathogenesis and immunogenetic diagnostics].

The complexity of treatment, which includes surgical removal of a tumor, radiotherapy, chemotherapy, and immune correction, makes the problem even more topical.

Modem classification of glial neoplasms is of no less importance, because treatment depends on the histologic structure of a tumor.

Thereupon, the authors of the article pay special attention to the modem WHO classification of gliomas.

However, there are no objective tests to verify the diagnosis of astrocytic glioma with reliable accuracy.

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(PMID = 16022111.001).

[ISSN] 0869-6047

[Journal-full-title] Vestnik Rossiiskoi akademii meditsinskikh nauk

[ISO-abbreviation] Vestn. Akad. Med. Nauk SSSR

[Language] RUS

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Russia (Federation)

[Chemical-registry-number] 0 / Antigens, CD; 0 / Lymphocyte Function-Associated Antigen-1; 0 / alpha-Fetoproteins; 126547-89-5 / Intercellular Adhesion Molecule-1

[Number-of-references] 45

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I trial combining SCH 66336 to temozolomide (TMZ) for patients with grade 3 or 4 malignant gliomas (MG).

METHODS: Eligibility included: adult patients with stable or recurrent MG (GBM, anaplastic astrocytoma [AA], anaplastic oligodendroglioma [AO]) previously treated with radiation therapy (RT) and with or without chemotherapy; interval of at least two weeks between prior RT, or four weeks between prior chemotherapy; Karnofsky ≥ 60%; and adequate hematologic, renal and liver function.

Radiographic evaluation reported: 2 partial responses, 14 stable disease for at least 4 cycles, and 11 disease progression after either the first or second cycle.

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(PMID = 27962751.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of recurrent malignant glioma with G207, a genetically engineered herpes simplex virus-1, followed by irradiation: Phase I study results.

Safety and efficacy of intracerebral inoculations of G207 to patients suffering from recurrent malignant gliomas have been demonstrated in previous clinical trials.

METHODS: In this phase I clinical trial, a total of 1 x 10⁹ plaque forming units (pfu) G207 were administered by five stereotactic injections of 0.2 mL each into regions of recurrent malignant glioma defined by MRI, followed by focal radiation therapy 24 hours post injection.

Included patients suffered from inoperable pathologically proven recurrent glioblastoma multiforme (GBM) or anaplastic astrocytoma (AA) which was progressive despite radiotherapy or chemotherapy and failed external beam radiotherapy > 5 Gray prior to study enrolment.

The 2 patients with initial PR (1xGBM, 1xAA) were re-treated with G207/Irradiation at time point of tumor recurrence, showing PR one month after re-treatment again.

Within persistent areas of tumor, HSV staining was present by using a polyclonal antibody for HSV, indicating intratumoral G207 replication (proof of concept).

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(PMID = 27964649.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Addition of temozolomide to radiotherapy for treatment of newly diagnosed anaplastic gliomas.

: e13037 Background: Anaplastic astrocytoma (AA), oligodendroglioma (AOD), and oligoastrocytoma (AOA) are rare tumors showing variable outcome due to their histological heterogeneity and different chemo- and radio-sensitivity.

Currently, the addition of chemotherapy to radiotherapy (RT) for newly diagnosed anaplastic gliomas is not sustained by available data.

We evaluated the addition of temozolomide (TMZ) to radiotherapy for newly diagnosed anaplastic gliomas in terms of tolerability, progression-free survival (PFS), and overall survival (OS).

METHODS: Since September 2004, following initial surgery, patients (pts) with histologically confirmed anaplastic glioma, Karnofsky Performance Status (KPS) ≥40, adequate organ function, no prior chemotherapy, were treated with RT to limited fields once daily at 2 Gy per fraction, 5 days a week, for a total of 60 Gy with concomitant TMZ (75 mg/m² for 7 days a week) followed by 6 cycles of maintenance TMZ at 200 mg/m² on days 1-5 every 28 days.

Nine pts (32%) underwent tumor complete resection, 10 partial resection (36%), and 9 (32%) tumor biopsy.

CONCLUSIONS: The addition of temozolomide to radiation therapy for newly diagnosed anaplastic gliomas is well tolerated and seems active; efficacy needs confirmation in a randomized clinical trial.

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(PMID = 27962859.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Efficacy of protracted dose-dense temozolomide (TMZ) in patients with progressive high-grade glioma.

: e13018 Background: The study was aimed to evaluate the efficacy of TMZ on a protracted dose-dense schedule after standard 5-day TMZ regimen in patients with progressive high-grade glioma.

METHODS: In this phase II prospective study, patients who had progression on standard 5-day TMZ for recurrence (group 1) or recurrence after concurrent radiotherapy+TMZ and ≥ 2 cycles of adjuvant TMZ (group 2) for high-grade glioma received TMZ 100 mg/m2× 21 q28 days until progression according to MacDonald's criteria.

The histopathology was glioblastoma in 18 and grade 3 glioma (anaplastic astrocytoma, anaplastic oligoastrocytoma or anaplastic oligodendroglioma) in 7.

The best response during treatment was partial response in 2 (8%), stable disease in 9 (36%), and progression in 9 (36%) out of 20 patients assessed.

CONCLUSIONS: Protracted dose-dense TMZ after 5-day schedule for recurrent or progressive disease has modest efficacy with tolerable toxicity.

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(PMID = 27962826.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: We retrospectively identified adults with newly diagnosed anaplastic oligodendroglioma (AO) or oligo-astrocytoma (AOA) seen at 17 medical centers from 1981-2007 exclusive of phase III or bone marrow transplant trials.

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(PMID = 27964586.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Impact of MGMT methylation status on 1p/19q intact anaplastic gliomas.

: e13003 Background: Chromosomes 1p/19q codeletion has been recognized as a prognostic and predictive factor in patients (pts) with grade 3 gliomas.

Non-codeleted (intact) anaplastic oligodendroglioma showed a survival comparable to that usually observed in pts with anaplastic astrocytomas; MGMT methylation status, moreover, has been found to be a prognostic factor in glioblastoma and anaplastic gliomas (AG).

Histology was anaplastic oligodendroglioma in 17 pts, anaplastic oligoastrocytoma in 20 pts, and anaplastic astrocytoma in 30 pts; all these pts were 1p19q intact and received surgery, RT, and CT.

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(PMID = 27962754.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A phase I trial of surgical resection with biodegradable carmustine (BCNU) wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma.

: 2033 Background: Our prior immunotherapy trials demonstrated efficacy in generating a tumor specific immune response in malignant glioma and the potential for high tumor-specific toxicity and sustained tumoricidal activity.

METHODS: We exploited this synergistic effect to maintain a cytotoxic environment around the tumor milieu.

Patients with high-grade glioma were eligible after maximal resection with biodegradable carmustine (BCNU) wafer placement.

Screening leukapheresis is used to isolate mononuclear cells which are differentiated into dendritic cells, pulsed with tumor lysate, and then 3 intradermal vaccines are administered at 2-week intervals.

The histology included 3 newly diagnosed glioblastoma multiforme (GBM), 8 recurrent GBM, 2 newly diagnosed anaplastic astrocytoma (AA), and 2 recurrent AA.

A stable disease interval of 13 to 90 weeks was observed for patients who received vaccine.

The 3 newly diagnosed GBM patients have stable disease (18 to 71 weeks).

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(PMID = 27964627.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] DNA methylation pattern of brain stem pilocytic astrocytomas in children.

: 10021 Background: Pilocytic astrocytoma (WHO grade I) comprises the most frequent brain tumor in childhood.

METHODS: To identify novel genes involved in astrocytoma pathogenesis, we performed a genome-wide DNA methylation analysis of 78 pilocytic astrocytoma samples from different tumor locations (diencephalic, cerebral, cerebellar, brain stem).

Two CpG sites were analyzed for each of a total of 14.000 promoters per sample.

Moreover, from 14 tumors clustering together with the brain stem tumors, 5 patients experienced disease recurrence (38%) as opposed to 20% in the remaining group.

Genes contained in the signature most interestingly included three homeobox family genes (HOXB1, HOXD3, and HOXD4), and NES, a tumor stem cell marker.

CONCLUSIONS: These data suggest that brain stem pilocytic astrocytomas display biologic features different from most tumors of other locations and share a methylation signature with tumors prone to disease recurrence from other locations.

We provide first evidence for a role of differentially methylated homeobox family genes in the pathogenesis of pilocytic astrocytoma.

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(PMID = 27962622.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Quantitative analysis of 0⁶-methylguanine-DNA methyltransferase (MGMT) promoter methylation in patients with low-grade gliomas.

: 2069 Background: Loss of heterozygosity (LOH) on the chromosomes 1p and 19q is associated with sensitivity to alkylating agents like temozolomide (TMZ) in patients with low-grade gliomas; whether methylation of the MGMT-promoter, a predictive factor in glioblastoma patients, also correlates with tumor response to TMZ in low-grade gliomas is unclear.

METHODS: We performed a retrospective analysis of patients with histologically verified low-grade gliomas (WHO Grade II) who were treated with TMZ for tumor progression at our hospital between November 1999 and November 2007.

Objective tumor response was assessed by MRI at 6-month intervals.

LOH of microsatellite markers on chromosomes 1p and 19q was determined by polymerase chain reaction (PCR) amplification of the matched pairs of blood and tumor DNA.

Seven patients had prior surgical resection of the tumor.

Histological classification revealed 10 oligodendrogliomas, 7 oligoastrocytomas, and 5 astrocytomas.

CONCLUSIONS: Quantitative methylation-specific PCR of the MGMT promoter correlates with radiological response to chemotherapy with temozolomide in WHO grade II gliomas.

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(PMID = 27964685.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I trial of vendetanib and oral etoposide for recurrent malignant gliomas.

: e13016 Background: Recurrent malignant gliomas have a poor prognosis, with a median survival of 6-15 months, with grade 4 glioblastomas more aggressive than grade 3 anaplastic astrocytomas or oligodendrogliomas.

Vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) are critically important in glioma biology.

We report a phase I trial of vandetanib in combination with oral etoposide for recurrent malignant glioma.

METHODS: Patients with histologically documented recurrent grade 3 or grade 4 malignant glioma were eligible.

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(PMID = 27962830.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Seizures in patients with glioma treated with phenytoin and levetiracetam.

: e13020 Background: Seizures are common in patients with glioma.

We compare seizure outcomes and side effects in patients with glioma treated with phenytoin and levetiracetam monotherapy.

METHODS: Retrospective analysis of consecutive patients with glioma.

RESULTS: 76 patients (34 female) with pathologically proven glioma and seizures were identified, 25 treated with phenytoin and 51 with levetiracetam.

64% had grade 4 astrocytoma.

When adjusting for age, gender, type of seizure, type of glioma, and dosage using univariate and multivariate models there were no differences between the treatment groups and none of these covariates were statistically significant for explaining the second seizure rates between treatment groups (all p values >0.05).

CONCLUSIONS: In this study, glioma patients treated with levetiracetam had similar seizure control as patients treated with phenytoin.

Levetiracetam is a safe, effective, and preferred alternative for seizure management in patients with glioma.

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(PMID = 27962817.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The infiltrative, diffuse pattern of recurrence in patients with malignant gliomas treated with bevacizumab.

: 2057 Background: There is no standard of care for recurrent gliomas; however, bevacizumab is often used as a salvage chemotherapy regimen.

A diffuse, infiltrative pattern of recurrence, as evidenced by MR imaging, was seen manifesting as multifocal disease or presumed CSF dissemination with subependymal spread.

METHODS: We conducted a retrospective analysis of 40 recurrent glioma patients followed at Moffitt Cancer Center from September 2006 through December 2008 treated with bevacizumab alone or in combination with irinotecan.

Histologies included glioblastoma (GB), anaplastic astrocytomas (AA), anaplastic oligodendrogliomas (AO), anaplastic oligoastrocytomas (AOA), and low-grade astrocytomas.

CONCLUSIONS: There appears to be an increase in a diffuse, infiltrative pattern of recurrence among recurrent glioma patients treated with bevacizumab as a salvage regimen.

It is unclear why the disparity among this subset of patients occurs, however, we hypothesize that this may once again highlight the distinct tumor biology among young glioma patients.

The impact of this observation on clinical decision making on whether to utilize bevacizumab in young recurrent glioma patients warrants further investigation.

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(PMID = 27964663.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Stable incidence of childhood and adult glioma in The Netherlands, 1989-2003.

Time trends in the incidence of glioma may reflect changes in the prevalence of environmental risk factors for glioma.

We therefore investigated trends in the incidence of childhood and adult glioma in The Netherlands from 1989 to 2003.

We calculated European standardised incidence rates for glioma, and stratified for age, gender and glioma subgroups.

Similar to other countries, the overall incidence of glioma was fairly stable in The Netherlands during the period 1989 to 2003, for both children and adults.

In adult astrocytic glioma, a significantly increasing incidence of high-grade astrocytoma was balanced by simultaneous decreases of low-grade astrocytoma, astrocytoma with unknown malignancy grade and glioma of uncertain histology.

Stable incidence rates of adult and childhood glioma suggest that no major changes in environmental risk factors have occurred, which influenced the incidence of glioma in the studied period.

[MeSH-major] Glioma / epidemiology

[MeSH-minor] Adolescent. Adult. Aged. Astrocytoma / epidemiology. Child. Child, Preschool. Cohort Studies. Ependymoma / epidemiology. Europe / epidemiology. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Netherlands / epidemiology. Oligodendroglioma / epidemiology. Sex Characteristics. United States / epidemiology

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(PMID = 16644569.001).

[ISSN] 0284-186X

[Journal-full-title] Acta oncologica (Stockholm, Sweden)

[ISO-abbreviation] Acta Oncol

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Norway

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Preparation and distribution of polyclonal antibodies against human PIWIL3 protein in tumor tissues].

The expression and distribution of PIWIL3 protein were detected by human tumor tissue biochips.

PIWIL3 proteins were expressed in the cytoplasma of human astrocytic glioma and meningioma.

These antibodies will have potential value for human PIWIL3 protein in human specific tumor pathogenesis.

[MeSH-minor] Astrocytoma / metabolism. Humans. Meningioma / metabolism. Peptides / chemical synthesis. Peptides / chemistry. Peptides / immunology

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(PMID = 18616918.001).

[ISSN] 1007-8738

[Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

[ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antibodies; 0 / Peptides; 0 / Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We have reported that the expression of PAX6 was significantly reduced in GBMs and that a low level of PAX6 expression is a harbinger of an unfavorable prognosis for patients with malignant astrocytic glioma.

Thus it is interesting to determine if repression of PAX6 expression is involved in anti-tumor suppression function in GBM.

Repeated subcutaneous and intracranial implantation experiments in nude mice using PAX6-stable transfectants provided solid evidence that PAX6 suppressed tumor growth in vivo and significantly extended mouse survival.

CONCLUSION: Our data demonstrate that PAX6exerts a tumor suppressor function that limits the growth of GBM cells.

[MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Genes, Tumor Suppressor. Humans. Loss of Heterozygosity / genetics. Mice. Mice, Nude. Paired Box Transcription Factors. Transfection

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(PMID = 15735909.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Repressor Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Here we show that HIV-1 Nef has an effect on the transcriptional levels of a cellular protein, anaplastic lymphoma kinase (ALK), that is preferentially expressed in the central and peripheral nervous system at late embryonic stages.

By its overexpression along with Nef, the authors demonstrate ALK ability to influence, at least in the U87MG astrocytic glioma cells, the mytogen-activated protein kinase (MAP-K)-dependent pathway.

Moreover, although in the absence of a physical direct interaction, Nef and ALK activate matrix metalloproteinases (MMPs), which are likely to contribute to blood-brain barrier (BBB) damage in HAD.

[MeSH-minor] Cell Line, Transformed. Cell Line, Tumor. Chemokine CCL5 / metabolism. Chemokine CXCL12 / metabolism. Humans. Receptor Protein-Tyrosine Kinases. Transcriptional Activation

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(PMID = 19455469.001).

[ISSN] 1538-2443

[Journal-full-title] Journal of neurovirology

[ISO-abbreviation] J. Neurovirol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CCL5; 0 / Chemokine CXCL12; 0 / nef Gene Products, Human Immunodeficiency Virus; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular genetic analysis of p53 intratumoral heterogeneity in human astrocytic brain tumors.

We investigated genetic heterogeneity of astrocytic gliomas using p53 gene mutations as a marker.

Different parts of morphologically heterogeneous astrocytic gliomas were microdissected, and direct DNA sequencing of p53 gene exons 5 through 8 was performed.

Thirty-five glioma samples and tumor-adjacent normal-appearing brain tissue from 11 patients were analyzed.

The mutations were present in grade II, III, and IV astrocytic glioma areas.

Both severe functionally dead mutants and mutants with remaining transcriptional activity could be observed in the same tumor.

We observed that morphologically different parts of a glioma could carry different or similar mutations in the p53 gene and could be either associated or not associated with the locus of heterozygosity at the mutant site.

Coexistence of p53 gene mutations and the locus of heterozygosity was common, at least in astrocytomas grade III and in glioblastomas, and also occurred in astrocytoma grade II areas.

Our results are of importance for a further understanding of the molecular mechanisms behind failure to treat glioma patients.

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Genes, p53 / genetics

[MeSH-minor] Adult. Aged. DNA Primers. DNA, Neoplasm / genetics. Female. Gene Frequency. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Microdissection. Middle Aged. Mutation / genetics. Mutation / physiology. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 17917588.001).

[ISSN] 0022-3069

[Journal-full-title] Journal of neuropathology and experimental neurology

[ISO-abbreviation] J. Neuropathol. Exp. Neurol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Up-regulation of VEGF expression and related neo-angiogenesis in childhood high-grade gliomas: implications for anti-angiogenic anti-neoplastic therapy.

There is considerable experimental evidence that VEGF isoforms are strongly involved in provoking neoangiogenesis of neoplastic cells and, consequently, the growth and progression of primary neoplasms (i.e., astrocytic gliomas), including the formation of an invasive and metastatic immunophenotype (IP).

During this immunohistochemical study, the presence and tissue localization of VEGF121 was observed in anaplastic, high-grade astrocytomas (AAs) and in glioblastoma multiforme (GBMs) employing the specific monoclonal antibody against it.

The immunoreactivity demonstrated a cytoplasmic, cell surface and extracellular matrix localization pattern in more than 90% of the tumor cells, with high intensity immunoreactivity (++++, A,B) in every high-grade astrocytic glioma tissue.

VEGF121 expression was identified mostly within the cytoplasm of tumor cells, suggesting an embryonic, undifferentiated and more malignant cellular IP of high-grade gliomas.

Tumor-related neo-angiogenesis and endothelial cell proliferation were also present.

The great majority of high-grade astrocytic gliomas are incurable with the three classic therapeutic modalities.

In the future, the development of targeted anti-neoplastic treatment strategies, adapted to individual patients, will require molecular identification of the different classes of neoplasm (including subtypes of astrocytomas) according to their stages, biology, prognosis and therapeutic options.

[MeSH-major] Gene Expression Regulation, Neoplastic. Glioma / blood supply. Glioma / pathology. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / metabolism

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(PMID = 16900782.001).

[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 / Antibodies, Monoclonal; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The current WHO classification of brain tumors defines gliomatosis cerebri (GC) as an extensively infiltrating astrocytic glioma involving at least three cerebral lobes.

The relation of GC to diffuse astrocytomas and glioblastoma is uncertain.

Recent reports showed IDH1 mutations in astrocytic and oligodendroglial tumors WHO grades II and III and in secondary glioblastomas with a frequency of up to 90%, whereas IDH1 mutations occurred in only 5% of primary glioblastomas.

We identified IDH1 mutations in 10/24 (42%) cases, which also included a solid tumor portion (type 2 GC), but not in 11 "classical" cases without solid tumor mass (type 1 GC).

Our data suggest that GC consists of two histological/molecular subtypes, type 1 being clearly distinct from diffuse astrocytoma, and type 2 sharing features with diffuse astrocytoma.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Arginine / genetics. Astrocytoma / secondary. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA Mutational Analysis. Female. Histidine / genetics. Humans. In Situ Hybridization, Fluorescence / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged. Oligodendroglioma / secondary. Polymorphism, Single Nucleotide / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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[CommentIn] Acta Neuropathol. 2010 Aug;120(2):269-70 [20532895.001]

(PMID = 20514489.001).

[ISSN] 1432-0533

[Journal-full-title] Acta neuropathologica

[ISO-abbreviation] Acta Neuropathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 4QD397987E / Histidine; 94ZLA3W45F / Arginine; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] MGMT methylation status as a prognostic factor in anaplastic astrocytomas.

However, further data on the epigenetic feature are needed before its role in rare diseases such as anaplastic astrocytomas (AA) can be established.

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(PMID = 27964674.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

Primary endpoints are drug safety in the setting of malignant gliomas and tumor response as measured according to MacDonald's criteria.

DISCUSSION: The aim of this study is to evaluate the safety and efficacy of Sulfasalazine as a treatment for recurring malignant gliomas.

[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]

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(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model.

Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2(+) transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.

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[Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]

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(PMID = 19477430.001).

[ISSN] 1878-3686

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS053900-03; United States / NINDS NIH HHS / NS / R01 NS053900; United States / NINDS NIH HHS / NS / 1R01 NS053900; United States / NINDS NIH HHS / NS / R01 NS053900-01; United States / NINDS NIH HHS / NS / NS053900-01; United States / NINDS NIH HHS / NS / R01 NS053900-02; United States / NINDS NIH HHS / NS / NS053900-02; United States / NINDS NIH HHS / NS / R01 NS073762; United States / NINDS NIH HHS / NS / NS053900-03

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53

[Other-IDs] NLM/ NIHMS112275; NLM/ PMC2721466

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] (131)I-chTNT-1/B mAb: tumour necrosis therapy for malignant astrocytic glioma.

Treatment of malignant glioma is therapeutically challenging.

Despite improvements in neurosurgery, radiotherapy and chemotherapy, few patients diagnosed with anaplastic astrocytoma (AA) or glioblastoma multiforme (GBM) (WHO grades 3 and 4, respectively) will live beyond 2 years.

Most malignant gliomas cannot be completely resected or irradiated due to their ability to infiltrate diffusely into normal brain tissue.

Brain tissue is protected from the systemic circulation via the blood-brain barrier (BBB), which impedes entry of water-soluble chemotherapeutic agents into the tumour at therapeutic concentrations. (131)I-chTNT-1/B mAb (Cotara) employs an innovative strategy to treat the invasive portion of the tumour and the core lesion. (131)I-chTNT-1/B mAb is a genetically engineered, radiolabelled, chimeric monoclonal antibody specific for a universal intracellular antigen (i.e., DNA/histone H1 complex) exposed in the necrotic core of malignant gliomas.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Astrocytoma / radiotherapy. Iodine Radioisotopes / therapeutic use

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(PMID = 16610983.001).

[ISSN] 1744-7682

[Journal-full-title] Expert opinion on biological therapy

[ISO-abbreviation] Expert Opin Biol Ther

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Histones; 0 / Iodine Radioisotopes; 9007-49-2 / DNA

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] MGMT expression in low-grade gliomas.

: e13001 Background: To evaluate the expression of MGMT in low-grade gliomas, and explore the relationship between its expression and the histological type of the tumour and the corresponding MRI characteristics.

METHODS: We assessed 389 low-grade gliomas (182 astrocytomas, 145 oligoastrocytomas, 61 oligodendrocytomas) with immunohistochemistry staining.

We also recorded the preoperational MRI criteria such as tumor volume on T2 image, enhancing volume, tumor location, and relationship with ventricles.

RESULTS: The expression of MGMT in astrocytomas, oligoastrocytomas, and oligocytomas were 1.67 ± 0.78, 1.41 ± 0.86,1.44 ± 0.78, respectively.

Significant stronger expression of MGMT was observed in astrocytomas than oligoastrocytomas and oligodendrocytomas (t = 3.00, p = 0.03), but no significant difference was observed between the latter two (t = 0.28, p = 0.78).

MGMT expression level was significantly correlated with the enhancing volume of the tumor (r = -0.605, p = 0.002), but did not correlate with the total tumor volume (p = 0.504).

This suggest that MGMT may contribute to the tumor resistance to radiotherapy and chemotherapy in low-grade gliomas.

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(PMID = 27962757.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Frequent promoter hypermethylation of Wnt pathway inhibitor genes in malignant astrocytic gliomas.

Recent studies suggested a role of Wnt signaling in gliomas, the most common primary brain tumors.

We investigated 70 gliomas of different malignancy grades for promoter hypermethylation in 8 genes encoding members of the secreted frizzled-related protein (SFRP1, SFRP2, SFRP4, SFRP5), dickkopf (DKK1, DKK3) and naked (NKD1, NKD2) families of Wnt pathway inhibitors.

While none of the tumors carried CTNNB1 mutations, we found frequent promoter hypermethylation of Wnt pathway inhibitor genes, with at least one of these genes being hypermethylated in 6 of 16 diffuse astrocytomas (38%), 4 of 14 anaplastic astrocytomas (29%), 7 of 10 secondary glioblastomas (70%) and 23 of 30 primary glioblastomas (77%).

Furthermore, SFRP1-hypermethylated gliomas showed significantly lower expression of the respective transcripts when compared with unmethylated tumors.

Taken together, our results suggest an important role of epigenetic silencing of Wnt pathway inhibitor genes in astrocytic gliomas, in particular, in glioblastomas, with distinct patterns of hypermethylated genes distinguishing primary from secondary glioblastomas.

[MeSH-major] Astrocytoma / genetics. DNA Methylation / genetics. Promoter Regions, Genetic. Wnt Proteins / genetics

[MeSH-minor] Carrier Proteins / genetics. Cell Line, Tumor. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Exons. Eye Proteins / genetics. Glioblastoma / genetics. Glioblastoma / secondary. Glioma / genetics. Glioma / pathology. Humans. Intercellular Signaling Peptides and Proteins / genetics. Membrane Proteins / genetics. Mutation. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. beta Catenin / genetics

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(PMID = 19847810.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NKD1 protein, human; 0 / NKD2 protein, human; 0 / Proto-Oncogene Proteins; 0 / SFRP1 protein, human; 0 / SFRP2 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human; 0 / Wnt Proteins; 0 / beta Catenin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical significance of EGFR amplification and the aberrant EGFRvIII transcript in conventionally treated astrocytic gliomas.

The aim of this study was to evaluate the clinical value of assessing epidermal growth factor receptor (EGFR) amplification and the common 5' rearrangement of EGFR resulting in the EGFRvIII transcript in astrocytic gliomas.

Amplification of EGFR was found in 41% (65/160) of glioblastomas (GBs) and 10% (4/41) of anaplastic astrocytomas (AAs).

There were no abnormalities of the EFGR or its transcript in grade II astrocytoma (AII).

We noted a tendency towards decreased survival with any EGFR abnormality in the 41 patients with AAs.

[MeSH-major] Astrocytoma / genetics. Central Nervous System Neoplasms / genetics. Gene Amplification. Glioblastoma / genetics. Glioma / genetics. Receptor, Epidermal Growth Factor / genetics

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(PMID = 16133418.001).

[ISSN] 0946-2716

[Journal-full-title] Journal of molecular medicine (Berlin, Germany)

[ISO-abbreviation] J. Mol. Med.

[Language] eng

[Grant] United Kingdom / Cancer Research UK / / CRUK/ A6618

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Biomarkers; 0 / epidermal growth factor receptor VIII; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

[Other-IDs] NLM/ PMC2815848; NLM/ UKMS2690

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Modeling prognosis for patients with malignant astrocytic gliomas: quantifying the expression of multiple genetic markers and clinical variables.

The disparate lengths of survival among patients with malignant astrocytic gliomas (anaplastic astrocytomas [AAs] and glioblastoma multiforme [GBM]) cannot be adequately accounted for by clinical variables (patient age, histology, and recurrent status).

We previously explicated the expression and prognostic value of PAX6, PTEN, VEGF, and EGFR in these glioma tissues and established a comprehensive prognostic model (Zhou et al., 2003).

This study attempts to improve that model by including four additional genetic markers, which exhibited a differential expression (P < 0.001) among tumor grades and between tumor and normal tissues.

This finding suggests that the expression of IGFBP2 is associated with pathways activated specifically in GBMs that result in enhancing invasiveness and angiogenesis.

[MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Models, Statistical

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(PMID = 16212813.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Ribosomal Proteins; 0 / ribosomal protein S9; EC 3.4.24.24 / Matrix Metalloproteinase 2

[Other-IDs] NLM/ PMC1871729

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Reduced expression of PDCD5 is associated with high-grade astrocytic gliomas.

However, the expression level of PDCD5 in human gliomas has not been investigated.

In the present study, we examined the expression of PDCD5 in 88 human glioma samples at both mRNA and protein levels by RT-PCR, Western blotting and immunohistochemistry.

We found that 53.3% (16/30) of the glioma samples had a reduced expression of PDCD5 mRNA and 70.5% (62/88) had a reduced expression of the PDCD5 protein as compared to normal brain tissue.

Furthermore, we studied the correlation of the expression level of PDCD5 with the clinicopathological grade and survival of patients with astrocytomas.

Although longitudinal studies of a cohort of patients with astrocytoma revealed that PDCD5 expression was not able to predict clinical outcome (p>0.05), a decreased expression of PDCD5 correlated significantly with high-grade astrocytomas (p<0.001).

In conclusion, our data suggest that reduced PDCD5 expression may contribute to the pathogenesis of human gliomas.

[MeSH-major] Apoptosis Regulatory Proteins / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Neoplasm Proteins / metabolism

[MeSH-minor] Adult. Blotting, Western. Female. Humans. Immunoenzyme Techniques. Male. Neoplasm Staging. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tumor Cells, Cultured

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(PMID = 18695908.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / RNA, Messenger

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].

OBJECTIVE: To study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas. METHODS:.

(1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.

RESULTS: The frequency of p53 mutation in diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas and secondary glioblastomas was 1/10, 4/19 (21.1%), 4/6 and 2/2, respectively and the frequency of EGFR overexpression was 5/10, 10/19 (52.6%), 5/6 and 2/2, respectively.

Both p53 accumulation and EGFR overexpression increased accompanied by a successive increase of degree of the glioma malignancy.

CONCLUSIONS: EGFR overexpression is not infrequently seen, however, p53 mutation is rarely seen in the low grade gliomas.

Consequently, EGFR overexpression and p53 gene mutation are not mutually exclusive in astrocytic gliomagenesis but synergistically to promote the glioma progression.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Receptor, Epidermal Growth Factor / genetics. Tumor Suppressor Protein p53 / genetics

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(PMID = 16776982.001).

[ISSN] 0529-5807

[Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology

[ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] RAF expression in human astrocytic tumors.

Only for A-RAF no link to tumorigenesis has been published so far.

Malignant gliomas are the most prevalent primary brain tumors of adults.

Although a role of the mitogenic Ras-RAF-MEK-ERK signalling cascade in brain tumor development is well established, there are only few reports available addressing alterations in RAF sequence or protein expression and function in human gliomas.

We analysed the mutational status of A-RAF and B-RAF in human glioblastomas (GBM) by sequencing.

Then we checked for RAF gene amplification by dot blot hybridization and examined RAF mRNA and protein expression patterns in human astrocytic gliomas of WHO grade II (LGA) and IV (GBM) by semiquantitative RT-PCR and Western blotting, respectively.

Finally, we performed functional assays to address a putative function of A-RAF in glioma cell proliferation and migration.

A-raf gene amplification was more often detected and overexpression of all three RAF proteins on mRNA and protein level was regularly found in human malignant gliomas.

Since neither A-RAF, nor C-RAF expression had any influence on proliferation and migration of GBM cells, putative functions of C-RAF in angiogenesis and of A-RAF in regulation of metabolism are discussed.

[MeSH-major] Astrocytoma / genetics. Glioblastoma / genetics. Proto-Oncogene Proteins A-raf / genetics. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins c-raf / genetics

[MeSH-minor] Cell Line, Tumor. Cell Movement. Cell Proliferation. Gene Expression Regulation. Humans. Mutant Proteins / genetics. Prognosis. RNA, Messenger / genetics. Sequence Analysis, DNA

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(PMID = 19082503.001).

[ISSN] 1107-3756

[Journal-full-title] International journal of molecular medicine

[ISO-abbreviation] Int. J. Mol. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Mutant Proteins; 0 / RNA, Messenger; EC 2.7.11.1 / Proto-Oncogene Proteins A-raf; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Contactin is expressed in human astrocytic gliomas and mediates repulsive effects.

Analyzing different types of astrocytic tumors, we detected an association between increasing malignancy grade and contactin expression.

Functionally, contactin had repellent effects on glioma cells in vitro, as demonstrated by adhesion and migration assays.

Our findings suggest that contactin has repellent effects on glioma cells to which it is presented as a ligand, but it does not alter the proliferative or adhesive capacities of cells that overexpress the molecule.

The repulsive properties of contactin may be a key factor in glioma disaggregation, and may contribute to the diffuse infiltration pattern characteristic of glioma cells in human brain.

[MeSH-major] Astrocytes / metabolism. Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Cell Adhesion Molecules, Neuronal / metabolism

[MeSH-minor] Cell Adhesion / physiology. Cell Aggregation / physiology. Cell Communication / physiology. Cell Line, Tumor. Cell Movement / physiology. Cell Proliferation. Contactins. Extracellular Matrix Proteins / metabolism. Gene Expression Regulation, Neoplastic / physiology. Glial Fibrillary Acidic Protein / metabolism. Humans. Ligands. Neoplasm Invasiveness. Protein Tyrosine Phosphatases / metabolism

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[Copyright] (c) 2005 Wiley-Liss, Inc.

(PMID = 16078236.001).

[ISSN] 0894-1491

[Journal-full-title] Glia

[ISO-abbreviation] Glia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules, Neuronal; 0 / Contactins; 0 / Extracellular Matrix Proteins; 0 / Glial Fibrillary Acidic Protein; 0 / Ligands; EC 3.1.3.48 / Protein Tyrosine Phosphatases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The oncogenic roles of Notch1 in astrocytic gliomas in vitro and in vivo.

Deregulation of Notch signaling has been implicated in some genetic diseases and tumorigenesis.

The function of Notch signaling in a variety of tumors can be either oncogenic or tumor-suppressive, depending on the cellular context.

In this study, Notch1 overexpression was observed in the majority of 45 astrocytic gliomas with different grades and in U251MG glioma cells.

Meanwhile, tumor growth was delayed in established subcutaneous gliomas in nude mice treated with Notch1 siRNA in vivo.

These results suggest that Notch1 plays an important oncogenic role in the development and progression of astrocytic gliomas.

[MeSH-major] Astrocytoma / genetics. Gene Expression Regulation, Neoplastic / physiology. Receptor, Notch1 / genetics

[MeSH-minor] Animals. Annexin A5 / metabolism. Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Disease Models, Animal. Flow Cytometry / methods. Humans. In Situ Nick-End Labeling / methods. Matrix Metalloproteinase 9 / metabolism. Mice. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. RNA, Small Interfering / pharmacology. RNA, Small Interfering / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Transfection / methods

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(PMID = 19771395.001).

[ISSN] 1573-7373

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Annexin A5; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Nestin expression in astrocytic tumors delineates tumor infiltration.

Nestin is an intermediate filament protein expressed in undifferentiated cells during central nervous system development, and glioma is known to be a highly infiltrative tumor.

We determined whether nestin was expressed in astrocytic tumors and could identify infiltrating tumor cells.

We screened 65 archival, paraffin-embedded adult astrocytic tumors using immunohistochemical staining and computerized overlaid photographs.

The intensity of nestin expression corresponded to the tumor grade.

All 33 glioblastoma cases showed positive and extensive staining, which was less positive in diffuse astrocytoma.

Overlaid images showed that nestin immunostaining delineated tumor invasion into adjacent gray and white matter.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Intermediate Filament Proteins / metabolism. Intermediate Filament Proteins / physiology. Nerve Tissue Proteins / metabolism. Nerve Tissue Proteins / physiology

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Child. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Nestin. Young Adult

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(PMID = 20425043.001).

[ISSN] 1861-387X

[Journal-full-title] Brain tumor pathology

[ISO-abbreviation] Brain Tumor Pathol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Further preliminary assessment of three human glioma cell lines as models of human astrocytic toxicity in vitro.

Three human astroglioma lines U251-MG, U373-MG and CCF-STTG1 have been evaluated further as possible models for astrocytotoxicity (GFAP and IL-6 release).

It is possible that batteries of astrocytic human glioma cell lines may be applicable to the sensitive evaluation of toxicants on astrogliotic expression markers such as GFAP and IL-6.

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[Copyright] Copyright © 2008 Elsevier B.V. All rights reserved.

(PMID = 21791377.001).

[ISSN] 1382-6689

[Journal-full-title] Environmental toxicology and pharmacology

[ISO-abbreviation] Environ. Toxicol. Pharmacol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Epigenetic downregulation of mitogen-activated protein kinase phosphatase MKP-2 relieves its growth suppressive activity in glioma cells.

Critical tumor suppression pathways in brain tumors have yet to be fully defined.

Using differential methylation hybridization, we identified a CpG-rich region of the promoter of the dual-specificity mitogen-activated protein kinase phosphatase-2 gene (DUSP4/MKP-2) that is hypermethylated in gliomas.

In 83 astrocytic gliomas and 5 glioma cell lines examined, hypermethylation of the MKP-2 promoter was found to occur relatively more frequently in diffuse or anaplastic astrocytomas and secondary glioblastomas relative to primary glioblastomas.

Our findings reveal MKP-2 as a common epigenetically silenced gene in glioma, the inactivation of which may play a significant role in glioma development.

[MeSH-major] Brain Neoplasms / pathology. Cell Proliferation. Dual-Specificity Phosphatases / genetics. Epigenesis, Genetic / physiology. Glioma / pathology. Mitogen-Activated Protein Kinase Phosphatases / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. DNA Methylation. Down-Regulation / physiology. Female. Gene Expression Regulation, Neoplastic / physiology. Gene Silencing / physiology. Genes, Tumor Suppressor / physiology. Humans. Male. Middle Aged

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(PMID = 20124482.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / DUSP4 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] mTOR promotes survival and astrocytic characteristics induced by Pten/AKT signaling in glioblastoma.

Combined activation of Ras and AKT leads to the formation of astrocytic glioblastoma multiforme (GBM) in mice.

We demonstrate here that loss of Pten is similar to AKT activation in the context of glioma formation in mice.

Blockade of mTOR results in regional apoptosis in these tumors and conversion in the character of surviving tumor cells from astrocytoma to oligodendroglioma.

These data suggest that mTOR activity is required for the survival of some cells within these GBMs, and mTOR appears required for the maintenance of astrocytic character in the surviving cells.

Furthermore, our study provides the first example of conversion between two distinct tumor types usually thought of as belonging to specific lineages, and provides evidence for signal transduction-mediated transdifferentiation between glioma subtypes.

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(PMID = 15967113.001).

[ISSN] 1522-8002

[Journal-full-title] Neoplasia (New York, N.Y.)

[ISO-abbreviation] Neoplasia

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U01CA894134-1

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 147336-22-9 / Green Fluorescent Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.67 / PTEN Phosphohydrolase; W36ZG6FT64 / Sirolimus

[Other-IDs] NLM/ PMC1501155

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Time trends in oligodendroglial and astrocytic tumor incidence.

BACKGROUND: We hypothesized that the incidences of oligodendrogliomas, anaplastic oligodendrogliomas, and mixed gliomas have significantly increased from the early 1990 s forward, while the incidences of anaplastic and grade II astrocytic tumors have significantly decreased.

METHODS: Data for the years 1973-2004 from the Surveillance, Epidemiology and End Results (SEER) public-use data and for 1985-2004 from six collaborating registries of the Central Brain Tumor Registry of the US (CBTRUS) were obtained.

RESULTS: Using CBTRUS data, the incidences (per 100,000 person-years) of oligodendrogliomas (APC = 4.7), mixed gliomas (APC = 3.9) and anaplastic oligodendrogliomas (APC = 12.5) have all increased over time, while the incidences of astrocytoma not otherwise specified (APC = -8.1) and fibrillary astrocytoma (APC = -2.1) have decreased.

CONCLUSIONS: This study has demonstrated that increases in oligodendroglial tumor incidence correspond to decreases in astrocytic tumor incidence over the same time period.

[MeSH-major] Astrocytoma / epidemiology. Brain Neoplasms / epidemiology. Glioma / epidemiology. Oligodendroglioma / epidemiology

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[Copyright] (c) 2008 S. Karger AG, Basel.

(PMID = 18259099.001).

[ISSN] 1423-0208

[Journal-full-title] Neuroepidemiology

[ISO-abbreviation] Neuroepidemiology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular analysis of the EGFR gene in astrocytic gliomas: mRNA expression, quantitative-PCR analysis of non-homogeneous gene amplification and DNA sequence alterations.

This report investigates the presence of mutations, amplification and/or over-expression of the EGFR gene in 86 glial tumours including 44 glioblastomas, 21 anaplastic astrocytomas, and 21 WHO grade II astrocytomas, using polymerase chain reaction/single-strand conformation polymorphism, semiquantitative reverse-transcription-polymerase chain reaction (RT-PCR) and Southern Blot techniques.

These findings corroborate that EGFR is non-randomly involved in malignant glioma development and that different mutant forms participate in aberrant activation of tyrosine kinase pathways.

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Epidermal Growth Factor / genetics. Gene Amplification

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(PMID = 16008822.001).

[ISSN] 0305-1846

[Journal-full-title] Neuropathology and applied neurobiology

[ISO-abbreviation] Neuropathol. Appl. Neurobiol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 62229-50-9 / Epidermal Growth Factor

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression and activity of l-isoaspartyl methyltransferase decrease in stage progression of human astrocytic tumors.

Here we investigated PIMT regulation in astrocytic tumors, which are the most common human brain tumors.

PIMT expression and enzyme activity were significantly decreased in all grades of human astrocytic tumors.

More precisely, PIMT levels were significantly lower by 76% in pilocytic astrocytomas (grade I), 46% in astrocytomas (grade II), 69% in anaplastic astrocytomas (grade III), and a marked 80% in glioblastomas (grade IV) as compared to normal brains.

Furthermore, the reduced PIMT levels correlated closely with a decrease in the number of neuron cells in astrocytic tumors as assessed by measuring the neuron-specific enolase level.

Many proteins with abnormal aspartyl residues accumulated in brain tumors and some were specific to individual grades of astrocytic tumors.

Similar results were obtained, either by measuring the reduction in PIMT activity and expression or by measuring the formation of abnormal proteins, in an orthotopic rat brain tumor model implanted with invasive CNS-1 glioma cells.

The novelty of these findings was to provide the first evidence for a marked reduction of PIMT expression and activity during stage progression of astrocytic tumors in humans.

[MeSH-major] Brain / enzymology. Brain Neoplasms / enzymology. Gene Expression Regulation, Neoplastic / physiology. Glioma / enzymology. Protein D-Aspartate-L-Isoaspartate Methyltransferase / metabolism

[MeSH-minor] Animals. Blotting, Northern. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry / methods. Male. Methylation. Neoplasm Transplantation / methods. Phosphopyruvate Hydratase / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred Lew. Reverse Transcriptase Polymerase Chain Reaction / methods

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(PMID = 15857672.001).

[ISSN] 0169-328X

[Journal-full-title] Brain research. Molecular brain research

[ISO-abbreviation] Brain Res. Mol. Brain Res.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / RNA, Messenger; EC 2.1.1.77 / Protein D-Aspartate-L-Isoaspartate Methyltransferase; EC 4.2.1.11 / Phosphopyruvate Hydratase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors.

Recent evidence indicates that miRNAs can function both as tumor suppressors and as oncogenes.

Expression of miR-21, 221, 128a, 128b, 128c, 181a, 181b, 181c was studied using real-time quantitative reverse transcriptase polymerase chain reaction and northern blotting for human astrocytic tumors with different grade of malignancy. miR-21 and 221 were overexpressed in glioma samples, whereas miRNA 181b was downregulated compared with normal brain tissue. miRNA-21 was hyperexpressed in all tumor samples whereas higher levels of miRNA-221 were found in high-grade gliomas.

This study is the first analysis of miRNAs in astrocytic tumor at different stages of malignancy.

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(PMID = 19159078.001).

[ISSN] 1573-7373

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MIRN21 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MIrn181 microRNA, human; 0 / MicroRNAs

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Human astrocytic bradykinin B(2) receptor modulates zymosan-induced cytokine expression in 1321N1 cells.

Bradykinin secreted from neurons affects astrocytic functions such as neurovascular coupling and astrocytic cytokine production.

In human astrocytes, however, the detailed mechanism of bradykinin-mediated modulation of astrocytic functions has not yet been fully elucidated.

Here, we report the functional expression of the bradykinin B(2) receptor and its modulation of zymosan-induced cytokine expression in human astrocytoma 1321N1 cells.

In contrast to the result in human glioma cells, bradykinin inhibits the zymosan-induced expression of TNF-alpha and IL-1beta in rat astrocytes, which shows a species-dependent manner.

These data suggest that bradykinin B(2) receptors are expressed in human astrocytoma cells and that they modulate the expression pattern of inflammatory cytokines.

[MeSH-minor] Animals. Bradykinin / analogs & derivatives. Bradykinin / metabolism. Calcium Signaling / physiology. Cell Line, Tumor. Humans. Inflammation / chemically induced. Inflammation / physiopathology. Interleukin-1beta / immunology. Rats. Species Specificity. Toll-Like Receptor 2 / metabolism. Tumor Necrosis Factor-alpha / immunology

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(PMID = 19854233.001).

[ISSN] 1873-5169

[Journal-full-title] Peptides

[ISO-abbreviation] Peptides

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Receptor, Bradykinin B2; 0 / Toll-Like Receptor 2; 0 / Tumor Necrosis Factor-alpha; 9010-72-4 / Zymosan; S8TIM42R2W / Bradykinin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of oligodendroglial and astrocytic lineage markers in diffuse gliomas: use of YKL-40, ApoE, ASCL1, and NKX2-2.

The phenotypic heterogeneity of astrocytic and oligodendroglial tumor cells complicates establishing accurate diagnostic criteria, and lineage-specific markers would facilitate diagnosis of glioma subtypes.

Based on data from the literature and from expression microarrays, we selected molecules relevant to gliogenesis and glial lineage specificity and then used immunohistochemistry to assess expression of these molecules in 55 diffuse gliomas, including 8 biphasic oligoastrocytomas, 21 oligodendrogliomas (all with 1p/19qloss), 21 astrocytomas, and 5 glioblastomas.

For the astrocytic lineage markers (GFAP, YKL-40, and ApoE), GFAP expression was significantly higher in the astrocytic component of oligoastrocytomas compared with the oligodendroglial part; similar patterns were detected for YKL-40 and ApoE, although the differences were not significant.

GFAP, YKL-40, and ApoE reliably distinguished grade II-III oligodendrogliomas from grade II-IV astrocytomas (p < 0.0001, p = 0.002, and p < 0.0001, respectively).

Among the oligodendroglial lineage markers (Olig2, Sox10, ASCL1, and NKX2-2), ASCL1 and NKX2-2 displayed significantly different immunostaining between oligodendrogliomas and astrocytomas (p = 0.017 and 0.004, respectively), but none clearly differentiated between the 2 glial populations of oligoastrocytomas.

In addition to GFAP, therefore, YKL-40, ApoE, ASCL1, and NKX2-2 represent promising tumor cell markers to distinguish oligodendrogliomas from astrocytomas.

[MeSH-major] Astrocytes / pathology. Biomarkers, Tumor / metabolism. Brain Neoplasms / diagnosis. Cell Lineage / genetics. Glioma / diagnosis. Oligodendroglia / pathology

[MeSH-minor] Adipokines. Apolipoproteins E / analysis. Apolipoproteins E / metabolism. Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / metabolism. Basic Helix-Loop-Helix Transcription Factors / analysis. Basic Helix-Loop-Helix Transcription Factors / metabolism. Diagnosis, Differential. Glial Fibrillary Acidic Protein / analysis. Glial Fibrillary Acidic Protein / metabolism. Glycoproteins / analysis. Glycoproteins / metabolism. Homeodomain Proteins / analysis. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Lectins. Oligodendroglioma / diagnosis. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. Predictive Value of Tests. Transcription Factors / analysis. Transcription Factors / metabolism

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(PMID = 17146289.001).

[ISSN] 0022-3069

[Journal-full-title] Journal of neuropathology and experimental neurology

[ISO-abbreviation] J. Neuropathol. Exp. Neurol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 57683; United States / NCI NIH HHS / CA / CA 95616

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / ASCL1 protein, human; 0 / Adipokines; 0 / Apolipoproteins E; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / CHI3L1 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Glycoproteins; 0 / Homeodomain Proteins; 0 / Lectins; 0 / Nkx-2.2 homedomain protein; 0 / Transcription Factors; 0 / apolipoprotein E1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Emerging targeted treatments for malignant glioma.

This paper focuses on the medical management of malignant gliomas, which is currently undergoing change.

The current therapies for glioma and the targeted agents in clinical trials are reviewed.

There is a general acceptance that temozolomide in combination with radiotherapy is replacing radiotherapy alone as first-line therapy in high-grade astrocytic gliomas.

[MeSH-major] Antineoplastic Agents / administration & dosage. Brain Neoplasms / drug therapy. Drug Delivery Systems / methods. Drugs, Investigational / administration & dosage. Glioma / drug therapy

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(PMID = 16262566.001).

[ISSN] 1744-7623

[Journal-full-title] Expert opinion on emerging drugs

[ISO-abbreviation] Expert Opin Emerg Drugs

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational

[Number-of-references] 56

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of interleukin-16 by tumor-associated macrophages/activated microglia in high-grade astrocytic brain tumors.

MATERIALS AND METHODS: Expression of IL-16 was analyzed by immunohistochemistry in human astrocytic brain tumors and the rat C6 glioblastoma tumor model.

IL-16 was detected in both human astrocytic brain tumors and rat C6 glioma.

RESULTS: Compared with human control brains, a significant increase in the percentages of parenchymal IL-16+ macrophages/microglia was observed already in grade II astrocytomas, indicating that IL-16+ immunostaining could be a descriptor of a macrophage/microglia subset in astrocytic brain tumors.

A further increase was observed at the transition from grade II to III astrocytomas.

This increase in IL-16 immunoreactivity correlated with WHO grades of human astrocytic brain tumors.

CONCLUSIONS: Therefore, IL-16 might be a so far unknown factor in the regulation of the local inflammatory milieu of human and experimental astrocytomas.

[MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology. Glioblastoma / immunology. Interleukin-16 / biosynthesis. Macrophages / immunology. Microglia / immunology

[MeSH-minor] Adult. Aged. Animals. Cell Line, Tumor. Female. Humans. Inflammation Mediators / metabolism. Male. Middle Aged. Rats. Rats, Sprague-Dawley

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[Cites] J Immunol. 2000 May 1;164(9):4429-32 [10779741.001]

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(PMID = 17221335.001).

[ISSN] 0004-069X

[Journal-full-title] Archivum immunologiae et therapiae experimentalis

[ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Inflammation Mediators; 0 / Interleukin-16

[Other-IDs] NLM/ PMC3234149

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumor.

PURPOSE: To retrospectively analyze the outcome of post-operative radiotherapy for spinal cord glioma with the emphasis on the hypofractionated radiotherapy boost for dose escalation as a treatment option for high-grade spinal cord astrocytic tumors.

MATERIALS AND METHODS: Forty-one patients with spinal cord glioma received post-operative radiotherapy between 1979 and 2003.

There were 12 low-grade astrocytic tumors, 11 high-grade astrocytic tumors, 16 low-grade ependymal tumors and 2 high-grade ependymal tumors.

Among 11 patients with high-grade astrocytic tumors, 5 with anaplastic astrocytoma and 1 with glioblastoma received hypofractionated radiotherapy boost for dose escalation.

RESULTS: The Kaplan-Meier survival rates at 10 years from the date of the first surgery were 64% for the entire group, 47% for the astrocytic tumors and 84% for the ependymal tumors, respectively (P=0.009).

Among 11 patients with high-grade astrocytic tumors, the actuarial survival rate at 10 years was 35%.

DISCUSSION: The results for ependymal tumors and low-grade astrocytic tumors were comparable to those reported in the literature.

Hypofractionated radiotherapy boost for dose escalation may help to prolong the survival of patients with high-grade astrocytic tumors.

[MeSH-major] Dose Fractionation. Glioma / radiotherapy. Spinal Cord Neoplasms / radiotherapy

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(PMID = 16314938.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Astrocytic regulation of human monocytic/microglial activation.

Recent reports have described reduced immunological responsiveness and stimulatory capacity among monocytes/microglia that infiltrate malignant human gliomas.

Herein, we demonstrate that culture of ex vivo human monocytes or primary human microglia with tumor cells isolated from glioblastoma multiforme (GBM) specimens renders them tolerogenic, capable of suppressing the function of ex vivo monocytes in the absence of tumor cells or their soluble factors.

We demonstrate that the tolerance induced in monocytes/microglia by GBM tumor cells is not associated with interference with the signaling cascade associated with TLR- or CD40-induced monocyte activation.

Rather, these tumor cells appear to up-regulate pathways that antagonize positive signaling pathways, including but not limited to STAT3 and STAT5.

Finally, we demonstrate that the tolerogenic properties of GBM tumor cells amplify properties inherent to nontransformed astrocytes.

Future studies that identify all of the molecular mechanisms by which astrocytes and malignant gliomas suppress monocyte/microglial function will have dual therapeutic benefits: suppressing these pathways may benefit patients with astrocytic tumors, while enhancing them may benefit patients with autoimmune processes within the CNS, such as multiple sclerosis.

[MeSH-major] Astrocytes / immunology. Glioma / immunology. Microglia / immunology. Monocytes / immunology

[MeSH-minor] Antigens, CD40 / immunology. Humans. Multiple Sclerosis / immunology. Multiple Sclerosis / pathology. Multiple Sclerosis / therapy. STAT3 Transcription Factor / immunology. STAT5 Transcription Factor / immunology. Signal Transduction / immunology. Toll-Like Receptors / immunology. Tumor Cells, Cultured

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(PMID = 18832699.001).

[ISSN] 1550-6606

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD40; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 0 / Toll-Like Receptors

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] PTPmu suppresses glioma cell migration and dispersal.

Glioblastomas (GBMs) are the highest grade of primary brain tumors with astrocytic similarity and are characterized by marked dispersal of tumor cells.

PTPmu expression was examined in human GBM, low-grade astrocytoma, and normal brain tissue.

These studies revealed a striking loss of PTPmu protein expression in highly dispersive GBMs compared to less dispersive low-grade astrocytomas and normal brain.

The migration of brain tumor cells was assessed in vitro using a scratch wound assay.

To assess migration, labeled U-87 MG glioma cells were injected into adult rat brain slices, and their movement was followed over time.

Together, these data suggest that loss of PTPmu in human GBMs contributes to tumor cell migration and dispersal, implicating loss of PTPmu in glioma progression.

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(PMID = 19304959.001).

[ISSN] 1523-5866

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS051520-04; United States / NEI NIH HHS / EY / P30 EY011373; United States / NINDS NIH HHS / NS / R01 NS051520; United States / NINDS NIH HHS / NS / R01-NS051520; United States / NCI NIH HHS / CA / K08 CA101954; United States / NINDS NIH HHS / NS / NS051520-04; United States / NEI NIH HHS / EY / P30 EY011373-119002; United States / NCI NIH HHS / CA / P20 CA103736; United States / NEI NIH HHS / EY / P30 EY011373-129002; United States / NCI NIH HHS / CA / P30 CA043703; United States / NEI NIH HHS / EY / P30 EY011373-139002; United States / NCI NIH HHS / CA / T32 CA059366; United States / NINDS NIH HHS / NS / NS051520-02; United States / NINDS NIH HHS / NS / NS051520-01A1; United States / NEI NIH HHS / EY / EY011373-139002; United States / NIGMS NIH HHS / GM / T32-GM007250; United States / NEI NIH HHS / EY / P30-EY11373; United States / NEI NIH HHS / EY / EY011373-119002; United States / NINDS NIH HHS / NS / NS051520-03; United States / NINDS NIH HHS / NS / R01 NS051520-02; United States / NINDS NIH HHS / NS / R01 NS051520-01A1; United States / NEI NIH HHS / EY / EY011373-129002; United States / NCI NIH HHS / CA / K08-CA101954; United States / NCI NIH HHS / CA / R01-CA116257; United States / NCI NIH HHS / CA / P30-CA043703; United States / NCI NIH HHS / CA / T32-CA059366; United States / NCI NIH HHS / CA / R01 CA116257; United States / NIGMS NIH HHS / GM / T32 GM007250; United States / NINDS NIH HHS / NS / R01 NS051520-03; United States / NCI NIH HHS / CA / P20-CA103736

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 2

[Other-IDs] NLM/ PMC2802397

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Establishment of prognostic models for astrocytic and oligodendroglial brain tumors with standardized quantification of marker gene expression and clinical variables.

BACKGROUND: Prognosis models established using multiple molecular markers in cancer along with clinical variables should enable prediction of natural disease progression and residual risk faced by patients.

In this study, multivariate Cox proportional hazards analyses were done based on overall survival (OS) of 100 glioblastoma multiformes (GBMs, 92 events), 49 anaplastic astrocytomas (AAs, 33 events), 45 gliomas with oligodendroglial features, including anaplastic oligodendroglioma (AO, 13 events) and oligodendraglioma (O, 9 events).

The modeling included two clinical variables (patient age and recurrence at the time of sample collection) and the expression variables of 13 genes selected based on their proven biological and/or prognosis functions in gliomas (ABCG2, BMI1, MELK, MSI1, PROM1, CDK4, EGFR, MMP2, VEGFA, PAX6, PTEN, RPS9, and IGFBP2).

Univariate models revealed opposing prognostic effects of ABCG2, MELK, BMI1, PROM1, IGFBP2, PAX6, RPS9, and MSI1 expressions for astrocytic (GBM and AA) and oligodendroglial tumors (AO_O).

Our success in establishing prognosis models for AA and AO_O was largely based on identification of a set of genes with independent prognostic values and application of standardized gene expression quantification to allow formation of a large cohort in analysis.

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(PMID = 21234290.001).

[ISSN] 1177-2719

[Journal-full-title] Biomarker insights

[ISO-abbreviation] Biomark Insights

[Language] ENG

[Publication-type] Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC3018892

[Keywords] NOTNLM ; gene expression markers / glioma / model / prognosis

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Slit2 involvement in glioma cell migration is mediated by Robo1 receptor.

Because similar molecular mechanisms may be utilized in glioma cell invasion and neuroblast migration, we studied the expression of Slit2 and its transmembrane receptor Robo1 as well as their functional role in migration in glioma cells. qRT-PCR and immunohistochemistry of human specimens revealed that Slit2 was distinctly expressed by non-neoplastic neurons, but at only very low levels in fibrillary astrocytoma and glioblastoma.

Robo1 also was mainly restricted to neurons in the normal brain, whereas astrocytic tumor cells in situ as well as glioblastoma cell lines overexpressed Robo1 at mRNA and protein levels.

Recombinant human Slit2 in a concentration of 0.45 nM was repulsive for glioma cell lines in a modified Boyden chamber assay.

RNAi-mediated knockdown of Robo1 in glioma cell lines neutralized the repulsive effect of Slit2, demonstrating that Robo1 served as the major Slit2 receptor.

Our findings suggest that a chemorepulsive effect mediated by interaction of Slit2 and Robo1 participates in glioma cell guidance in the brain.

[MeSH-major] Brain Neoplasms / metabolism. Cell Movement / physiology. Glioma / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Nerve Tissue Proteins / metabolism. Receptors, Immunologic / metabolism

[MeSH-minor] Astrocytes / metabolism. Blotting, Western. Cell Line, Tumor. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Neurons / metabolism. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

Genetic Alliance. consumer health - Glioma.

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(PMID = 17968499.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Immunologic; 0 / Slit homolog 2 protein; 0 / roundabout protein