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MATERIAL: Seventy-nine cases were distributed in the following manner: ependymomas, 38; astrocytomas, 22; oligodendrogliomas, four; gangliogliomas, two; hemangioblastomas, 10 (nine sporadic cases and one case of Von Hippel-Lindau disease); primitive melanoma, one; and intramedullary neurinomas, two.

Tumor removal was complete in the cases of ependymoma and hemangioblastoma and subtotal in the cases of astrocytoma.

Astrocytomas: 22 cases, with 14 cases of astrocytoma, two pilocytic astrocytoma, four malignant astrocytoma, and two glioblastoma.

Diagnostic delay: malignant tumors, one to nine months; low grades; three to six years (range, eight months to 25 years).

[MeSH-minor] Adolescent. Adult. Aged. Delayed Diagnosis. Female. Follow-Up Studies. France / epidemiology. Humans. Magnetic Resonance Imaging. Male. Microsurgery. Middle Aged. Neoplasm Recurrence, Local. Neurosurgical Procedures. Treatment Outcome. Young Adult

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[Copyright] Copyright (c) 2010 Elsevier Masson SAS. All rights reserved.

(PMID = 20097390.001).

[ISSN] 1773-0619

[Journal-full-title] Neuro-Chirurgie

[ISO-abbreviation] Neurochirurgie

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

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[Title] Progesterone and estradiol effects on SRC-1 and SRC-3 expression in human astrocytoma cell lines.

In this study, we determined progesterone and estrogen receptor isoform expression in two human astrocytoma cell lines with different evolution grade (U373, grade III; and D54, grade IV) by Western Blot.

Our data suggest that SRC-1 and SRC-3 expression is differentially regulated by sex steroid hormones in astrocytomas and that P(4) regulates SRC-1 expression depending on the evolution grade of human astrocytoma cells.

[MeSH-major] Astrocytoma / metabolism. Estradiol / metabolism. Gene Expression Regulation, Neoplastic. Glioblastoma / metabolism. Nuclear Receptor Coactivator 1 / metabolism. Nuclear Receptor Coactivator 3 / metabolism. Progesterone / metabolism

[MeSH-minor] Blotting, Western. Cell Line, Tumor. Humans. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Receptors, Estradiol / metabolism. Receptors, Estrogen / metabolism. Receptors, Progesterone / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors

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(PMID = 20963570.001).

[ISSN] 1559-0100

[Journal-full-title] Endocrine

[ISO-abbreviation] Endocrine

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Estradiol; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / NCOA3 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1; EC 2.3.1.48 / Nuclear Receptor Coactivator 3

   

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[Title] Expression of PROX1 Is a common feature of high-grade malignant astrocytic gliomas.

PROX1 is a prospero-related transcription factor that plays a critical role in the development of various organs including the mammalian lymphatic and central nervous systems; it controls cell proliferation and differentiation through different transcription pathwaysand has both oncogenic and tumor-suppressive functions.

We investigated PROX1 expression patterns in 56 human astrocytic gliomas of different grades using immunohistochemistry.

An average of 79% of cells in World Health Organization Grade IV (glioblastoma, n = 15) and 57% of cells in World Health Organization Grade III (anaplastic astrocytoma, n = 13) were strongly PROX1 positive; low-grade diffuse astrocytomas (Grade II, n = 13) had 21% of cells that were strongly positive; Grade I tumors (n = 15) had 1.5%; and non-neoplastic brain tissue (n = 15) had 3.7% of cells that were PROX1 positive.

Analyses of coexpression with proliferation markers suggest that PROX1+ cells have a marginally lower rate of proliferation than other tumor cells but are still mitotically active.

We conclude that PROX1 may constitute a useful tool for the diagnosis and grading ofastrocytic gliomas and for distinguishing Grade III and Grade IV tumors from Grade I and Grade II tumors.

[MeSH-major] Astrocytoma / metabolism. Astrocytoma / pathology. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Homeodomain Proteins / metabolism. Tumor Suppressor Proteins / metabolism

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(PMID = 20084020.001).

[ISSN] 1554-6578

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

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

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins; 0 / Nerve Tissue Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / neuronal nuclear antigen NeuN, human; 0 / prospero-related homeobox 1 protein

   

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[Title] Influence of histological subtype on survival after combined therapy of surgery and radiation in WHO grade 3 glioma.

World Health Organization (WHO) grade 3 glioma is one of the common brain tumors and has three main histological subtypes, including anaplastic astrocytoma (AA), anaplastic oligoastrocytoma (AOA) and anaplastic oligodendroglioma (AO).

In this study, 68 patients with histologically proven WHO grade 3 glioma, consecutively received postoperative radiotherapy at the Gunma University Hospital, Japan, between 1983 and 2005, were investigated to assess the impact of histological subtype on the survival.

In our study, histological subtype was one of the most important prognostic factors of WHO grade 3 glioma.

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

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(PMID = 20921826.001).

[ISSN] 1349-9157

[Journal-full-title] Journal of radiation research

[ISO-abbreviation] J. Radiat. Res.

[Language] eng

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

[Publication-country] Japan

   

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[Title] c -MYC amplification and expression in astrocytic tumors.

The aim of this study was to evaluate the nuclear and cytoplasmic expression of c-MYC protein in human astrocytic tumors of different histopathological grades and to determine whether its expression correlates with c-MYC gene amplification.

An immunohistochemical study of c-MYC protein was performed in 140 paraffin-embedded astrocytic tumors of different grades.

The distribution of the positive cases according to the tumor grade increased in both nuclear and cytoplasmic staining with malignancy.

The median nuclear LI also increased with tumor grade, with highest c-MYC nuclear expression in grade III.

The median cytoplasmic labeling scores showed a significant difference between grade I tumors and diffuse tumors, which presented high and similar median scores.

FISH results disclosed that the presence of two signals was inversely correlated with histopathological grade, while the presence of >/=5 signals increased according to degree of malignancy.

These results indicate that c-MYC expression in astrocytic tumors is strongly associated with increased c-MYC gene copy number and suggest that c-MYC plays a role in the early tumorigenesis of astrocytomas.

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

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(PMID = 18369647.001).

[ISSN] 0001-6322

[Journal-full-title] Acta neuropathologica

[ISO-abbreviation] Acta Neuropathol.

[Language] eng

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

[Publication-country] Germany

   

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[Title] Salvage chemotherapy with CPT-11 for recurrent temozolomide-refractory anaplastic astrocytoma.

BACKGROUND: The primary objective of this prospective phase 2 study of CPT-11 in adult patients with recurrent temozolomide-refractory anaplastic astrocytoma (AA) was to evaluate 6-month progression-free survival (PFS).

The median time to tumor progression was 4.1 month.

[MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Camptothecin / analogs & derivatives. Dacarbazine / analogs & derivatives. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy / methods

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(PMID = 18361434.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Clinical Trial, Phase II; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; XT3Z54Z28A / Camptothecin

   

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[Title] Use of Gliadel (BCNU) wafer in the surgical treatment of malignant glioma: a 10-year institutional experience.

BACKGROUND: Gliadel (polifeprosan 20 with carmustine [BCNU] implant) is commonly used for local delivery of BCNU to high-grade gliomas after resection and is associated with increased survival.

We set out to characterize Gliadel-associated morbidity in our 10-year experience with Gliadel wafers for treatment of malignant glioma.

METHODS: We retrospectively reviewed records of 1013 patients undergoing craniotomy for resection of malignant brain astrocytoma (World Health Organization grade III/IV disease).

RESULTS: A total of 1013 craniotomies were performed for malignant brain astrocytoma.

A total of 288 (28%) received Gliadel wafer (250 glioblastoma multiforme (GBM), 38 anaplastic astrocytoma/anaplastic oligodendroglioma (AA/AO), 166 primary resection, 122 revision resection).

Patients in Gliadel versus non-Gliadel cohorts had similar incidences of perioperative surgical site infection (2.8% vs. 1.8%, P = .33), cerebrospinal fluid leak (2.8% vs. 1.8%, P = .33), meninigitis (.3% vs. .3%, P = 1.00), incisional wound healing difficulty (.7% vs. .4%, P = .63), symptomatic malignant edema (2.1% vs. 2.3%, P = 1.00), 3-month seizure incidence (14.6% vs. 15.7%, P = .65), deep-vein thrombosis (6.3% vs. 5.2%, P = .53), and pulmonary embolism (PE) (4.9% vs. 3.7%, P = .41).

CONCLUSION: In our experience, use of Gliadel wafer was not associated with an increase in perioperative morbidity after surgical treatment of malignant astrocytoma.

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(PMID = 18636295.001).

[ISSN] 1534-4681

[Journal-full-title] Annals of surgical oncology

[ISO-abbreviation] Ann. Surg. Oncol.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biocompatible Materials; 0 / Decanoic Acids; 0 / Drug Carriers; 0 / Polyesters; 90409-78-2 / decanedioic acid-4,4'-(1,3-propanediylbis(oxy))bis(benzoic acid) copolymer; U68WG3173Y / Carmustine

   

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Temozolomide (TMZ) was approved for second-line therapy of recurrent anaplastic astrocytoma.

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(PMID = 19920915.001).

[ISSN] 1177-8881

[Journal-full-title] Drug design, development and therapy

[ISO-abbreviation] Drug Des Devel Ther

[Language] eng

[Publication-type] Journal Article

[Publication-country] New Zealand

[Other-IDs] NLM/ PMC2761188

[Keywords] NOTNLM ; carrier molecules / drug delivery / facilitated transport / glioblastoma multiforme / temozolomide

   

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[Title] Podocalyxin expression in malignant astrocytic tumors.

Recently, we revealed that highly sulfated KS or another mucin-like transmembrane sialoglycoprotein podoplanin/aggrus is upregulated in malignant astrocytic tumors.

The aim of this study is to examine the relationship between podocalyxin expression and malignant progression of astrocytic tumors.

In this study, 51 astrocytic tumors were investigated for podocalyxin expression using immunohistochemistry, Western blot analysis, and quantitative real-time PCR.

Immunohistochemistry detected podocalyxin on the surface of tumor cells in six of 14 anaplastic astrocytomas (42.9%) and in 17 of 31 glioblastomas (54.8%), especially around proliferating endothelial cells.

In diffuse astrocytoma, podocalyxin expression was observed only in vascular endothelial cells.

Podocalyxin might be associated with the malignant progression of astrocytic tumors, and be a useful prognostic marker for astrocytic tumors.

[MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / analysis. Central Nervous System Neoplasms / pathology. Sialoglycoproteins / analysis

[MeSH-minor] Blotting, Western. Humans. Immunohistochemistry. Polymerase Chain Reaction. Prognosis. RNA, Messenger / analysis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Cells, Cultured

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(PMID = 18639524.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Sialoglycoproteins; 0 / podocalyxin

   

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1. A human glioma cell line, NG97, was established by Grippo et al. in 2001 from tissue obtained from a grade III astrocytoma (WHO, 2000).

The injection of NG97 cells into nude mice induced an aggressive tumor characterized by: severe cytological atypia, vascular proliferation and pseudopalisading necrosis (glioblastoma multiforme features).

2. The purpose of the present study was to characterize the immunophenotype and ultrastructural aspects of this cell line, using the parental tumor, cultured cells and the xenotransplant, in order to assess its glial nature and possible divergent differentiation.

GFAP was similarly expressed in the parental tumor and in the cells in culture, but decreased in the xenotransplant.

The xenotransplant's ultrastructural features were those of a highly undifferentiated tumor.

4. Thus, our data demonstrate that NG97 cells constitute a pure glial-committed cell line, which may prove useful as a malignant glioma model in studies addressing pathophysiological, diagnostic and therapeutic issues.

[MeSH-major] Brain Neoplasms / pathology. Cell Culture Techniques / standards. Cell Line, Tumor. Glioblastoma / pathology

[MeSH-minor] Animals. Biomarkers. Cell Differentiation. Humans. Immunophenotyping. Mice. Mice, Nude. Microscopy, Electron. Neoplasm Transplantation. Neuroglia / cytology. Reproducibility of Results. Transplantation, Heterologous

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(PMID = 16133944.001).

[ISSN] 0272-4340

[Journal-full-title] Cellular and molecular neurobiology

[ISO-abbreviation] Cell. Mol. Neurobiol.

[Language] eng

[Publication-type] Journal Article; Validation Studies

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers

   

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METHODS: Thirty-six patients with an MTL tumor were studied.

The tumors were confined to the MTL (Schramm Type A) in 25 patients (69%).

Extension of the tumor into the fusiform gyrus (Schramm Type C) and temporal stem (Schramm Type D) was observed in 4 and 7 patients (11 and 19%), respectively.

There was a significant difference in the tumor size according to Schramm types (p = 0.001).

Complete tumor resection was achieved in 26 patients (72%).

All tumors were low-grade lesions except for 1 anaplastic astrocytoma.

The degree of tumor resection was significantly related to the tumor control failure (p < 0.001) and malignant transformation of a low-grade tumor (p < 0.001).

Univariate analyses using a Cox proportional hazards model showed that the following factors were significantly associated with a failure to control the tumor:.

1) extent of the tumor (Schramm Type D; p = 0.003, relative risk [RR] 12.04);.

2) size of the tumor (p = 0.033, RR 1.052/mm);.

Complete tumor resection is strongly recommended for long-term tumor control.

Older age, short duration of epilepsy, and tumor size are all associated with poor outcome.

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(PMID = 19645561.001).

[ISSN] 1092-0684

[Journal-full-title] Neurosurgical focus

[ISO-abbreviation] Neurosurg Focus

[Language] eng

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

[Publication-country] United States

   

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BACKGROUND: Better treatments are required urgently for patients with malignant glioma, which currently is incurable.

Death ligands, such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), may offer promise for the treatment high-grade glioma if such ligands induce apoptotic signaling in vivo in glioma cells.

It also may act as a tumor suppressor protein.

METHODS: Eleven glioblastomas, 5 anaplastic astrocytomas, and 3 low-grade astrocytomas were studied.

[MeSH-major] Astrocytoma / pathology. Biomarkers, Tumor / metabolism. Brain Neoplasms / pathology. Caspases / metabolism. Glioblastoma / pathology

[MeSH-minor] Base Sequence. Blotting, Northern. Caspase 10. Caspase 8. DNA Methylation. DNA, Neoplasm / analysis. Female. Humans. Male. Molecular Sequence Data. Probability. Reverse Transcriptase Polymerase Chain Reaction / methods. Risk Assessment. Sampling Studies. Sensitivity and Specificity. Statistics, Nonparametric. Tissue Culture Techniques

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(PMID = 16080161.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CASP10 protein, human; 0 / DNA, Neoplasm; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 10; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases

   

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BACKGROUND: A recent genomewide mutational analysis of glioblastomas (World Health Organization [WHO] grade IV glioma) revealed somatic mutations of the isocitrate dehydrogenase 1 gene (IDH1) in a fraction of such tumors, most frequently in tumors that were known to have evolved from lower-grade gliomas (secondary glioblastomas).

RESULTS: We identified mutations that affected amino acid 132 of IDH1 in more than 70% of WHO grade II and III astrocytomas and oligodendrogliomas and in glioblastomas that developed from these lower-grade lesions.

Tumors with IDH1 or IDH2 mutations had distinctive genetic and clinical characteristics, and patients with such tumors had a better outcome than those with wild-type IDH genes.

CONCLUSIONS: Mutations of NADP(+)-dependent isocitrate dehydrogenases encoded by IDH1 and IDH2 occur in a majority of several types of malignant gliomas.

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[Copyright] 2009 Massachusetts Medical Society

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[CommentIn] N Engl J Med. 2009 May 21;360(21):2248; author reply 2249 [19458374.001]

[CommentIn] N Engl J Med. 2009 May 21;360(21):2248-9; author reply 2249 [19469031.001]

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(PMID = 19228619.001).

[ISSN] 1533-4406

[Journal-full-title] The New England journal of medicine

[ISO-abbreviation] N. Engl. J. Med.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA043460-27; United States / NCI NIH HHS / CA / CA57345; United States / NCI NIH HHS / CA / R01CA118822; United States / NCI NIH HHS / CA / R37 CA043460; United States / NCI NIH HHS / CA / R37 CA043460-27; United States / NCI NIH HHS / CA / P50 CA108786; United States / NINDS NIH HHS / NS / P50 NS020023; United States / NCI NIH HHS / CA / 2P30-CA-14236; United States / NCI NIH HHS / CA / 5P50-CA-108786; United States / NCI NIH HHS / CA / CA121113; United States / NCI NIH HHS / CA / CA062924-150012; United States / NCI NIH HHS / CA / R37 CA043460-26; United States / NCI NIH HHS / CA / 5R37-CA-11898; United States / NCI NIH HHS / CA / R37CA11898-34; United States / NCI NIH HHS / CA / R01 CA121113; United States / NCI NIH HHS / CA / R01 CA140316; United States / NCI NIH HHS / CA / CA43460; United States / NCI NIH HHS / CA / CA043460-26; United States / NCI NIH HHS / CA / R01 CA121113-04; United States / NINDS NIH HHS / NS / NS20023-21; United States / NCI NIH HHS / CA / CA057345-17; United States / NCI NIH HHS / CA / R37 CA057345-17; United States / NCI NIH HHS / CA / R37 CA057345; United States / NCI NIH HHS / CA / P30 CA014236; United States / NCI NIH HHS / CA / P50 CA062924-150012; United States / NCI NIH HHS / CA / R01 CA057345; United States / NCI NIH HHS / CA / R01 CA118822; United States / NINDS NIH HHS / NS / 5P50-NS-20023; United States / NCI NIH HHS / CA / R37 CA011898

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

[Publication-country] United States

[Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human

[Other-IDs] NLM/ NIHMS107443; NLM/ PMC2820383

   

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[Title] PIK3CA alterations in primary (de novo) and secondary glioblastomas.

We assessed alterations in the EGFR/PTEN/PI3K pathway in 107 primary (de novo) glioblastomas and 32 secondary glioblastomas that progressed from low-grade or anaplastic astrocytomas.

Furthermore, this signaling pathway was altered by either PTEN mutations or PIK3CA amplification in 10 of 12 (83%) malignant glioma cell lines analyzed.

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(PMID = 17235514.001).

[ISSN] 0001-6322

[Journal-full-title] Acta neuropathologica

[ISO-abbreviation] Acta Neuropathol.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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[Title] Proteomic identification of biomarkers in the cerebrospinal fluid (CSF) of astrocytoma patients.

In this report, we used two proteomic techniques, two-dimensional gel electrophoresis (2-DE), and cleavable Isotope-Coded Affinity Tag (cICAT) to compare CSF proteomes to identify tumor- and grade-specific biomarkers in patients bearing brain tumors of differing histologies and grades.

Retrospective analyses were performed on 60 samples derived from astrocytomas WHO grade II, III, and IV, schwannomas, metastastic brain tumors, inflammatory samples, and non-neoplastic controls.

We identified 103 potential tumor-specific markers of which 20 were high-grade astrocytoma-specific.

These investigations allowed us to identify a spectrum of signature proteins that could be used to distinguish CSF derived from control patients versus those with low- (AII) or high-grade (AIV) astrocytoma.

These candidate biomarkers may also have functional properties that play a critical role in the development and malignant progression of human astrocytomas, thus possibly representing novel therapeutic targets for this highly lethal disease.

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(PMID = 17269713.001).

[ISSN] 1535-3893

[Journal-full-title] Journal of proteome research

[ISO-abbreviation] J. Proteome Res.

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / RR 02878; United States / NCI NIH HHS / CA / R01 CA086335; United States / NCI NIH HHS / CA / R01 CA086335-05; United States / NCRR NIH HHS / RR / M01 RR000039; United States / NCRR NIH HHS / RR / RR 12878; United States / NCRR NIH HHS / RR / M01 RR 00039; United States / NCRR NIH HHS / RR / RR 13948; United States / NCI NIH HHS / CA / CA 86335

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

[Publication-country] United States

[Chemical-registry-number] 0 / Affinity Labels; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Proteome

[Other-IDs] NLM/ NIHMS61862; NLM/ PMC2566942

   

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[Title] Malignant progression in pleomorphic xanthoastrocytoma: personal experience and review of the literature.

Pleomorphic xanthoastrocytoma (PXA) is a rare primary low-grade astrocytic tumor, recently classified as a neuroglial tumor.

It generally occurs in children and young adults and shows benign behaviour (WHO II), although an anaplastic variant and malignant potential have been described.

Pleomorphic xanthoastrocytomas with malignant transformation have been reported in three out of eight patients operated on for this type of tumor in our department in the last 15 years.

Histological examination revealed simple PXA in two patients and a PXA with anaplastic foci in the other.

Mean recurrence time was 5.7 years, with the original xanthoastrocytoma evolving to glioblastoma in two cases and anaplastic astrocytoma in the third.

Two died from tumor progression and one from brain edema after intracerebral haemorrhage.

A review of the available PXA literature dating back to 1979 revealed 16 cases of primary anaplastic astrocytoma and 21 cases of PXA with malignant transformation.

Our experience adds three more cases of malignant transformations, outlining once again the potential malignancy of pleomorphic xanthoastrocytomas and the fact that prognosis in these cases is the same as for primary anaplastic astrocytoma and glioblastoma.

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

[MeSH-minor] Adult. Cell Transformation, Neoplastic. Child. Disease Progression. Fatal Outcome. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Neoplasm Recurrence, Local / pathology. Tomography, X-Ray Computed

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(PMID = 17189643.001).

[ISSN] 0022-510X

[Journal-full-title] Journal of the neurological sciences

[ISO-abbreviation] J. Neurol. Sci.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] Netherlands

[Number-of-references] 52

   

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[Title] Malignant supratentorial astrocytoma treated with postoperative radiation therapy: prognostic value of pretreatment quantitative diffusion-weighted MR imaging.

PURPOSE: To retrospectively evaluate whether the minimum apparent diffusion coefficient (ADC) of the tumor seen on pretreatment magnetic resonance (MR) images is of prognostic value in patients with malignant supratentorial astrocytoma.

Between June 1996 and November 2003, 79 patients (44 male, 35 female; age range, 16-76 years) with malignant supratentorial astrocytoma underwent pretreatment MR imaging.

Patient age, symptom duration, neurologic function, mental status, Karnofsky performance scale (KPS) score, extent of surgery, histopathologic diagnosis, tumor component enhancement, and minimum ADC were assessed at factor analysis of survival.

RESULTS: Twenty-nine patients had anaplastic astrocytoma, and 50 had glioblastoma multiforme.

The minimum ADC was significantly lower in patients with glioblastoma multiforme than in those with anaplastic astrocytoma (P < .001).

CONCLUSION: The minimum ADC at pretreatment MR imaging is a useful clinical prognostic biomarker for survival in patients with malignant supratentorial astrocytoma.

[MeSH-major] Astrocytoma / diagnosis. Diffusion Magnetic Resonance Imaging / methods. Radiotherapy, Adjuvant / methods. Supratentorial Neoplasms / diagnosis. Supratentorial Neoplasms / therapy

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(PMID = 17356177.001).

[ISSN] 0033-8419

[Journal-full-title] Radiology

[ISO-abbreviation] Radiology

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

   

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[Title] The incidence, correlation with tumor-infiltrating inflammation, and prognosis of phosphorylated STAT3 expression in human gliomas.

We sought to determine the incidence of phosphorylated STAT3 (p-STAT3) expression in malignant gliomas of different pathologic types, whether p-STAT3 expression is a negative prognostic factor, and whether p-STAT3 expression influences the inflammatory response within gliomas.

RESULTS: We did not detect p-STAT3 expression in normal brain tissues or low-grade astrocytomas.

We observed significant differences in the incidence of p-STAT3 expression between the different grades of astrocytomas and different pathologic glioma types. p-STAT3 expression was associated with the population of tumor-infiltrating immune cells but not with that of T regulatory cells.

On univariate analysis, we found that p-STAT3 expression within anaplastic astrocytomas was a negative prognostic factor.

CONCLUSIONS: p-STAT3 expression is common within gliomas of both the astrocytic and oligodendroglial lineages and portends poor survival in patients with anaplastic astrocytomas. p-STAT3 expression differs significantly between gliomas of different pathologic types and grades and correlated with the degree of immune infiltration.

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(PMID = 19088040.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA120813-01A1; United States / NCI NIH HHS / CA / R01 CA120813; United States / NCI NIH HHS / CA / R01 CA120813-01A1

[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 / STAT3 Transcription Factor; 0 / STAT3 protein, human

[Other-IDs] NLM/ NIHMS78715; NLM/ PMC2605668

   

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[Title] Revisiting anaplastic astrocytomas II: further characterization of an expansive growth pattern with visually enhanced diffusion tensor imaging.

PURPOSE: To seek to distinguish and visualize the different magnetic resonance imaging (MRI) growth patterns among malignant gliomas utilizing visually enhanced diffusion tensor imaging (DTI).

MATERIALS AND METHODS: Nineteen consecutive patients undergoing image-guided resection of a newly diagnosed malignant glioma underwent add-on acquisition of DTI data based on an Institutional Review Board (IRB)-approved imaging protocol during preoperative MRI scans for routine intraoperative image guidance.

Tumor growth patterns were assigned to expansive or mixed/infiltrative classes as described in the companion article (24).

Infiltrating tumors were WHO Grade IV astrocytomas and all expansive tumors were either WHO Grade III astrocytomas or WHO Grade II astrocytomas.

DTI-based white matter tractography was conducted and the DTI data were fused with anatomical images using an in-house software package we developed to enhance the visualization of the tumor/fiber interface.

RESULTS: Out of the 19 tumor patients studied, 11 had infiltrative tumors and the other 8 had expansive tumors.

While less clear with 2D axial diffusion color maps, visually enhanced 3D reconstructions of the tumor/fiber interface successfully corroborated distinctive growth patterns.

This was particularly evident when viewed in 3D video loops of each tumor/fiber interface.

CONCLUSION: We have successfully developed software that visually enhances the anatomic details of the tumor/fiber interface in patients with anaplastic astrocytomas.

These data support the existence of a subgroup of patients within the WHO Grade III classification with expansive tumors and a significantly better prognosis.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Diffusion Magnetic Resonance Imaging / methods. Image Enhancement / methods. Image Processing, Computer-Assisted

[MeSH-minor] Adult. Aged. Female. Humans. Imaging, Three-Dimensional. Magnetic Resonance Imaging, Interventional. Male. Middle Aged. Neoplasm Staging

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[Copyright] (c) 2008 Wiley-Liss, Inc.

(PMID = 19025901.001).

[ISSN] 1053-1807

[Journal-full-title] Journal of magnetic resonance imaging : JMRI

[ISO-abbreviation] J Magn Reson Imaging

[Language] eng

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

[Publication-country] United States

   

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Eleven tumours (11/44) appeared hyperintense on DWI: eight metastases from lung cancer (mean ADC value 0.86 mm(2)/s, range 0.75-1.2 mm(2)/s), two GBMs (mean 0.7 mm(2)/s, range 0.67-0.76 mm(2)/s) and one anaplastic astrocytoma (ADC value 1.24 mm(2)/s).

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(PMID = 24300002.001).

[ISSN] 1971-4009

[Journal-full-title] The neuroradiology journal

[ISO-abbreviation] Neuroradiol J

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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Extracellular matrix metalloproteinase inducer (EMMPRIN), a member of the immunoglobulin superfamily, is present on the surface of tumor cells where it stimulates adjacent fibroblasts to produce matrix metalloproteinases (MMPs).

The intensively positive expression rates of EMMPRIN (22/27) and MMP2 (21/27) in anaplastic astrocytoma and glioblastoma tissues were significantly higher than those in normal brain and low-grade astrocytoma tissues (2/28 and (1/2)8, respectively).

The positive expression of EMMPRIN and MMP2 was associated with higher grade gliomas.

[MeSH-major] Antigens, CD147 / metabolism. Astrocytoma / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / mortality. Matrix Metalloproteinase 2 / metabolism

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[Cites] Am J Pathol. 2002 Apr;160(4):1215-21 [11943706.001]

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(PMID = 18795327.001).

[ISSN] 1432-1076

[Journal-full-title] European journal of pediatrics

[ISO-abbreviation] Eur. J. Pediatr.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / BSG protein, human; 136894-56-9 / Antigens, CD147; EC 3.4.24.24 / Matrix Metalloproteinase 2

   

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[Title] Clinical results of BNCT for malignant brain tumors in children.

It is very difficult to treat the patients with malignant brain tumor in children, especially under 3 years, because the conventional irradiation cannot be applied due to the damage of normal brain tissue.

However, boron neutron capture therapy (BNCT) has tumor selectivity such that it can make damage only in tumor cells.

We evaluated the clinical results and courses in patients with malignant glioma under 15 years.

There were 3 glioblastomas (GBM), 6 anaplastic astrocytomas(AAS), 7 primitive neuroectodermal tumors (PNET), 6 pontine gliomas and 1 anaplastic ependymoma.

All GBM and PNET patients died due to CSF and/or CNS dissemination without local tumor regrowth.

All pontine glioma patients died due to regrowth of the tumor.

Four of 6 anaplastic astrocytoma and 1 anaplastic ependymoma patients alive without tumor recurrence.

BNCT can be applied to malignant brain tumors in children, especially under 3 years instead of conventional radiation.

[MeSH-minor] Adolescent. Astrocytoma / pathology. Astrocytoma / radiotherapy. Child. Child, Preschool. Ependymoma / pathology. Ependymoma / radiotherapy. Fatal Outcome. Female. Glioblastoma / pathology. Glioblastoma / radiotherapy. Humans. Infant. Magnetic Resonance Angiography. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness / pathology. Neuroectodermal Tumors, Primitive / pathology. Neuroectodermal Tumors, Primitive / radiotherapy

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(PMID = 19406652.001).

[ISSN] 1872-9800

[Journal-full-title] Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine

[ISO-abbreviation] Appl Radiat Isot

[Language] eng

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

[Publication-country] England

   

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

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

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

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

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

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

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

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

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

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(PMID = 17917588.001).

[ISSN] 0022-3069

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

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

[Language] eng

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

[Publication-country] United States

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

   

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[Title] Mediastinal metastasis of glioblastoma multiforme evolving from anaplastic astrocytoma.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Glioblastoma / pathology. Mediastinal Neoplasms / pathology. Mediastinal Neoplasms / secondary

[MeSH-minor] Adult. Disease Progression. Fatal Outcome. Follow-Up Studies. Gene Deletion. Genes, p16. Glial Fibrillary Acidic Protein / metabolism. Homozygote. Humans. Male. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / radiotherapy. Salvage Therapy. Survival Analysis. Time Factors. Tomography, X-Ray Computed

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[Cites] Cancer. 1985 Oct 1;56(7 Suppl):1778-82 [4027909.001]

[Cites] Arch Anat Cytol Pathol. 1995;43(5-6):342-9 [8729851.001]

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(PMID = 16132499.001).

[ISSN] 0167-594X

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

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein

   

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RESULTS: A > 90% resection was achieved in 42%, and 70-90% tumor removal was accomplished in 51% of cases.

For example, in neurologically intact patients < or = 40 years of age with WHO Grade I-III tumors, good outcomes (Karnofsky Performance Scale Score 80-100) were seen in 91% of cases.

Surprisingly good survival rates were seen after surgery for anaplastic gliomas.

The median survival for patients with anaplastic astrocytomas (WHO Grade III) was 5 years, and the 5-year survival rate for those with anaplastic oligodendroglial tumors was 80%.

Independent predictors of survival included younger age, favorable histological features (WHO Grade I and oligodendroglial tumors), Yaşargil Type 5A/B tumors with frontal extensions, and more extensive resections.

CONCLUSIONS: Insular tumor surgery carries substantial complication rates.

In view of the oncological benefits of resective surgery, our data would therefore argue for microsurgery as the primary treatment for most patients with a presumed WHO Grade I-III tumor.

[MeSH-minor] Adolescent. Adult. Age Factors. Aged. Astrocytoma / surgery. Child. Female. Humans. Male. Middle Aged. Postoperative Complications. Survival Rate. Treatment Outcome

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(PMID = 19099379.001).

[ISSN] 0022-3085

[Journal-full-title] Journal of neurosurgery

[ISO-abbreviation] J. Neurosurg.

[Language] eng

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

[Publication-country] United States

   

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[Title] Ovarian malignant mixed mesodermal tumor with neuroectodermal differentiation: a multifaceted evaluation.

Malignant mixed mesodermal tumors (MMMTs) of the ovary are rare, highly aggressive neoplasms that arise most commonly in postmenopausal women.

Histologically, they consist of a mixed population of malignant epithelial and mesenchymal elements.

Histologically, the tumor was composed of epithelial, mesenchymal, and neuroectodermal elements.

The neuroectodermal component was predominantly that of a medulloepithelioma, with scattered areas displaying features of an anaplastic astrocytoma, including rare ganglion cell differentiation.

DNA ploidy analysis was also performed on the various components of the tumor and compared with 3 additional cases of MMMT without neuroectodermal differentiation and 2 ovarian immature teratomas.

Our findings suggest that the neuroectodermal component may arise from a separate clone or at least evolves at an earlier stage of tumor development.

[MeSH-major] Mixed Tumor, Mesodermal / pathology. Neuroectodermal Tumors / pathology. Ovarian Neoplasms / pathology

[MeSH-minor] Aged. Cell Differentiation / physiology. DNA, Neoplasm / genetics. Female. Humans. Immunohistochemistry. Microscopy, Electron, Transmission. Ploidies

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(PMID = 20407321.001).

[ISSN] 1538-7151

[Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists

[ISO-abbreviation] Int. J. Gynecol. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

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

   

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Three had pilocytic astrocytomas, two had anaplastic astrocytomas, three had ependymomas (two anaplastic), four had medulloblastomas, three had atypical teratoid/rhabdoid tumors, three had craniopharyngiomas, and three had other pathologies.

RESULTS: Local control was achieved in the patients with pilocytic and anaplastic astrocytoma, three of the patients with medulloblastoma, and the three with craniopharyngioma, but not for those with ependymoma.

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[Copyright] (c) 2004 Wiley-Liss, Inc.

(PMID = 15558704.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Epidermal growth factor receptor serum levels and prognostic value in malignant gliomas.

Increased EGFR expression might therefore be a strong prognostic feature in multiple tumor types, and inhibition of its cellular actions may have substantial therapeutic benefit.

METHODS AND STUDY DESIGN: Serum samples obtained from 50 healthy individuals and 65 brain cancer patients (35 glioblastoma multiforme and 30 anaplastic astrocytomas) were collected before and after treatment and assayed for EGFR extracellular domain serum concentrations by a sandwich ELISA.

There was a significant difference in the mean serum levels of EGFR between glioblastoma multiforme patients (96.2 +/- 12 ng/ml) and anaplastic astrocytoma patients (71.6 +/- 18 ng/ml, P = 0.04).

For all patients, median overall survival was 13 months (anaplastic astrocytoma, 18 months; glioblastoma multiforme, 12.5 months).

In 47 patients with high EGFR serum levels, overall survival was reduced (P = 0.01), with a median survival time corresponding to 11.5 months (anaplastic astrocytoma, 14.5 months; glioblastoma multiforme, 10.5 months).

[MeSH-major] Biomarkers, Tumor / blood. Brain Neoplasms / blood. Glioma / blood. Neoplasm Proteins / blood. Receptor, Epidermal Growth Factor / blood

[MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / blood. Astrocytoma / drug therapy. Astrocytoma / mortality. Astrocytoma / radiotherapy. Astrocytoma / surgery. Chemotherapy, Adjuvant. Combined Modality Therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Disease-Free Survival. Enzyme-Linked Immunosorbent Assay. Female. Follow-Up Studies. Glioblastoma / blood. Glioblastoma / drug therapy. Glioblastoma / mortality. Glioblastoma / radiotherapy. Glioblastoma / surgery. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Protein Structure, Tertiary. Radiotherapy, Adjuvant. Signal Transduction. Survival Analysis. Treatment Outcome

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(PMID = 17679463.001).

[ISSN] 0300-8916

[Journal-full-title] Tumori

[ISO-abbreviation] Tumori

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 7GR28W0FJI / Dacarbazine; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; YF1K15M17Y / temozolomide

   

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PATIENTS AND METHODS: Fifteen patients (male: n = 8; female: n = 7; median age, 14.6 years) received bevacizumab for recurrent or progressive solid tumors (carcinoma: n = 3; neuroblastoma: n = 2; astrocytoma grade III: n = 2; rhabdomyosarcoma: n = 2; nephroblastoma: n = 2; benign vascular tumors: n = 2; synovial sarcoma: n = 1; and malignant hemangiopericytoma: n = 1) on a compassionate basis.

Radiographic objective responses (partial responses) were observed in two patients with astrocytoma grade III and in one patient each with neuroblastoma and pleomorphic rhabdomyosarcoma, respectively.

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(PMID = 18056650.001).

[ISSN] 1569-8041

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab

   

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[Title] Prognostic significance of histological grading, p53 status, YKL-40 expression, and IDH1 mutations in pediatric high-grade gliomas.

The objective of this study was to evaluate, in a series of 43 pediatric high-grade gliomas (21 anaplastic astrocytoma WHO grade III and 22 glioblastoma WHO grade IV), the prognostic value of histological grading and expression of p53 and YKL-40.

The prognostic stratification for histological grading showed no difference in overall (OS) and progression-free survival (PFS) between glioblastomas and anaplastic astrocytomas.

TP53 mutations were detected in five of 27 (18%) cases (four glioblastomas and one anaplastic astrocytoma).

Our results suggest that in pediatric high-grade gliomas: (i) histological grading does not have strong prognostic significance, (ii) YKL-40 overexpression is less frequent than adult high-grade gliomas and does not correlate with a more aggressive behavior, (iii) TP53 mutations but not p53 expression may correlate with a more aggressive behavior, and (iv) IDH1 mutations are absent.

These observations support the concept that, despite identical histological features, the biology of high-grade gliomas in children differs from that in adults, and therefore different prognostic factors are needed.

[MeSH-major] Astrocytoma / genetics. Astrocytoma / metabolism. Glycoproteins / metabolism. Isocitrate Dehydrogenase / genetics. Lectins / metabolism. Mutation / genetics. Tumor Suppressor Protein p53 / genetics

[MeSH-minor] Adipokines. Adolescent. Adult. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Child. Child, Preschool. Chitinase-3-Like Protein 1. DNA, Neoplasm / genetics. Female. Humans. Immunoenzyme Techniques. Infant. Infant, Newborn. Male. Neoplasm Staging. Polymerase Chain Reaction. Prognosis. Young Adult

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[Cites] Curr Oncol Rep. 2009 Jan;11(1):68-72 [19080744.001]

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(PMID = 20174854.001).

[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 / Adipokines; 0 / CHI3L1 protein, human; 0 / Chitinase-3-Like Protein 1; 0 / DNA, Neoplasm; 0 / Glycoproteins; 0 / Lectins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human

   

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[Title] Phase 2 study of T138067-sodium in patients with malignant glioma: Trial of the National Cancer Institute of Canada Clinical Trials Group.

We studied the activity of T138067-sodium in patients with malignant gliomas.

Patients with recurrent anaplastic astrocytoma or glioblastoma multiforme were treated intravenously with 330 mg/m(2) of T138067-sodium weekly.

There were two patients with anaplastic astrocytoma and 16 with glioblastoma multiforme.

Our results suggest that given in this dose and schedule T138067-sodium does not have activity in this population of anaplastic astrocytoma and glioblastoma multiforme.

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(PMID = 15831236.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] eng

[Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Sulfonamides; T4NP8G3K6Q / batabulin

[Other-IDs] NLM/ PMC1871890

   

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OBJECTIVE: Balancing the benefits of extensive tumor resection with the consequence of potential postoperative deficits remains a challenge in malignant astrocytoma surgery.

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(PMID = 19687690.001).

[ISSN] 1524-4040

[Journal-full-title] Neurosurgery

[ISO-abbreviation] Neurosurgery

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Integrated molecular analysis suggests a three-class model for low-grade gliomas: a proof-of-concept study.

INTRODUCTION: We used an integrated molecular analysis strategy to perform class discovery on a population of low-grade gliomas (astrocytomas, oligodendrogliomas, and mixed gliomas) to improve our understanding of the molecular relationships among these tumors and to reconcile genotypic relationships with current histologic and molecular strategies for tumor classification.

Unsupervised class discovery algorithms identified and validated tumor clusters with genotypic similarity, and these data were integrated with chromosomal copy number assays and RT-PCR data to define molecular tumor subclasses.

RESULTS: Molecular class discovery suggested a three-class model for low-grade gliomas.

One discrete cluster of gliomas identified the pilocytic astrocytomas, a second grouped the 1p/19q codeleted oligodendrogliomas, and the mixture of remaining 1p/19q intact gliomas, including astrocytomas, oligodendrogliomas, and oligoastrocytomas, formed a third cluster with a discrete pattern of expression.

CONCLUSIONS: Integration of genomic, transcriptomic, and morphologic data for class discovery suggests a three-class model for low-grade gliomas.

Class I represents tumors with molecular similarity to pilocytic astrocytomas, class II tumors are similar to 1p/19q codeleted oligodendrogliomas, and class III represents infiltrative low-grade gliomas.

This classification is similar to current clinical paradigms for low-grade gliomas; our work suggests a molecular basis for such models.

This classification may supplement or may serve as the basis for a molecular pathologic alternative to current grading schemes for low-grade gliomas and may highlight potential targets for future biologically based treatments or strategies for future clinical trials.

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(PMID = 19835948.001).

[ISSN] 1089-8646

[Journal-full-title] Genomics

[ISO-abbreviation] Genomics

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 63231-63-0 / RNA

   

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Apolipoprotein D (apoD) expression has been shown to correlate both with cell cycle arrest and with prognosis in several types of malignancy, including central nervous system astrocytomas and medulloblastomas.

Sixteen poorly infiltrating WHO grade I glial neoplasms (i.e., pilocytic astrocytomas and gangliogliomas) showed an average 20-fold higher apoD expression level compared with the 20 diffusely infiltrating glial neoplasms (i.e., glioblastoma, anaplastic astrocytoma, oligodendrogliomas; p=0.00004).

Analyzed as individual tumor groups, poorly infiltrating grade I pilocytic astrocytomas and gangliogliomas differed significantly from each tumor type within the diffusely infiltrating higher-grade category (p<0.05 for each comparison) but not from each other (p>0.05).

Conversely, each individual tumor type within the diffusely infiltrating category differed significantly from both pilocytic astrocytomas and gangliogliomas (p<0.05) but did not vary from other infiltrating tumors (p>0.05).

Ependymomas, non-infiltrating grade II neoplasms, expressed levels of apoD similar to or lower than levels expressed by the diffusely infiltrating gliomas.

In addition, apoD expression was 5-fold higher in the slowly proliferating grade I glial neoplasms compared with non-proliferating normal brain tissue (p=0.01), suggesting that apoD expression is not simply an inverse measure of proliferation.

ApoD expression measured by quantitative RT-PCR may be useful in the differential diagnosis of primary brain tumors, particularly pilocytic astrocytomas and gangliogliomas.

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(PMID = 16055749.001).

[ISSN] 0022-1554

[Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society

[ISO-abbreviation] J. Histochem. Cytochem.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Apolipoproteins; 0 / Apolipoproteins D; 0 / Fixatives; 0 / Ki-67 Antigen; 1HG84L3525 / Formaldehyde; 8002-74-2 / Paraffin

   

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[Title] Radiation-induced malignant gliomas: is there a role for reirradiation?

PURPOSE: To review the literature regarding the role of radiotherapy (RT) in the treatment of patients with radiation-induced malignant gliomas (RIMGs).

RESULTS: Initial tumor types treated with RT included brain tumor in 37 patients (40%), acute lymphoblastic leukemia in 33 (36%), benign disease in 11 (12%), and other in 11 (12%).

Type of RIMG was glioblastoma in 69 (75%) and anaplastic astrocytoma in 23 (25%).

One-, 2-, and 5-year overall survival rates were 29.3%, 7.3%, and 0% for patients with glioblastoma and 59.7%, 30.3%, and 20.2% for patients with anaplastic astrocytoma.

[MeSH-minor] Astrocytoma / radiotherapy. Glioblastoma / radiotherapy. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Retreatment. Survival Rate

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[CommentIn] Int J Radiat Oncol Biol Phys. 2008 Sep 1;72(1):304-5; author reply 305 [18722290.001]

(PMID = 18262733.001).

[ISSN] 0360-3016

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 62

   

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[Title] Results of a phase I dendritic cell vaccine trial for malignant astrocytoma: potential interaction with adjuvant chemotherapy.

Dendritic cell vaccination has been applied to the treatment of a variety of cancers, including malignant astrocytoma.

We have treated 13 patients with malignant astrocytoma using dendritic cell vaccination and have shown that this treatment is safe and is likely to be effective in combination with standard adjuvant therapy.

[MeSH-major] Astrocytoma / therapy. Brain Neoplasms / therapy. Cancer Vaccines / therapeutic use. Chemotherapy, Adjuvant / methods. Dendritic Cells / immunology. Immunotherapy, Active / methods

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(PMID = 18083572.001).

[ISSN] 0967-5868

[Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia

[ISO-abbreviation] J Clin Neurosci

[Language] eng

[Publication-type] Clinical Trial, Phase I; Journal Article

[Publication-country] Scotland

[Chemical-registry-number] 0 / Antigens, CD8; 0 / Cancer Vaccines; EC 3.1.3.48 / Antigens, CD45

   

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OBJECTIVE: The uptake of L-methyl-11C-methionine (MET) by gliomas is greater than that by intact tissue, making methionine very useful for evaluation of tumor extent.

Tumors included diffuse astrocytoma, anaplastic astrocytoma, glioblastoma, ependymoma, oligodendroglioma, medulloblastoma, dysembryoplastic neuroepithelial tumor, choroid plexus papilloma, central neurocytoma, optic glioma, gliomatosis cerebri, pleomorphic xanthoastrocytoma, and ganglioglioma.

Tumor activity and degree of malignancy were evaluated using Ki-67LI (LI: labeling index) and Kaplan-Meier survival curves.

The correlations between methionine uptake and tumor proliferation (tumor versus contralateral gray matter ratio (T/N) and Ki-67LI) were determined for the group of all subjects.

The existence of significant correlations between T/N and Ki-67LI and between SUV and Ki-67LI was determined for astrocytic tumors.

Receiver operating characteristics (ROC) analysis of T/N and standardized uptake value (SUV) was performed for the group of astrocytic tumors.

Ki-67LI differed significantly between the high-grade group and low-grade group at T/N levels between 1.5 and 1.8 on analysis using tumor proliferative potential (p = 0.019-0.031).

The prognosis differed significantly between the high-grade and low-grade groups when T/N was in the range of 1.6-1.8 (p = 0.028-0.032).

CONCLUSIONS: When analysis was confined to cases of astrocytic tumor, a correlation was noted between methionine accumulation and Ki-67LI.

For the astrocytic tumors, T/N ratio seemed to be more useful as a diagnostic indicator than SUV.

The cut-off level of T/N ratio for distinction between high-grade and low-grade astrocytoma appears to lie between 1.5 and 1.6.

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(PMID = 16444993.001).

[ISSN] 0914-7187

[Journal-full-title] Annals of nuclear medicine

[ISO-abbreviation] Ann Nucl Med

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Radiopharmaceuticals; 58576-49-1 / carbon-11 methionine; AE28F7PNPL / Methionine

   

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[Title] MGMT promoter hypermethylation correlates with a survival benefit from temozolomide in patients with recurrent anaplastic astrocytoma but not glioblastoma.

AIMS: To investigate the correlation between O(6)-methylguanine-DNA-methyltransferase (MGMT) promoter methylation and benefit from temozolomide in patients with recurrent high-grade glioma.

RESULTS: A subgroup of 38 patients who were chemotherapy-naive at recurrence was analysed (22 glioblastoma, 12 anaplastic astrocytoma [AA] and 4 anaplastic oligoastrocytoma [AOA]); none had 1p/19q loss.

By Cox multivariate analysis, tumour grade and MGMT promoter methylation correlated with time to progression (p<0.05); MGMT promoter methylation correlated with superior overall survival in AA/AOA but not in glioblastoma.

[MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic

[MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Methylation. Female. Glioblastoma / drug therapy. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality. Prognosis. Retrospective Studies. Survival Rate. Young Adult

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(PMID = 18945611.001).

[ISSN] 1879-0852

[Journal-full-title] European journal of cancer (Oxford, England : 1990)

[ISO-abbreviation] Eur. J. Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

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[Title] Lyn kinase activity is the predominant cellular SRC kinase activity in glioblastoma tumor cells.

As we have found that Lyn, but not Fyn, activity promotes migration of glioblastoma cells in response to the cooperative signal generated by platelet-derived growth factor receptor beta and integrin alpha(v)beta3, we compared the activity and expression of Lyn and Fyn in glioblastoma (grade IV) tumor biopsy samples with that in anaplastic astrocytoma (grade III) tumors, nonneoplastic brain, and normal autopsy brain samples.

Lyn kinase activity was significantly elevated in glioblastoma tumor samples.

The levels of phosphorylation of the autophosphorylation site were consistent with significantly higher Lyn activity in glioblastoma tumor tissue than nonneoplastic brain.

Immunostaining revealed that Lyn is located primarily in the glioblastoma cells in the tumor biopsies.

These data indicate that Lyn kinase activity is significantly elevated in glioblastoma tumors and suggest that it is the Lyn activity that promotes the malignant phenotype in these tumors.

[MeSH-minor] Astrocytoma / enzymology. Astrocytoma / genetics. Astrocytoma / pathology. Biopsy. Brain / enzymology. Endothelial Cells / enzymology. Humans. Immunohistochemistry. Phosphotransferases / genetics. Phosphotransferases / metabolism. Protein-Tyrosine Kinases. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-fyn. RNA, Messenger / genetics. RNA, Messenger / metabolism

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(PMID = 15994925.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA97110; United States / NCI NIH HHS / CA / P50 CA97247

[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 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 2.7.- / Phosphotransferases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / FYN protein, human; EC 2.7.10.2 / Proto-Oncogene Proteins c-fyn; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases

   

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[Title] Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene.

PURPOSE: Allelic loss at 1p is seen in 70% to 85% of oligodendrogliomas (typically in association with 19q allelic loss) and 20-30% of astrocytomas.

Because most 1p deletions in gliomas involve almost the entire chromosome arm, narrowing the region of the putative tumor suppressor gene has been difficult.

The latter group included both low-grade tumors (oligodendroglioma, diffuse astrocytoma, and "oligoastrocytoma") and high-grade tumors (anaplastic oligodendrogliomas, anaplastic astrocytomas, anaplastic oligoastrocytomas).

RESULTS: Allelic losses on 1p and 19q, either separately or combined, were more common in classic oligodendrogliomas than in either astrocytomas or oligoastrocytomas (P < 0.0001).

There was no significant difference in 1p/19q LOH status between low-grade and anaplastic oligodendrogliomas.

In contrast, no astrocytomas and only 6 of 30 (20%) oligoastrocytic tumors had combined 1p/19q loss.

Although rare, 1p deletions were more often segmental in astrocytomas (5 of 6, 83%) than in oligodendrogliomas (3 of 35, 9%; P = 0.006).

Eleven tumors (6 oligodendrogliomas or having oligodendroglial components, 5 purely astrocytic) with small segmental 1p losses underwent further detailed LOH mapping.

All informative tumors in the oligodendroglial group and 2 of 3 informative astrocytomas showed LOH at 1p36.23, with a 150-kb MDR located between D1S2694 and D1S2666, entirely within the CAMTA1 transcription factor gene.

[MeSH-minor] Adult. Astrocytoma / genetics. Astrocytoma / pathology. Calcium-Binding Proteins / genetics. Chromosome Deletion. Chromosome Mapping. Expressed Sequence Tags. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Microsatellite Repeats. Mutation. Oligodendroglioma / genetics. Oligodendroglioma / pathology. Reverse Transcriptase Polymerase Chain Reaction. Trans-Activators / genetics

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(PMID = 15709179.001).

[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] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / CAMTA1 protein, human; 0 / Calcium-Binding Proteins; 0 / Trans-Activators

   

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[Title] Immunobiological and experimental aspects of malignant astrocytoma.

Starting from 1992, the goal of our studies was to obtain new biological data on malignant astrocytomas to better understand the basic biology of the tumour and these are reviewed here.

[MeSH-major] Astrocytoma / immunology. Brain Neoplasms / immunology

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(PMID = 19596914.001).

[ISSN] 1791-7530

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Greece

[Chemical-registry-number] 0 / Interleukin-2

[Number-of-references] 51

   

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[Transliterated title] Syndrome de Turcot confirmé par biologie moléculaire.

INTRODUCTION: Turcot's syndrome is characterized clinically by the concurrence of a primary brain tumor and a familial adenomatous polyposis or a hereditary nonpolyposis colorectal cancer.

OBSERVATION: We report a case of a 45-year-old woman who underwent in 1995 neuro-oncological treatment for an anaplastic astrocytoma (grade III according to the World Health Organization classification).

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(PMID = 16840983.001).

[ISSN] 0035-3787

[Journal-full-title] Revue neurologique

[ISO-abbreviation] Rev. Neurol. (Paris)

[Language] fre

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein

   

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[Title] Salvage chemotherapy with bevacizumab for recurrent alkylator-refractory anaplastic astrocytoma.

A retrospective study of bevacizumab only in adults with recurrent temozolomide (TMZ)-refractory anaplastic astrocytoma (AA) with a primary objective of determining progression free survival (PFS).

Bevacizumab-related toxicity included fatigue (14 patients; 2 grade 3), leukopenia (7; 1 grade 3), deep vein thrombosis (5; 2 grade 3), hypertension (5; 1 grade 3), anemia (4; 0 grade 3) and wound dehiscence (1; 1 grade 3).

Time to tumor progression ranged from 1 to 20 months (median: 7).

[MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Astrocytoma / drug therapy. Astrocytoma / mortality. Brain Neoplasms / drug therapy. Brain Neoplasms / mortality. Neoplasm Recurrence, Local

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(PMID = 18953491.001).

[ISSN] 1573-7373

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

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab

   

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[Title] Metal binding of metallothioneins in human astrocytomas (U87 MG, IPDDC-2A).

For this reason astroglia cells possess high cytosolic levels of metallothioneins I, II and III (MT-I,II,III).

Our aim was to establish the inducibility and metal binding of MTs in two human astrocytoma cell lines, U87 MG (astrocytoma-glioblastoma, grade IV) and IPDDC-2A (astrocytoma, grade II), on exposure to cadmium chloride (1 microM).

We showed that MTs are constitutively expressed in both human astrocytoma cell lines.

In accordance with the higher malignancy grade of U87 MG, the amount of MTs was higher in U87 MG than in IPDDC-2A cells.

Isoform III (identified by chromatographic separation of isoform III from I/II) was present at all exposure times, but only in traces with respect to the prevailing amounts of MT-I/II isoforms.

[MeSH-major] Astrocytoma / metabolism. Metallothionein / metabolism. Metals / metabolism

[MeSH-minor] Cadmium Chloride / metabolism. Cadmium Chloride / pharmacology. Cadmium Chloride / toxicity. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. Protein Binding / physiology

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(PMID = 17115260.001).

[ISSN] 0966-0844

[Journal-full-title] Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine

[ISO-abbreviation] Biometals

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Metals; 9038-94-2 / Metallothionein; J6K4F9V3BA / Cadmium Chloride

   

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[Title] Assessment of 1p/19q status by fluorescence in situ hybridization assay: A comparative study in oligodendroglial, mixed oligoastrocytic and astrocytic tumors.

Astrocytomas and the astrocytic component of oligoastrocytomas showed a diffuse fibrillary type of staining.

None of the astrocytomas including two pediatric cases showed this alteration (P < 0.05).

p53 was expressed in 57.1% of astrocytomas (8/14), 33% of mixed oligoastrocytomas (3/9) and 10% of oligodendrogliomas (2/20).

In contrast, all astrocytomas (Grade II and III) were EGFR negative.

CONCLUSION: Loss of 1p/19q is strongly associated with oligodendroglial phenotype, while astrocytic tumors are more likely to show p53 over-expression. p53 expression and 1p/19q status appear to be mutually exclusive.

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosomes, Human, Pair 19. In Situ Hybridization, Fluorescence / methods. Oligodendroglioma / genetics

[MeSH-minor] Adolescent. Adult. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Receptor, Epidermal Growth Factor / metabolism. Retrospective Studies. Tumor Suppressor Protein p53 / metabolism. Young Adult

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(PMID = 19934553.001).

[ISSN] 0028-3886

[Journal-full-title] Neurology India

[ISO-abbreviation] Neurol India

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] India

[Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

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Intra-axial pathology ranged from anaplastic astrocytoma to metastasis while extra-axial lesions included meningiomas and skull-based metastases.

[MeSH-minor] Adenoma / surgery. Astrocytoma / surgery. Breast Neoplasms / surgery. Craniopharyngioma / surgery. Esthetics. Eyebrows. Eyelids. Female. Follow-Up Studies. Frontal Lobe / surgery. Humans. Male. Meningeal Neoplasms / surgery. Meningioma / surgery. Middle Aged. Pituitary Neoplasms / surgery. Postoperative Complications / etiology. Treatment Outcome

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[Copyright] (c) Georg Thieme Verlag KG Stuttgart . New York.

(PMID = 20376737.001).

[ISSN] 1439-2291

[Journal-full-title] Minimally invasive neurosurgery : MIN

[ISO-abbreviation] Minim Invasive Neurosurg

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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[Title] TRAIL induces MMP-9 expression via ERK activation in human astrocytoma cells.

Matrix metalloproteinase-9 (MMP-9) is an important angiogenic and prognostic factor in malignant tumors.

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as the death ligand, which induces preferential apoptosis of transformed tumor cells.

We demonstrated that TRAIL induces MMP-9 expression in human astrocytoma cells, which is preceded by activation of extracellular signal-regulated protein kinase (ERK).

These findings indicate that TRAIL treatment in human astrocytoma cells leads to the activation of NF-kappaB and subsequent expression of MMP-9, which are dependent on ERK activation.

Collectively, these results suggest that TRAIL has alternative biological functions in addition to its role in inducing apoptosis in human malignant astrocytoma cells.

[MeSH-major] Astrocytoma / enzymology. Extracellular Signal-Regulated MAP Kinases / metabolism. Matrix Metalloproteinase 9 / biosynthesis. TNF-Related Apoptosis-Inducing Ligand / physiology

[MeSH-minor] Butadienes / pharmacology. Cell Line, Tumor. Enzyme Activation. Humans. NF-kappa B / metabolism. Nitriles / pharmacology. Protein Kinase Inhibitors

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(PMID = 18834856.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Butadienes; 0 / NF-kappa B; 0 / Nitriles; 0 / Protein Kinase Inhibitors; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / U 0126; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9

   

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Partial resection of the tumor was safely performed, with slight temporary neurological worsening.

The histological diagnosis was anaplastic astrocytoma.

Individual adjuvant therapy based on the results of real-time reverse transcription-polymerase chain reaction of O6-methylguanine-deoxyribonucleic acid methyltransferase achieved an almost complete tumor response.

[MeSH-major] Astrocytoma / surgery. Brain Mapping. Brain Stem Neoplasms / surgery. Evoked Potentials, Motor. Mesencephalon / physiopathology. Neurosurgical Procedures / methods

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(PMID = 15699622.001).

[ISSN] 0470-8105

[Journal-full-title] Neurologia medico-chirurgica

[ISO-abbreviation] Neurol. Med. Chir. (Tokyo)

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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[Title] Prognostic factors for anaplastic astrocytomas.

Anaplastic astrocytomas (WHO grade III) constitute about 10% of all gliomas.

Definitive data on predictive and prognostic factors are lacking for these neoplasms that are considered the most enigmatic entity among the whole spectrum of astrocytic tumors because of their unclear biologic behavior and variable clinical outcome.

Currently, only few factors have been identified as useful for prognosis of anaplastic astrocytoma: age and Karnofsky Performance Status.

Potential prognostic biomarkers concern tumor suppressor genes on chromosome 9q that are involved in the RB1 pathway; PTEN, the PI3k/Akt/p70s6k cascade, survivin gene, Formylpeptide receptor, minichromosome maintenance protein 3 and genes on chromosome 7.

The state of the art pictured here underlie the recent interest on gene expression profile to identify aberrations useful to understand the biologic behavior of astrocytic tumors.

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

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(PMID = 17001519.001).

[ISSN] 0167-594X

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

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

[Number-of-references] 55

   

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We previously found that FoxM1B is overexpressed in human glioblastomas and that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of highly angiogenic glioblastoma in nude mice.

Our findings provide both clinical and mechanistic evidence that FoxM1 contributes to glioma progression by enhancing VEGF gene transcription and thus tumor angiogenesis.

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(PMID = 18974115.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA116528-03; United States / NCI NIH HHS / CA / CA116528-03; United States / NCI NIH HHS / CA / R01-CA-116528; United States / NCI NIH HHS / CA / R01 CA116528; United States / NCI NIH HHS / CA / R01 CA116528-02; United States / NCI NIH HHS / CA / CA116528-02

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Vascular Endothelial Growth Factor A

[Other-IDs] NLM/ NIHMS67455; NLM/ PMC2597644