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The expression of protein RCAS1 (receptor-binding cancer antigen expressed on SiSo cells), possibly involved in the mechanisms of evasion of immune surveillance by tumours, has been studied in brain astrocytomas grade III and IV and in metastatic carcinomas to the brain by means of double immunofluorescence with antibodies against RCAS1 and respectively anti-GFAP (astroglia) or CD68 or CD74 (macrophages/microglia).

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(PMID = 19813143.001).

[ISSN] 1641-4640

[Journal-full-title] Folia neuropathologica

[ISO-abbreviation] Folia Neuropathol

[Language] ENG

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

[Publication-country] Poland

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / EBAG9 protein, human

   

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

The aim is to define the histological type of glioma (astrocytic, oligodendrocytic or mixed) and the grade in order to classify the patients and give them an accurate treatment.

According to the WHO classification, infiltrative gliomas encompass astrocytic gliomas (diffuse astrocytomas grade II, anaplastic astrocytomas grade III and glioblastomas grade IV), oligodendroglial tumours (oligodendrogliomas grade II, anaplastic oligodendrogliomas grade III) and mixed gliomas (oligoastrocytomas grade II and anaplastic oligoastrocytomas grade III).

Circumscribed gliomas mainly corresponds to pilocytic astrocytomas (grade I).

Three distinct tumour growth patterns may be seen in gliomas, type I: tumor tissue only, type II: tumour tissue and isolated tumor cells permeating the brain parenchyma (ITC) and type III: ITCs only and no tumor tissue.

According to the Sainte Anne classification, gliomas are divided into astrocytic gliomas (pilocytic astrocytomas, structure type I, glioblastomas structure type II) and oligodendrogliomas and mixed oligoastrocytomas (grade A: lack of contrast enhancement and lack of endothelial hyperplasia, structure type III; and grade B: contrast enhancement or endothelial hyperplasia, structure type II and III).

[MeSH-minor] Astrocytoma / pathology. Humans. Neoplasms, Complex and Mixed / classification. Neoplasms, Complex and Mixed / pathology. Oligodendroglioma / pathology. Reproducibility of Results. World Health Organization

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(PMID = 15888386.001).

[ISSN] 1769-6917

[Journal-full-title] Bulletin du cancer

[ISO-abbreviation] Bull Cancer

[Language] fre

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

[Publication-country] France

   

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

Tumorigenesis involves alterations in the tumor suppressor genes (p53), protooncogenes (BCL-2), and housekeeping genes (human MutS homologue-2 (hMSH2).

To test our hypothesis and to examine these issues, we immunostained 60 specimens entailing normal brain tissues, gliosis, and gliomas (Grade I, II, III, IV) for p53, BCL-2, and hMSH2 protein expression.

As compared with the normal brain and gliosis, examination of the average weighted scores in gliomas (Grade I, II, III, IV, respectively) showed significant up-regulation of: (i) p53 protein (0.0 +/- 0.0; 0.0 +/- 0.0; 0.9 +/- 0.5; 1.6 +/- 0.8; 1.7 +/- 0.5; and 4.1 +/- 0.8, P < 0.0001) (ii) hMSH2 (1.3 +/- 0.3; 1.5 +/- 0.7; 1.9 +/- 1.1; 2.2 +/- 0.5; 4.1 +/- 1.5; and 4.7 +/- 1.1, P < 0.0006), and (iii) BCL-2 (0.8 +/- 0.5; 1.9 +/- 0.5; 1.9 +/- 0.6; 2.0 +/- 0.6; 4.4 +/- 1.2; and 4.6 +/- 0.8, P < 0.001).

The expression values (p53, BCL-2, and hMSH2) were statistically significantly higher (P < 0.05) in astrocytomas (Grade III) than in other gliomas.

[MeSH-major] Brain Neoplasms / chemistry. Gene Expression Regulation, Neoplastic. Glioma / chemistry. MutS Homolog 2 Protein / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis. Tumor Suppressor Protein p53 / analysis

[MeSH-minor] Astrocytoma / chemistry. Brain Chemistry. Case-Control Studies. Gliosis / metabolism. Humans. Immunohistochemistry / methods

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(PMID = 16875495.001).

[ISSN] 0959-9673

[Journal-full-title] International journal of experimental pathology

[ISO-abbreviation] Int J Exp Pathol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein

[Other-IDs] NLM/ PMC2517375

   

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

[Title] Histomorphometry of tumour cell nuclei in astrocytomas using shape analysis, densitometry and topometric analysis.

Although tumour cell nuclei are important histological structures for grading of astrocytomas according to the WHO-classification of brain tumours, there is no reported morphometric study of astrocytomas which describes quantitatively the four main morphologic criteria of tumour cell nuclei: size, shape, texture (densitometric characteristics) and spatial relationships between the nuclei (topometric analysis).

Using a set of morphometric parameters describing these criteria as well as the Ki67-proliferation index, 74 astrocytomas from 74 patients were studied by means of a digital image analysis system.

The objective of the study was to test, if these morphometric parameters were sufficient for statistical discrimination between pilocytic astrocytomas WHO-grade I, astrocytomas grade II and anaplastic astrocytomas grade III.

Our results showed a correct reclassification of 97.3% (72/74) of the cases with respect to the tumour grade by means of cross-validated discriminant analysis.

In conclusion, the present morphometric procedure provided good discrimination between the tumour grades, supporting the view that histomorphometry of tumour cell nuclei could be a valuable tool for grading of astrocytomas.

[MeSH-major] Astrocytoma / pathology. Astrocytoma / ultrastructure. Brain Neoplasms / pathology. Brain Neoplasms / ultrastructure. Cell Nucleus / pathology. Cell Nucleus / ultrastructure

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(PMID = 15634229.001).

[ISSN] 0305-1846

[Journal-full-title] Neuropathology and applied neurobiology

[ISO-abbreviation] Neuropathol. Appl. Neurobiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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

[Title] Attractin is elevated in the cerebrospinal fluid of patients with malignant astrocytoma and mediates glioma cell migration.

The goal of our study was to find reliable markers that could be used for disease monitoring as well as to identify new targets for the therapeutic intervention for malignant astrocytoma (WHO grades 3 and 4).

EXPERIMENTAL DESIGN: We employed proteomic techniques to identify secreted proteins in the cerebrospinal fluid that were specific to patients with malignant astrocytoma.

RESULTS: Among 60 cerebrospinal fluid samples of patients with various central nervous system diseases, attractin was consistently found to be elevated in the samples of patients with malignant astrocytoma.

To independently validate these results, we examined attractin expression in a new set of 108 normal and tumoral brain tissue specimens and found elevated expression in 97% of malignant astrocytomas, with the highest levels in grade 4 tumors.

Using immunohistochemistry, we further showed that attractin is produced and secreted by the tumor cells.

Finally, we showed that cerebrospinal fluid from brain tumor patients induces glioma cell migration and that attractin is largely responsible for this promigratory activity.

CONCLUSIONS: Our results find attractin to be a reliable secreted marker for high-grade gliomas.

Additionally, our migration studies suggest that it may be an important mediator of tumor invasiveness, and thus, a potential target in future therapies.

[MeSH-major] Astrocytoma / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Cell Movement / physiology. Glioma / cerebrospinal fluid. Membrane Proteins / cerebrospinal fluid

[MeSH-minor] Blotting, Western. Electrophoresis, Gel, Two-Dimensional. Humans. Immunohistochemistry. Neoplasm Invasiveness

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(PMID = 17085642.001).

[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 / CA 86335

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

[Publication-country] United States

[Chemical-registry-number] 0 / ATRN protein, human; 0 / Membrane Proteins

   

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

[Title] Osteopontin expression correlates with angiogenesis and survival in malignant astrocytoma.

The aim of the study was to analyze the expression of OPN in human astrocytomas and to correlate it with angiogenesis and patients' outcome.

Seventy-six human astrocytomas including eight pilocytic astrocytomas (grade I), 10 diffuse astrocytomas (grade II), 8 anaplastic astrocytomas (grade III) and 50 glioblastomas (grade IV) were immunohistochemically stained for OPN protein.

Astrocytomas were heterogeneous regarding the OPN expression.

Our results indicate the overexpression of OPN protein in astrocytoma cells and suggest the role of OPN in astrocytoma progression and angiogenesis.

[MeSH-major] Astrocytoma / blood supply. Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / blood supply. Brain Neoplasms / metabolism. Neovascularization, Pathologic / metabolism. Osteopontin / metabolism

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(PMID = 18493866.001).

[ISSN] 1219-4956

[Journal-full-title] Pathology oncology research : POR

[ISO-abbreviation] Pathol. Oncol. Res.

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Biomarkers, Tumor; 106441-73-0 / Osteopontin

   

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

[Title] Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma.

Malignant astrocytoma includes anaplastic astrocytoma (grade III) and glioblastoma (grade IV).

Among them, glioblastoma is the most common primary brain tumor with dismal responses to all therapeutic modalities.

We performed a large-scale, genome-wide microRNA (miRNA) (n=756) expression profiling of 26 glioblastoma, 13 anaplastic astrocytoma and 7 normal brain samples with an aim to find deregulated miRNA in malignant astrocytoma.

More importantly, we identified a most discriminatory 23-miRNA expression signature, by using PAM, which precisely distinguished glioblastoma from anaplastic astrocytoma with an accuracy of 95%.

The differential expression pattern of nine miRNAs was further validated by real-time RT-PCR on an independent set of malignant astrocytomas (n=72) and normal samples (n=7).

Thus we have identified the miRNA expression signature for malignant astrocytoma, in particular glioblastoma, and showed the miRNA involvement and their importance in astrocytoma development.

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

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(PMID = 20711171.001).

[ISSN] 1530-0285

[Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

[ISO-abbreviation] Mod. Pathol.

[Language] eng

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

[Publication-country] United States

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

   

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

Five patients had low-grade gliomas (grade II), three had anaplastic astrocytomas (grade III), and seven had glioblastomas (grade IV).

For semiquantitative analysis, the standardized uptake value (SUV) and tumor to contralateral normal gray matter (T/N) ratio were calculated.

The sensitivity for detection of high-grade gliomas was calculated using visual analysis.

ACE and FDG SUV in high-grade gliomas were significantly higher than that in low-grade gliomas.

CONCLUSIONS: ACE PET is a potentially useful radiotracer for detecting brain gliomas and differentiating high-grade gliomas.

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[CommentIn] Mol Imaging Biol. 2009 Jul-Aug;11(4):223 [19326176.001]

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(PMID = 18543041.001).

[ISSN] 1536-1632

[Journal-full-title] Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging

[ISO-abbreviation] Mol Imaging Biol

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Acetates; 0 / Carbon Isotopes; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AE28F7PNPL / Methionine

   

[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.

RT-PCR analysis showed that levels of type I PIMT mRNA were up-regulated while those of type II PIMT mRNA were down-regulated in glioblastomas.

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-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] 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

   

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

[Title] Proteomics of tumor-specific proteins in cerebrospinal fluid of patients with astrocytoma: usefulness of gelsolin protein.

Changes in cerebrospinal fluid (CSF) composition have been shown to accurately reflect pathological processes in the CNS, and are potential indicators of abnormal CNS states, such as tumor growth.

To detect biomarkers in high-grade astrocytomas, the differential expression of proteins in the cerebrospinal fluid was analyzed from two cases each of diffuse astrocytoma (grade II), and glioblastoma (grade IV) using agarose 2-D gel electrophoresis (2-DE).

It was found that the expression of gelsolin protein decreased with histological grade.

To examine whether gelsolin is a useful indicator of tumor aggressiveness or patient outcome, its expression was further studied on immunohistochemistry in 41 formalin-fixed and paraffin-embedded astrocytomas.

The positive cell rate of gelsolin in tumors was 59.4% in grade II, 30.0% in grade III and 29.4% in grade IV, respectively.

Gelsolin expression was significantly lower in high-grade astrocytomas (grade III or IV) than in low-grade astrocytomas (grade II; P < 0.05).

Moreover, in astrocytomas the overall survival of patients in the low-expression group was significantly poorer than in the high expression group (P < 0.05).

These data suggest that gelsolin is a prognostic factor in astrocytoma.

[MeSH-major] Astrocytoma / cerebrospinal fluid. Biomarkers, Tumor / cerebrospinal fluid. Brain Neoplasms / cerebrospinal fluid. Gelsolin / cerebrospinal fluid

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(PMID = 19883430.001).

[ISSN] 1440-1827

[Journal-full-title] Pathology international

[ISO-abbreviation] Pathol. Int.

[Language] eng

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

[Publication-country] Australia

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

   

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

[Title] Expression of Ki-67, topoisomerase IIalpha and c-MYC in astrocytic tumors: correlation with the histopathological grade and proliferative status.

Astrocytomas represent the most frequent primary tumors of the central nervous system.

Recently, the determination of the proliferative index of astrocytic tumors by different methods has been proposed as a valuable tool for tumor grading and also as a prognostic marker.

The aim of the present study was to evaluate the expression of cell proliferation-related proteins in human astrocytic tumors of different histopathological grades (WHO).

An immunohistochemical study of the Ki-67, Topoisomerase IIalpha (Topo IIalpha) and c-MYC proteins using the avidin-biotin-peroxidase method was performed in 55 astrocytomas (13 grade I, 14 grade II, 7 grade III and 21 grade IV) and five samples of non-tumor brain tissue (control group).

Ki-67, Topo IIalpha and c-MYC positive indices tended to increase according to malignant progression, were absent in non-tumor brain tissue and showed maximum values in high-grade astrocytomas (III and IV).

Ki-67 antigen detection in more than 8.0% of the tumor cells distinguished astrocytoma grade IV, while a labeling index between 1.5 and 8.0% characterized astrocytomas grade III and values below 1.5% discriminated low-grade tumors (I and II).

These results indicate that Topo IIalpha and c-MYC expression is associated with cell proliferation in astrocytomas, although not in an exclusive way.

Moreover, Ki-67 antigen was found to be the best marker of cellular proliferation, and its expression predicts the grade of astrocytic tumors.

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

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, Neoplasm / metabolism. Cell Division. Child. Child, Preschool. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. Female. Glioblastoma / metabolism. Glioblastoma / pathology. Humans. Immunohistochemistry. Infant. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Proto-Oncogene Proteins c-myc / metabolism

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(PMID = 17203587.001).

[ISSN] 0919-6544

[Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology

[ISO-abbreviation] Neuropathology

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-myc; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha

   

[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.

Out of 80 cycles received there was no anemia; 5 (6%) grade 1, 8 (10%) grade 2, 2 (3%) grade 3 leucopenia; 1 (1%) grade 1, 2 (3%) grade 2, 1 (1%) grade 3, 1 (1%) grade 4 thrombocytopenia; 9 (11%) grade 1, 7 (9%) grade 2, 32 (40%) grade 3, and 11 (14%) grade 4 lymphopenia.

Study was terminated in 2 patients (one with grade 4 thrombocytopenia and the other with grade 4 hepatic 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.

[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.

Frequent mild toxicities were grade 1-2 nausea/vomiting (17 pts-63%), and grade 1-2 asthenia (8 pts-30%).

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] 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.

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.

There was more hematologic toxicity than expected, with 3/6 of the patients enrolled at dose level 1 developing grade 4 neutropenia.

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

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

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.

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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] 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.

Dose-limiting toxicities were: deep venous thrombosis (1 grade 3); nausea and vomiting (1 grade 3); diarrhea (1 grade 3); elevated ALT (1 grade 3); elevated creatinine (1 grade 3); and fatigue (1 grade 3).

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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] 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.

Our preliminary data on 15 patients and 39 courses of Dendritic Cell vaccines demonstrate one grade 3 toxicity of fever/chest pain.

CONCLUSIONS: This phase I study demonstrates the safety, feasibility of dendritic cell vaccination with biodegradable carmustine (BCNU) wafers with one grade 3 AE.

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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] 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] Could changes in the regulation of the PI3K/PKB/Akt signaling pathway and cell cycle be involved in astrocytic tumor pathogenesis and progression?

The most frequent alterations found in astrocytomas are two major groups of signaling proteins: the cell cycle and the growth factor-regulated signaling pathways.

The aim of our study was to detect changes in expression of the following proteins: the tumor suppressors PTEN, p53, and p21Waf1/Cip1, glial fibrillary acidic protein (GFAP, as a marker of astroglial differentiation), the phosphorylated form of protein kinase B/Akt (PKB/Akt), which is downstream to the epidermal growth factor receptor (EGFR), and MDM2, which degrades p53.

Paraffin-embedded astrocytoma tissue samples from 89 patients were divided into low grade (grade I-II; 42 samples) and high grade astrocytomas (grade III-IV; 47 samples).

EGFR protein was detected in 29 % of low grade and in 60 % of high grade astrocytomas.

The expression of phosphorylated PKB/Akt was found in roughly the same proportions: in 86% of low grade and in 79% of high grade astrocytomas.

PTEN was not found in most of astrocytomas, 64% of low grade and 74% of high grade tumors showed no PTEN staining.

Overexpression of the mutated form of p53 or loss of p53 expression, however, was found in about 63% in both groups of astrocytomas with no differences between them.

GFAP expression was decreased in tumor astrocytes compared to normal astrocytes and this decreased with grading.

GFAP positive tumor cells were detected in only 50% of low grade, and 32% of high grade astrocytomas.

Loss of p21Waf1/Cip1 expression was shown in 20% of low and in 45% of high grade tumors.

In the subgroup of high grade tumors with wild type p53, 86% showed p21Waf1/Cip1 expression, whereas in the subgroup of high grade tumors with altered p53, only 35% displayed p21Waf1/Cip1.

We conclude that EGFR expression increases with astrocytoma grading.

PTEN defects may also participate in aggressive tumor behaviour through activation of the PKB/Akt pathway.

The alteration of p53 supports the finding that the cell cycle regulation is also disrupted during development of astrocytomas.

EGFR is one of the factors, which drives the progression of astrocytomas from low to high grade stage.

[MeSH-major] Astrocytoma / metabolism. Cell Cycle. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Glial Fibrillary Acidic Protein / metabolism. Humans. Male. Middle Aged. Mutation / genetics. Oligodendroglioma / metabolism. Oligodendroglioma / pathology. PTEN Phosphohydrolase / metabolism. Phosphorylation. Proto-Oncogene Proteins c-mdm2 / metabolism. Receptor, Epidermal Growth Factor / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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(PMID = 17822324.001).

[ISSN] 0028-2685

[Journal-full-title] Neoplasma

[ISO-abbreviation] Neoplasma

[Language] eng

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

[Publication-country] Slovakia

[Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2

   

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

[Title] Collision tumor of meningioma and malignant astrocytoma.

The pathology of tumors reported collision tumors composed of meningioma and malignant astrocytoma.

[MeSH-major] Astrocytoma / surgery. Brain Neoplasms / surgery. Meningeal Neoplasms / surgery. Meningioma / surgery

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[Copyright] Copyright © 2011 S. Karger AG, Basel.

(PMID = 21389747.001).

[ISSN] 1423-0305

[Journal-full-title] Pediatric neurosurgery

[ISO-abbreviation] Pediatr Neurosurg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

   

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

[Title] p53 abnormality and tumor invasion in patients with malignant astrocytoma.

Malignant astrocytomas are characterized by diffusely infiltrating nature, and the abnormality of p53 is a cytogenetic hallmark of astrocytic tumors.

To elucidate the relationship between p53 abnormality and invasiveness of the tumors, we studied mutation and protein expression of p53 in 48 consecutive patients with malignant astrocytoma (14 anaplastic astrocytomas and 34 glioblastoma multiformes).

The tumors were classified into three categories according to the features of magnetic resonance imaging, and 5, 7, and 36 tumors were classified into diffuse, multiple, and single type, respectively.

We then examined how these tumor types correlate with MIB-1 staining index, TP53 gene mutation, and p53 protein expression.

Furthermore, diffuse- and multiple-type tumors were significantly correlated with poor progression-free survival, whereas only multiple-type tumors were significantly correlated with poor overall survival.

As diffuse and multiple features on imaging modalities represent invasive characteristics of the tumors, p53 abnormalities may affect the invasive and aggressive nature of malignant astrocytomas.

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

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. DNA, Neoplasm / genetics. Female. Glial Fibrillary Acidic Protein / genetics. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Mitotic Index. Mutation / genetics. Mutation / physiology. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Survival Analysis. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / metabolism. Young Adult

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(PMID = 21046311.001).

[ISSN] 1861-387X

[Journal-full-title] Brain tumor pathology

[ISO-abbreviation] Brain Tumor Pathol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Glial Fibrillary Acidic Protein; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A

   

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

[Title] Screening for motility-associated genes in malignant astrocytoma cell lines.

The most characteristic feature of a malignant astrocytoma is its early and extensive infiltration into adjacent parenchymal structures.

We focused on detecting the possible expression changes as the determining factors for malignant astrocytoma's motile ability.

These findings suggest that the genes identified may be important for determining high motility in astrocytoma cell lines.

These findings may help us understand the molecular invasion mechanism in astrocytomas.

[MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Cell Movement. Gene Expression Profiling

[MeSH-minor] Humans. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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(PMID = 17048098.001).

[ISSN] 0167-594X

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

[ISO-abbreviation] J. Neurooncol.

[Language] eng

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

[Publication-country] United States

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

   

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

[Title] Drug/diet synergy for managing malignant astrocytoma in mice: 2-deoxy-D-glucose and the restricted ketogenic diet.

BACKGROUND: Astrocytomas are largely dependent on glycolysis to satisfy their bioenergetic requirements for growth and survival.

Therapies that target glycolysis can potentially manage astrocytoma growth and progression.

Dietary restriction of the high fat/low carbohydrate ketogenic diet (KD-R) reduces glycolysis and is effective in managing experimental mouse and human astrocytomas.

The goal here was to determine if low doses of 2-DG could act synergistically with the KD-R to better manage growth of the CT-2A malignant mouse astrocytoma.

METHODS: The therapeutic effect of a KD-R supplemented with a low dose of 2-DG (25 mg/kg) was examined in adult C57BL/6J mice bearing the syngeneic CT-2A malignant astrocytoma grown orthotopically.

Mice were fed the standard unrestricted diet for the first 3 days after tumor implantation prior to their separation into one of four diet groups fed either a standard rodent diet in unrestricted amounts (SD-UR) or a KD-R with or without 2-DG for 10 days.

2-DG was initiated 6 days after tumor implantation and was continued for 7 days.

RESULTS: Energy intake, body weights, and CT-2A tumor weights were similar in the SD-UR and the SD-UR+2-2DG mouse groups over the dietary treatment period (days 3-13).

Tumor weights were about 48% and 80% lower in the KD-R and in the KD-R+2-DG groups, respectively, than in the SD-UR group.

CONCLUSION: Astrocytoma growth was reduced more in the KD-R mouse group supplemented with 2-DG than in the mouse groups receiving either dietary restriction or 2-DG alone, indicating a synergistic interaction between the drug and the diet.

The results suggest that management of malignant astrocytoma with restricted ketogenic diets could be enhanced when combined with drugs that inhibit glycolysis.

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(PMID = 19032781.001).

[ISSN] 1743-7075

[Journal-full-title] Nutrition & metabolism

[ISO-abbreviation] Nutr Metab (Lond)

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA102135; United States / NINDS NIH HHS / NS / R01 NS055195; United States / NINDS NIH HHS / NS / R56 NS055195

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2607273

   

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

[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

   

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

[Title] [Malignant astrocytoma as a recurrance of astrocytoma II WHO after 13 years. Case report and literature review].

Astrocytomas--neroepithelial originated tumors that belong to the big, differential group of tumors, which derive from astrocytic glial.

They include slow growing tumors such as fibillary astrocytoma or very malignant glioblastoma multiforme.

The case which is being presented is of a forty nine year old woman operated in July 1997 because of a protoplasmic astrocytoma II WHO in the left frontal lobe.

Due to this adverse event MRI was ordered and suspicion of tumor recurrence was put forward.

Histopathology identified anaplastic astrocytoma III WHO.

According to literature, the factors regarding remission time, tumor malignancy and therapeutic aim were analyzed.

[MeSH-major] Brain Neoplasms / radiotherapy. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / diagnosis

[MeSH-minor] Adult. Astrocytoma. Female. Frontal Lobe. Humans. Reoperation. Seizures / etiology

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(PMID = 21473001.001).

[ISSN] 1427-440X

[Journal-full-title] Annales Academiae Medicae Stetinensis

[ISO-abbreviation] Ann Acad Med Stetin

[Language] pol

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

[Publication-country] Poland

   

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

[Title] Reirradiation of recurrent WHO grade III astrocytomas using fractionated stereotactic radiotherapy (FSRT).

PURPOSE: To assess the effect of reirradiation in recurrent WHO grade III astrocytomas.

PATIENTS AND METHODS: From January 1995 to July 2003, 40 patients with grade III gliomas were treated with fractionated stereotactic reirradiation at the time point of recurrence.

No toxicities > CTC grade 2 developed.

CONCLUSION: Fractionated stereotactic radiotherapy is well tolerated and effective in patients with recurrent grade III astrocytomas.

[MeSH-major] Astrocytoma / mortality. Astrocytoma / surgery. Brain Neoplasms / mortality. Brain Neoplasms / surgery. Neoplasm Recurrence, Local / mortality. Neoplasm Recurrence, Local / surgery. Radiosurgery / statistics & numerical data

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(PMID = 16362786.001).

[ISSN] 0179-7158

[Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]

[ISO-abbreviation] Strahlenther Onkol

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Germany

   

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

[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

   

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

[Title] Regression of grade III astrocytoma during the treatment of CML with imatinib mesylate.

Astrocytomas are central nervous system neoplasms, which are derived predominately from astrocytes.

On the basis of the histopathologic characteristics astrocytomas are graded from I to IV.

The cells that demonstrate the greatest degree of anaplasia are used to determine the histologic grade of the tumor.

The mean age of survival are approximately 10 years from the time of diagnosis for pilocystic astrocytomas (World Health Organization grade I), more than 5 years for patients with low-grade diffuse astrocytomas (WHO grade II), 2 to 5 years for those with anaplastic astrocytomas (WHO grade III), and less than 1 year for patients with glioblastoma (WHO grade IV).

The treatment is a combination of surgery, radiation, and chemotherapy depending of the grade of astrocytoma.

We present a case of 31-year-old man with grade III astrocytoma with subsequent chronic myelogenous leukemia treated with imatinib mesylate as part of his chronic myelogenous leukemia treatment failing to show recurrence of the astrocytoma 10 years after standard treatment for astrocytoma.

[MeSH-major] Antineoplastic Agents / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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(PMID = 16988542.001).

[ISSN] 1075-2765

[Journal-full-title] American journal of therapeutics

[ISO-abbreviation] Am J Ther

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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

[Title] Intracranial Metastases of Cervical Intramedullary Low-Grade Astrocytoma without Malignant Transformation in Adult.

The first case of intracranial metastases of a cervical intramedullary low-grade astrocytoma without malignant transformation in adult is presented in this report.

Seven years ago, a 45 year-old male patient underwent biopsy to confirm pathologic characteristics and received craniocervical radiation and chemotherapy for a grade II astrocytoma in the cervical spinal cord.

The tumor at the cervical and brain lesions was classified as an astrocytoma (WHO grade II).

When a patient with low-grade astrocytoma in the spinal cord has new cranial symptoms after surgery, radiaton, and chemotherapy, the possibility of its metastasis should be suspected because it can spread to the intracranial cavity even without malignant transformation as shown in this case.

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[Cites] J Neurooncol. 2000 Dec;50(3):239-43 [11263503.001]

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(PMID = 19609424.001).

[ISSN] 2005-3711

[Journal-full-title] Journal of Korean Neurosurgical Society

[ISO-abbreviation] J Korean Neurosurg Soc

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2711238

[Keywords] NOTNLM ; Astrocytoma / Cranial metastases / Intramedullary / Spinal cord tumor

   

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

[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

   

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

[Title] Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas.

AIMS: The involvement of various growth factors, growth factor receptors and proliferative markers in the molecular pathogenesis of astrocytic neoplasms are being studied extensively.

Since EGFR and proliferating cell nuclear antigen (PCNA) are involved in mitogenic signal transduction and cellular proliferation pathway, we have studied the correlation between the expression of EGFR and PCNA labeling index in astrocytic tumors.

MATERIALS AND METHODS: We investigated the immunohistochemical expression of EGFR and PCNA using the appropriate monoclonal antibodies in 40 cases of astrocytic tumors of which 21 cases were glioblastoma, eight cases were Grade III or anaplastic astrocytomas and six cases were Grade II or diffuse astrocytomas and five cases were Grade I or pilocytic astrocytomas.

RESULTS: Both the EGFR expression and PCNA labeling index increase with increasing grades of astrocytomas with a significantly high percentage of cells showing positive staining for both EGFR and PCNA in GBM and Grade III astrocytomas compared to Grade II astrocytomas.

The expression levels of both EGFR and PCNA were low in Grade I or pilocytic astrocytomas.

CONCLUSIONS: A significant correlation was found between EGFR overexpression and PCNA labeling index in Grade III and Grade II astrocytomas and glioblastoma.

These suggest that the tumor proliferation, at least in higher grades of astrocytomas is dependent in some measure on EGF and EGFR-related signaling pathways.

[MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Receptor, Epidermal Growth Factor / metabolism

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NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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(PMID = 19127042.001).

[ISSN] 0028-3886

[Journal-full-title] Neurology India

[ISO-abbreviation] Neurol India

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 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] Recent advances in the treatment of malignant astrocytoma.

Malignant gliomas, including the most common subtype, glioblastoma multiforme (GBM), are among the most devastating of neoplasms.

Limited delivery and tumor heterogeneity are two fundamental factors that have critically hindered therapeutic progress.

The simultaneous development of multiple advanced therapies based on specific tumor biology may finally offer glioma patients improved survival.

[MeSH-major] Astrocytoma / therapy. Central Nervous System Neoplasms / therapy

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(PMID = 16525180.001).

[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

[Grant] United States / NCI NIH HHS / CA / 1 P20 CA096890; United States / NCI NIH HHS / CA / CA11898; United States / NCRR NIH HHS / RR / MO1 RR 30; United States / NINDS NIH HHS / NS / NS20023

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

[Publication-country] United States

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

[Number-of-references] 209

   

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

[Title] A new scoring system for malignant astrocytomas.

BACKGROUND: Currently there are a few scoring systems for malignant astrocytoma, but they are not widely accepted.

The aim of this study was to create a scoring system for supratentorial malignant astrocytoma, which could be used in both developed and developing societies.

METHODS: This study was performed in 128 patients who had supratentorial malignant astrocytoma (grade III or IV).

By using the most appropriate four parameters (age, KPS, initial seizure and histopathological grade) we created a scoring system - MAS (Malignant Astrocytoma Score).

CONCLUSIONS: We are of the opinion that MAS represents a useful scoring system to determine the severity of the illness and make a prognosis for both individuals and groups of patients with malignant supratentorial astrocytoma.

[MeSH-major] Astrocytoma / pathology. Supratentorial Neoplasms / pathology

[MeSH-minor] Female. Humans. Kaplan-Meier Estimate. Karnofsky Performance Status. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Neurosurgical Procedures / mortality. Prognosis. Proportional Hazards Models. ROC Curve. Survival Analysis. Tomography, X-Ray Computed

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(PMID = 18444219.001).

[ISSN] 0044-4251

[Journal-full-title] Zentralblatt für Neurochirurgie

[ISO-abbreviation] Zentralbl. Neurochir.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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

[Title] Tumor angiogenic and hypoxic profiles predict radiographic response and survival in malignant astrocytoma patients treated with bevacizumab and irinotecan.

PURPOSE: The combination of a vascular endothelial growth factor (VEGF) -neutralizing antibody, bevacizumab, and irinotecan is associated with high radiographic response rates and improved survival outcomes in patients with recurrent malignant gliomas.

The aim of these retrospective studies was to evaluate tumor vascularity and expression of components of the VEGF pathway and hypoxic responses as predictive markers for radiographic response and survival benefit from the bevacizumab and irinotecan therapy.

PATIENTS AND METHODS: In a phase II trial, 60 patients with recurrent malignant astrocytomas were treated with bevacizumab and irinotecan.

Tumor specimens collected at the time of diagnosis were available for further pathologic studies in 45 patients (75%).

RESULTS: Of 45 patients, 27 patients had glioblastoma multiforme, and 18 patients had anaplastic astrocytoma.

CONCLUSION: In this patient cohort, tumor expression levels of VEGF, the molecular target of bevacizumab, were associated with radiographic response, and the upstream promoter of angiogenesis, hypoxia, determined survival outcome, as measured from treatment initiation.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy

[MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Biomarkers, Tumor / analysis. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Female. Humans. Hypoxia. Male. Middle Aged. Neovascularization, Pathologic. Proportional Hazards Models. Radiography. Retrospective Studies. Survival Analysis. Treatment Outcome. Vascular Endothelial Growth Factor A / analysis

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(PMID = 18182667.001).

[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

[Grant] United States / NINDS NIH HHS / NS / NS054276; United States / NCI NIH HHS / CA / R01 CA116659; United States / NCI NIH HHS / CA / CA116659; United States / NINDS NIH HHS / NS / K02 NS047409; United States / NINDS NIH HHS / NS / NS047409; United States / NINDS NIH HHS / NS / R01 NS054276

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; 0H43101T0J / irinotecan; 2S9ZZM9Q9V / Bevacizumab; XT3Z54Z28A / Camptothecin

[Other-IDs] NLM/ NIHMS508913; NLM/ PMC3930173

   

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

[Title] High-grade intramedullary astrocytomas: 30 years' experience at the Neurosurgery Department of the University of Rome "Sapienza".

OBJECT: The goal in this study was to review a series of patients who underwent surgical removal of intramedullary high-grade gliomas, focusing on the functional outcome, recurrence rates, and technical problems continually debated in neurosurgical practice.

METHODS: Between December 1976 and December 2006, 22 patients underwent removal of intramedullary high-grade gliomas.

RESULTS: Histological examinations showed 10 Grade III astrocytomas and 12 glioblastomas.

Only 2 of the 22 high-grade astrocytomas could be completely removed.

In this series, multimodality treatment of intramedullary high-grade astrocytomas has been shown to increase length of survival without improving the neurological status.

[MeSH-major] Astrocytoma / surgery. Spinal Cord Neoplasms / surgery

[MeSH-minor] Adolescent. Adult. Cervical Vertebrae. Child. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Neurosurgical Procedures / methods. Neurosurgical Procedures / mortality. Rome. Spinal Cord / pathology. Spinal Cord / surgery. Thoracic Vertebrae. Time Factors. Treatment Outcome. Young Adult

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[CommentIn] J Neurosurg Spine. 2010 Feb;12(2):141-2; discussion 142-3 [20121347.001]

(PMID = 20121348.001).

[ISSN] 1547-5646

[Journal-full-title] Journal of neurosurgery. Spine

[ISO-abbreviation] J Neurosurg Spine

[Language] eng

[Publication-type] Case Reports; 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] Neural and cancer stem cells in tumor suppressor mouse models of malignant astrocytoma.

Malignant astrocytomas are highly invasive brain tumors that portend poor prognosis and dismal survival.

We previously reported tumor suppressor mouse models based on conditional inactivation of human astrocytoma-relevant genes p53, Nf1, and Pten.

These mice develop, with full penetrance, varying grades of astrocytic malignancy that recapitulate the human condition histologically and molecularly.

Our studies indicate a central role for neural stem cells and stem-cell-like cancer cells in tumor initiation and progression.

These mouse models thus represent powerful tools for investigating various aspects of tumor development that otherwise cannot be explored in humans.

[MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Neoplastic Stem Cells / pathology. Neurons / pathology

[MeSH-minor] Animals. Disease Models, Animal. Genes, Tumor Suppressor. Humans. Mice. Models, Neurological. Mutation

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(PMID = 19022744.001).

[ISSN] 1943-4456

[Journal-full-title] Cold Spring Harbor symposia on quantitative biology

[ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / P50NS05260602

[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] 43

   

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

[Title] The basic morphological characteristics of astrocytomas in Vojvodina in the period 2001-2006.

PURPOSE: Astrocytomas are the most common primary intracranial neoplasms.

The aim of this investigation was to register the age, sex, tumor localization, frequency and histological types of patients with astrocytomas.

Tumor histological studies were carried out in the Laboratory of the Centre for Pathology and Histology of the Clinical Centre of Vojvodina.

Out of 490 patients with diagnosed intracranial tumors, 139 (28.4%) had astrocytomas.

RESULTS: Astrocytomas were more frequent in males (63.3%) and were most common in the 50-59-year age group (39.5%).

In regard to other histological types of intracranial tumors, astrocytomas were more frequent in males (34.8%).

Grade III astrocytomas were most common (55.4%).

The frequency of hemorrhage and thrombosis showed a positive correlation with the histological grade of astrocytomas.

CONCLUSION: The typical patient with astrocytoma is a male of 50-59 years.

The tumor is grade III located in the right frontal region.

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

[MeSH-minor] Adult. Age Factors. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Sex Factors. Yugoslavia

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(PMID = 20148453.001).

[ISSN] 1107-0625

[Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology

[ISO-abbreviation] J BUON

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

   

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

[Title] Genomic alterations in low-grade, anaplastic astrocytomas and glioblastomas.

To extend our understanding of potential stepwise genetic alterations that may underlie tumor progression from low-grade astrocytomas to glioblastomas, histopathologic and comparative genomic hybridization analyses were performed on tumor specimens from 68 primary lesions, including 40 glioblastomas, 10 anaplastic and 18 low-grade astrocytomas.

The number of aberrations per case increased towards the higher grade tumors (grade II: 1.66+/-1.49; grade III: 2.80+/-1.68; grade IV: 3.02+/-1.07; F=6.955, p=0.002).

A gain of 7/7q was common and the most frequently seen aberration in low-grade astrocytomas, whereas loss of 10q was the most frequently seen anomaly in anaplastic astrocytomas and glioblastomas.

Chromosome 10/10q deletion and combination of 1p, 19q and 17p deletions were specific to high-grade astrocytic tumors.

The genomic copy deletions of chromosomes 1p and 19q might provide an alternative mechanism in the genesis of astrocytomas.

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Chromosome Aberrations. Chromosome Deletion. Glioblastoma / genetics

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[Cites] Acta Neurol Belg. 2002 Jun;102(2):53-62 [12161900.001]

[Cites] Am J Pathol. 1999 Aug;155(2):375-86 [10433931.001]

[Cites] Cancer Res. 1994 Mar 15;54(6):1397-401 [8137236.001]

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(PMID = 17387387.001).

[ISSN] 1219-4956

[Journal-full-title] Pathology oncology research : POR

[ISO-abbreviation] Pathol. Oncol. Res.

[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] Proteomic analysis of low- to high-grade astrocytomas reveals an alteration of the expression level of raf kinase inhibitor protein and nucleophosmin.

The aim of this study was to identify differentially expressed proteins in diffuse astrocytoma grade II, anaplastic astrocytoma grade III and glioblastoma multiforme grade IV in human tumor samples and in non-neoplastic brain tissue as control using 2-DE and MS.

Tumor and control brain tissue dissection was guided by histological hematoxylin/eosin tissue sections to provide more than 90% of tumor cells and astrocytes.

Six proteins were detected as up-regulated in higher grade astrocytomas and the most important finding was nucleophosmin (NPM) (p<0.05), whereas four proteins were down-regulated, among them raf kinase inhibitor protein (RKIP) (p<0.05).

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics. Phosphatidylethanolamine Binding Protein / genetics. Proteomics

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(PMID = 20533335.001).

[ISSN] 1615-9861

[Journal-full-title] Proteomics

[ISO-abbreviation] Proteomics

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Nuclear Proteins; 0 / Phosphatidylethanolamine Binding Protein; 0 / Proteins; 117896-08-9 / nucleophosmin

   

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

[Title] Distribution of nuclear size and internuclear distance are important criteria for grading astrocytomas.

AIM: The differentiation between low-grade astrocytomas and anaplastic astrocytomas is susceptible to considerable inter-observer variability.

In order to contribute to a better standardization of astrocytoma-grading based on quantitative data, the present study focuses on two important aspects not being considered in previous morphometric studies: elaboration of a decision flow chart for tumor grading based on morphometric parameters and appropriate cut-off-values, easily performed using low-cost equipment such as measuring oculars; investigation of the distribution (histograms) of parameters describing nuclear size and internuclear distance, which had been represented in previous studies by their mean and standard deviation only.

MATERIAL AND METHODS: At least 300 tumor cell nuclei per case were investigated in paraffin sections from surgical specimen of 75 patients with astrocytomas WHO grade II (n = 23) and anaplastic astrocytomas WHO grade III (n = 52) by means of a digital image analysis system.

According to multivariate analysis, the best contribution to tumor grading was achieved by means of parameters concerning the distribution of values for nuclear diameters and internuclear distances.

A decision tree was constructed using a knowledge based algorithm, which provided astrocytoma grading based on the distribution of values for nuclear diameter, as well as the numerical nuclear density and proliferation index.

CONCLUSION: The study demonstrates that a morphometric examination of tumor cell nuclei in paraffin sections supports the clinically important differential diagnosis between low-grade and high-grade astrocytomas.

The method for classification and the data published in the present study constitute a good basis for a standardized and reproducible grading procedure for astrocytomas, which can be performed in any histologic laboratory even without a digital image analysis system.

[MeSH-major] Astrocytoma / classification. Astrocytoma / pathology. Brain Neoplasms / classification. Brain Neoplasms / pathology. Cell Nucleus / ultrastructure

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(PMID = 16465775.001).

[ISSN] 0722-5091

[Journal-full-title] Clinical neuropathology

[ISO-abbreviation] Clin. Neuropathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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

[Title] Expression of phosphoprotein enriched in astrocytes 15 kDa (PEA-15) in astrocytic tumors: a novel approach of correlating malignancy grade and prognosis.

Despite its many important roles, the clinical significance of PEA-15 expression levels in astrocytic tumors has yet to be properly defined.

We studied the PEA-15 expression pattern of 65 patients [diagnosed according to World Health Organization (WHO) criteria] with diffuse astrocytoma (WHO grade II), anaplastic astrocytoma (grade III), and glioblastoma (grade IV).

In grade II astrocytoma (diffuse astrocytoma) and grade III astrocytoma (anaplastic astrocytoma), 100% and 88.9% of patients expressed high PEA-15 levels, respectively, while a smaller number (50%) of patients with grade IV astrocytoma (glioblastoma) expressed high PEA-15 levels.

PEA-15 expression level was inversely associated with WHO grade (P = 0.0006).

Next, we evaluated prognosis and PEA-15 expression levels in 43 patients with high-grade astrocytomas based on the following parameters: age, gender, WHO grade, surgical resection extent, MIB-1 labeling index (LI), and PEA-15 expression level.

Multivariable analyses revealed that high PEA-15 expression level displayed a significant correlation with longer overall survival (OS) in high-grade astrocytomas (P = 0.0024).

In conclusion, PEA-15 expression level was inversely associated with WHO grade and may serve as an important prognostic factor for high-grade astrocytomas.

[MeSH-major] Astrocytoma / diagnosis. Astrocytoma / metabolism. Brain Neoplasms / diagnosis. Brain Neoplasms / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Phosphoproteins / metabolism. Statistics as Topic

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(PMID = 20455002.001).

[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 / Intracellular Signaling Peptides and Proteins; 0 / Ki-67 Antigen; 0 / PEA15 protein, human; 0 / Phosphoproteins

   

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

[Title] Identification of COL6A1 as a differentially expressed gene in human astrocytomas.

Gliomas are classified by the WHO according to their histopathological and clinical characteristics into four classes: grade I (pilocytic astrocytoma), grade II (diffuse astrocytoma), grade III (anaplastic astrocytoma), and grade IV (glioblastoma multiforme).

Several genes have already been correlated with astrocytomas, but many others are yet to be uncovered.

By analyzing the public SAGE data from 21 patients, comprising low malignant grade astrocytomas and glioblastomas, we found COL6A1 to be differentially expressed, confirming this finding by real time RT-PCR in 66 surgical samples.

The expression of this gene has significantly different means when normal glia is compared with low-grade astrocytomas (grades I and II) and high-grade astrocytomas (grades III and IV), with a tendency to be greater in higher grade samples, thus rendering it a powerful tumor marker.

[MeSH-major] Astrocytoma / genetics. Collagen Type VI / genetics. Gene Expression Profiling

[MeSH-minor] Gene Expression Regulation, Neoplastic. Humans. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18551403.001).

[ISSN] 1676-5680

[Journal-full-title] Genetics and molecular research : GMR

[ISO-abbreviation] Genet. Mol. Res.

[Language] eng

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

[Publication-country] Brazil

[Chemical-registry-number] 0 / Collagen Type VI; 0 / RNA, Neoplasm

   

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

[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

   

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

[Title] Analysis of PIK3CA and B-RAF gene mutations in human astrocytomas: association with activation of ERK and AKT.

OBJECTIVE: The analysis of the presence of PIK3CA and B-RAF gene mutations in relation to ERK and AKT activation in diffusely infiltrating astrocytomas, in order to determine their potential role in tumor aggressiveness.

Neither low grade astrocytomas nor anaplastic astrocytomas revealed any mutations in these genes.

Moreover, pERK nuclear expression increased in parallel with tumor grade (II, III v/s IV, p = 0.0262).

pAKT cytoplasmic expression increased with increasing tumor grade (II,III v/s IV, p = 0.0930), although the latter relationship was of marginal significance. pAKT cytoplasmic expression was also positively correlated with pERK nuclear expression (p = 0.0156).

CONCLUSIONS: Our study reports the low frequency of PIK3CA and B-RAF mutations in astrocytomas, despite the presence of activated ERK and AKT proteins.

Moreover, the correlation of pERK nuclear and pAKT cytoplasmic expression with tumor grade suggests the possible crucial role of the activation of these proteins in human gliomagenesis.

[MeSH-major] Astrocytoma / genetics. Brain Neoplasms / genetics. MAP Kinase Signaling System / physiology. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics. Proto-Oncogene Proteins B-raf / genetics

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(PMID = 20569675.001).

[ISSN] 0722-5091

[Journal-full-title] Clinical neuropathology

[ISO-abbreviation] Clin. Neuropathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases

   

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

[Title] Methylation of the PTEN promoter defines low-grade gliomas and secondary glioblastoma.

Glioblastoma multiforme (GBM) can present as either de novo or secondary tumors arising from previously diagnosed low-grade gliomas.

Although these tumor types are phenotypically indistinguishable, de novo and secondary GBMs are associated with distinct genetic characteristics.

PTEN mutations, which result in activation of the phosphoinositide 3-kinase (PI3K) signal transduction pathway, are frequent in de novo but not in secondary GBMs or their antecedent low-grade tumors.

Results we present here show that grade II astrocytomas, oligodendrogliomas, and oligoastrocytomas commonly display methylation of the PTEN promoter, a finding that is absent in nontumor brain specimens and rare in de novo GBMs.

Our results also demonstrate frequent methylation of the PTEN promoter in grade III astrocytomas and secondary GBMs, consistent with the hypothesis that these tumors arise from lower grade precursors.

PTEN methylation is rare in de novo GBMs and is mutually exclusive with PTEN mutations.

We conclude that methylation of the PTEN promoter may represent an alternate mechanism by which PI3K signaling is increased in grade II and III gliomas as well as secondary GBMs, a finding that offers new therapeutic approaches in these patients.

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[Cites] Cancer Res. 2001 Feb 1;61(3):1122-8 [11221842.001]

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(PMID = 17504928.001).

[ISSN] 1522-8517

[Journal-full-title] Neuro-oncology

[ISO-abbreviation] Neuro-oncology

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA97257; United States / NCI NIH HHS / CA / R01 CA52689; United States / NCI NIH HHS / CA / P50 CA097257; United States / NCI NIH HHS / CA / R01 CA082783-06; United States / NCI NIH HHS / CA / R01 CA082783; United States / NCI NIH HHS / CA / CA082783-06; United States / NCI NIH HHS / CA / R01 CA052689

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

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

[Other-IDs] NLM/ PMC1907411

   

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

[Title] Anaplastic astrocytomas: biology and treatment.

Anaplastic astrocytomas (AA), WHO grade III gliomas, comprise 10-15% of all glial neoplasms.

The most important predictor of response to therapy and survival in AA tumors is the presence or absence of the 1p19q co-deletion, a translocation that defines a subset of oligodendroglial tumors, and anaplastic oligodendrogliomas in particular.

[MeSH-major] Astrocytoma / diagnosis. Astrocytoma / therapy. Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Clinical Trials as Topic

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(PMID = 18416660.001).

[ISSN] 1744-8360

[Journal-full-title] Expert review of neurotherapeutics

[ISO-abbreviation] Expert Rev Neurother

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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

[Title] Progression-associated genes in astrocytoma identified by novel microarray gene expression data reanalysis.

Astrocytoma is graded as pilocytic (WHO grade I), diffuse (WHO grade II), anaplastic (WHO grade III), and glioblastoma multiforme (WHO grade IV).

The progression from low- to high-grade astrocytoma is associated with distinct molecular changes that vary with patient age, yet the prognosis of high-grade tumors in children and adults is equally dismal.

Whether specific gene expression changes are consistently associated with all high-grade astrocytomas, independent of patient age, is not known.

To address this question, we reanalyzed the microarray datasets comprising astrocytomas from children and adults, respectively.

We identified nine genes consistently dysregulated in high-grade tumors, using four novel tests for identifying differentially expressed genes.

Four genes encoding ribosomal proteins (RPS2, RPS8, RPS18, RPL37A) were upregulated, and five genes (APOD, SORL1, SPOCK2, PRSS11, ID3) were downregulated in high-grade by all tests.

Expression results were validated using a third astrocytoma dataset.

APOD, the most differentially expressed gene, has been shown to inhibit tumor cell and vascular smooth muscle cell proliferation.

This suggests that dysregulation of APOD may be critical for malignant astrocytoma formation, and thus a possible novel universal target for therapeutic intervention.

Further investigation is needed to evaluate the role of APOD, as well as the other genes identified, in malignant astrocytoma development.

[MeSH-major] Astrocytoma / genetics. Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Gene Expression. Oligonucleotide Array Sequence Analysis / methods

[MeSH-minor] Adult. Child. Chromosomes, Human. Cluster Analysis. Data Interpretation, Statistical. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Models, Genetic. Neoplasm Recurrence, Local. Reproducibility of Results

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(PMID = 17634619.001).

[ISSN] 1064-3745

[Journal-full-title] Methods in molecular biology (Clifton, N.J.)

[ISO-abbreviation] Methods Mol. Biol.

[Language] eng

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

[Publication-country] United States

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

[Number-of-references] 49

   

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

[Title] Early inactivation of p53 tumor suppressor gene cooperating with NF1 loss induces malignant astrocytoma.

Malignant astrocytoma, the most prevalent primary brain tumor, is resistant to all known therapies and frequently harbors mutations that inactivate p53 and activate Ras signaling.

We have generated mouse strains that lack p53 and harbor a conditional allele of the NF1 tumor suppressor that negatively regulates Ras signaling.

The mice develop malignant astrocytomas with complete penetrance.

The majority of tumors display characteristics of glioblastoma multiforme with concomitant alteration of signaling pathways previously described in the human counterparts of this neoplasm.

We find that the sequence of tumor suppressor inactivation influences tumorigenicity and that earliest evidence of tumor formation localizes to regions of the brain that contain a multipotent stem cell population capable of in vivo differentiation into neurons and glia.

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(PMID = 16098465.001).

[ISSN] 1535-6108

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS034296-07; United States / NINDS NIH HHS / NS / NS034296-07; United States / NCI NIH HHS / CA / P20 CA086354; United States / NINDS NIH HHS / NS / R01 NS034296-06; United States / NINDS NIH HHS / NS / R01 NS034296; United States / NINDS NIH HHS / NS / NS034296-06; United States / NCI NIH HHS / CA / P20 CA86354

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

[Publication-country] United States

[Other-IDs] NLM/ NIHMS263629; NLM/ PMC3024718

   

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

[Title] Proliferating cell nuclear antigen, p53 and micro vessel density: Grade II vs. Grade III astrocytoma.

Histological classification and grading are prime procedures in the management of patients with astrocytoma, providing vital data for therapeutic decision making and prognostication.

However, it has limitations in assessing biological tumor behavior.

This study was carried out to compare proliferative indices using proliferating cell nuclear antigen (PCNA), extent of p53 expression and micro vessel morphometric parameters in patients with low grade and anaplastic astrocytoma.

Twenty-five patients, each of grade II and grade III astrocytoma were evaluated using monoclonal antibodies to PCNA, p53 protein and factor VIII related antigen.

Patients with grade III astrocytoma had higher PCNA and p53 labeling indices as compared with grade II astrocytoma (29.14 plus/minus 9.87% vs. 16.84 plus/minus 6.57%, p 0.001; 18.18 plus/minus 6.14% vs. 6.14 plus/minus 7.23%, p 0.001, respectively).

Micro vessel percentage area of patients with grade III astrocytoma was also (4.26 plus/minus 3.70 vs. 1.05 plus/minus 0.56, p 0.001), higher along with other micro vessel morphometric parameters.

Discordance between histology and one or more IHC parameters was seen in 5/25 (20%) of patients with grade III astrocytoma and 9/25 (36%) of patients with grade II disease.

Increased proliferative fraction, genetic alterations and neovascularization mark biological aggressiveness in astrocytoma.

[MeSH-major] Astrocytoma / diagnosis. Astrocytoma / pathology. Neovascularization, Pathologic. Proliferating Cell Nuclear Antigen / analysis. Tumor Suppressor Protein p53 / analysis

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(PMID = 20090216.001).

[ISSN] 0974-5130

[Journal-full-title] Indian journal of pathology & microbiology

[ISO-abbreviation] Indian J Pathol Microbiol

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Proliferating Cell Nuclear Antigen; 0 / Tumor Suppressor Protein p53

   

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

[Title] Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines.

In malignant astrocytoma cells, it was reported that NF-kappaB was activated aberrantly and promoted their proliferation.

Thus, inhibition of NF-kappaB activity is considered to be a promising therapeutic strategy for malignant astrocytoma.

In this study, we investigated inhibitory effects of curcumin on NF-kappaB activity and cellular proliferation, and induction of apoptosis by curcumin in human malignant astrocytoma cell lines.

Alteration of NF-kappaB activity in NP-2 human malignant astrocytoma cell line after treatment with curcumin was examined using electrophoretic mobility shift assay.

Alterations of DNA synthesis and cellular growth in five human malignant astrocytoma cell lines after treatment with curcumin were examined using [(3)H]thymidine incorporation assay and the trypan blue dye exclusion method, respectively.

Induction of apoptosis by curcumin in NP-2 and NP-3 human malignant astrocytoma cell lines was examined by DNA-fragmentation analysis and morphological observation.

The DNA synthesis and the cellular growth were inhibited by curcumin in dose-dependent manner in all the five malignant astrocytoma cell lines.

These results indicate that curcumin inhibits the cellular proliferation and induces apoptosis in human malignant astrocytoma cell lines.

[MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Astrocytoma / drug therapy. Cell Proliferation / drug effects. Curcumin / therapeutic use. NF-kappa B / drug effects

[MeSH-minor] Electrophoretic Mobility Shift Assay. Humans. Thymidine / metabolism. Tumor Cells, Cultured

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(PMID = 16193380.001).

[ISSN] 0167-594X

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

[ISO-abbreviation] J. Neurooncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; IT942ZTH98 / Curcumin; VC2W18DGKR / Thymidine