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Items 1 to 18 of about 18
1. Shuangshoti S, Rushing EJ, Mena H, Olsen C, Sandberg GD: Supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients. Cancer; 2005 Jun 15;103(12):2598-605
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  • [Title] Supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients.
  • BACKGROUND: Published research on the clinicopathologic features of extraventricular ependymal neoplasms of the cerebral hemispheres has been scant.
  • The left cerebral hemisphere was 1.5 times more commonly involved.
  • Ki-67 proliferation index paralleled tumor grade.
  • Flow cytometry performed in 27 tumors revealed diploidy in 20 cases and aneuploidy in 4 cases (3 anaplastic and 1 classic ependymomas), with S-phase fraction ranging from 0.2-9.7.
  • Eleven subjects were additionally treated with radiotherapy, and 3 with chemotherapy.
  • CONCLUSIONS: The results of the current study suggest that there is no significant relation between histopathology, Ki-67 proliferation index, p53 immunolabeling, tumor ploidy, and biologic behavior.
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Flow Cytometry. Humans. Infant. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Prognosis. S Phase. Tumor Suppressor Protein p53

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  • [Copyright] Published 2005 by the American Cancer Society.
  • (PMID = 15861411.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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2. Rahman R, Osteso-Ibanez T, Hirst RA, Levesley J, Kilday JP, Quinn S, Peet A, O'Callaghan C, Coyle B, Grundy RG: Histone deacetylase inhibition attenuates cell growth with associated telomerase inhibition in high-grade childhood brain tumor cells. Mol Cancer Ther; 2010 Sep;9(9):2568-81
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  • [Title] Histone deacetylase inhibition attenuates cell growth with associated telomerase inhibition in high-grade childhood brain tumor cells.
  • Aberrant epigenetic regulation of gene expression contributes to tumor initiation and progression.
  • The present study investigates the anticancer effects of the HDACi trichostatin A in high-grade childhood brain tumor cells.
  • In contrast, no cytotoxicity was observed in primary ependymal cells with respect to cilia function.
  • Thus, inhibition of histone deacetylases leads to antiproliferative and proapoptotic effects in childhood brain tumor cells, likely to involve altered chromatin regulation at the human telomerase reverse transcriptase promoter.
  • [MeSH-major] Brain Neoplasms / drug therapy. Histone Deacetylase Inhibitors / pharmacology. Histone Deacetylases / metabolism. Telomerase / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Growth Processes / drug effects. Child. Epigenesis, Genetic. Gene Expression / drug effects. Humans. Hydroxamic Acids / pharmacology. Rats. Rats, Wistar. Tumor Cells, Cultured

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  • (PMID = 20643785.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 3X2S926L3Z / trichostatin A; EC 2.7.7.49 / Telomerase; EC 3.5.1.98 / Histone Deacetylases
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3. Heimberger AB, Suki D, Yang D, Shi W, Aldape K: The natural history of EGFR and EGFRvIII in glioblastoma patients. J Transl Med; 2005 Oct 19;3:38
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  • METHODS: Biopsed or partially/subtotally resected GBM patients (N = 54) underwent adjuvant conformal radiation and chemotherapy.
  • RESULTS: In our study of GBM patients with less than GTR, 42.6% (n = 23) failed to express EGFR, 25.9% (n = 14) had over expression of the wild-type EGFR only and 31.5 % (n = 17) expressed the EGFRvIII.
  • Patients within groups expressing the EGFR, EGFRvIII, or lacking EGFR expression did not differ in age, Karnofsky Performance Scale (KPS) score, extent of tumor resection.
  • They all had received postoperative radiation and chemotherapy.
  • The median overall survival times for patients with tumors having no EGFR expression, over expressed EGFR only, or EGFRvIII were 12.3 (95% CI, 8.04-16.56), 11.03 (95% CI, 10.18-11.89) and 14.07 (95% CI, 7.39-20.74) months, respectively, log rank test p > 0.05).
  • Patients with tumors that over expressed the EGFR and EGFRvIII were more likely to present with ependymal spread, 21.4% and 35.3% respectively, compared to those patients whose GBM failed to express either marker, 13.0%, although the difference was not statistically significant.
  • CONCLUSION: The over expressed wild-type EGFR and EGFRvIII are not independent predictors of median overall survival in the cohort of patients who did not undergo extensive tumor resection.

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  • (PMID = 16236164.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1298339
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4. Agaoglu FY, Ayan I, Dizdar Y, Kebudi R, Gorgun O, Darendeliler E: Ependymal tumors in childhood. Pediatr Blood Cancer; 2005 Sep;45(3):298-303
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  • [Title] Ependymal tumors in childhood.
  • BACKGROUND: Ependymal tumors are classified as ependymoma (benign or low grade) versus anaplastic ependymoma (malignant or high grade).
  • Ependymomas represent 5-10% of intracranial neoplasm in children.
  • In this study, demographic data and the treatment results of pediatric patients with ependymal tumors, treated in a single institute, is reported.
  • PATIENTS AND METHODS: Between 1989 and 2001, 40 (22 M/18 F) previously untreated patients with a median age of 5.5 years (3 months-15 years), of histologically proven ependymal tumors (except ependymoblastomas) were referred to the Institute of Oncology, University of Istanbul.
  • Total tumor resection was performed in 20 patients (50%), subtotal in 18 patients (45%), and biopsy only in 2 patients (5%).
  • Postoperative treatment consisted of regional (8 patients) or craniospinal (CSI) (9 patients) radiotherapy (RT) in patients with ependymoma; regional (7 patients) or CSI RT (14 patients) with chemotherapy (ChT) in patients with anaplastic ependymoma; ChT only (1 patient) in patients less than 3 years of age.
  • The standard technique for posterior fossa irradiation was parallel-opposed lateral fields and total dose was 45-54 Gy.
  • Median time for progression or relapse was 24.3 months and there were 19 patients (43.6%) with relapse or progression.
  • CONCLUSIONS: The majority of complete responders were patients who had total tumor removal.
  • Treatment failure occurred mainly within the first 2 years, and outcome was dismal for patients who relapsed or had progressive disease.

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15770637.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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5. Brisson C, Lelong-Rebel I, Mottolèse C, Jouvet A, Fèvre-Montange M, Saint Pierre G, Rebel G, Belin MF: Establishment of human tumoral ependymal cell lines and coculture with tubular-like human endothelial cells. Int J Oncol; 2002 Oct;21(4):775-85
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  • [Title] Establishment of human tumoral ependymal cell lines and coculture with tubular-like human endothelial cells.
  • Treatment of ependymomas relies on surgery combined with radio- or chemotherapy, but the efficiency of chemotherapy is limited, probably because of their multidrug resistance (MDR) phenotype.
  • Progress in the therapy of these neoplasms is dramatically limited by the absence of cell line models.
  • Histological, immunological, and ultrastructural studies showed that the morphological features (microvilli, cilia, and caveolae) of these cultured cells were similar to those of the tumor in vivo.
  • The expression of P-gp, EGF-R, and caveolin-1 by these tumoral ependymocytes could be useful in studies on new drugs.
  • This coculture model might represent a new powerful tool to study new therapeutic delivery strategies in tumoral cells.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Culture Techniques / methods. Endothelium, Vascular / cytology. Ependymoma / pathology. Tumor Cells, Cultured
  • [MeSH-minor] Adolescent. Adult. Aged. Cells, Cultured. Child. Child, Preschool. Coculture Techniques. Collagen / pharmacology. Drug Combinations. Female. Humans. Immunohistochemistry. Infant. Laminin / pharmacology. Male. Microscopy, Electron. Microscopy, Fluorescence. Middle Aged. P-Glycoprotein / metabolism. Proteoglycans / pharmacology. Time Factors. Umbilical Veins / cytology

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  • (PMID = 12239616.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / P-Glycoprotein; 0 / Proteoglycans; 119978-18-6 / matrigel; 9007-34-5 / Collagen
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6. Moynihan TJ: Ependymal tumors. Curr Treat Options Oncol; 2003 Dec;4(6):517-23
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  • [Title] Ependymal tumors.
  • Ependymal tumors are rare malignancies that arise from the cells that line the ventricles and central canal of the spinal cord.
  • Although they are more common in children, adults may also be effected by ependymal tumors.
  • Prognosis is dependent on tumor location, histology, especially for myxopapillary tumors that tend to occur in the lumbar spine, extent of surgical resection, and stage of disease.
  • Standard therapy consists of complete resection when feasible.
  • Patients with known residual disease may benefit from local radiation therapy, but the extent of radiation field and total dose are controversial.
  • Even in patients treated with involved field radiotherapy, most relapses occur within the original tumor bed, thus local control remains the biggest obstacle to effective therapy.
  • Chemotherapy has little impact against this tumor and has no role in the adjuvant setting, outside of a well designed clinical trial, with the possible exception of children younger than 5 years in an effort to delay radiation.
  • A minority of patients may respond to one of several chemotherapy regimens at the time of recurrence, but the impact of this therapy is limited.
  • Newer treatment strategies are needed.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Ependymoma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Emergency Medical Services. Humans. Life Style. Neoplasm Staging. Neurosurgical Procedures. Radiotherapy

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  • (PMID = 14585232.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 28
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7. Mendrzyk F, Korshunov A, Benner A, Toedt G, Pfister S, Radlwimmer B, Lichter P: Identification of gains on 1q and epidermal growth factor receptor overexpression as independent prognostic markers in intracranial ependymoma. Clin Cancer Res; 2006 Apr 1;12(7 Pt 1):2070-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our aim was to screen for novel genomic imbalances and prognostic markers in ependymal tumors.
  • Novel recurrent genomic gains were validated by fluorescence in situ hybridization using a tissue microarray consisting of 170 intracranial ependymomas.
  • Candidate genes were also tested for mRNA expression by quantitative real-time PCR, and protein expression was determined by immunohistochemistry on the tissue microarray.
  • Gain of 1q21.1-32.1 was associated with tumor recurrence in intracranial ependymomas (P < 0.001).
  • Moreover, EGFR might serve as therapeutic target for more specific chemotherapy applications.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 1 / genetics. Ependymoma / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Receptor, Epidermal Growth Factor / genetics

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  • (PMID = 16609018.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 9007-49-2 / DNA; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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8. Hwang HJ, Sohn JH, Han SJ, Kim TS, Lee YS, Kim JH: Multi-disciplinary treatment of a rare pelvic cavity ependymoma. Yonsei Med J; 2007 Aug 31;48(4):719-22
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  • [Title] Multi-disciplinary treatment of a rare pelvic cavity ependymoma.
  • Histologically, the tumor was characterized by compact columnar neoplastic cells divided by fibrovascular septae.
  • The neoplastic cells formed true ependymal rosettes and perivascular pseudorosettes.
  • The tumor was thus diagnosed as an ependymoma arising from the pelvic cavity.
  • The patient was treated with a debulking operation and chemotherapy based upon the in vitro chemosensitivity test results.
  • This is a rare case of extraneural ependymoma for which an in vitro chemosensitivity test was critical in determining the multidisciplinary approach for treatment.

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  • (PMID = 17722249.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2628065
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9. De Tommasi A, De Tommasi C, Occhiogrosso G, Cimmino A, Parisi M, Sanguedolce F, Ciappetta P: Primary intramedullary primitive neuroectodermal tumor (PNET)--case report and review of the literature. Eur J Neurol; 2006 Mar;13(3):240-3
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  • [Title] Primary intramedullary primitive neuroectodermal tumor (PNET)--case report and review of the literature.
  • Following the WHO 2000 classification, PNETs have been considered embryonal tumors composed of undifferentiated neuroepithelial cells with a capacity of differentiation into different cellular lines, such as astrocytic, ependymal, melanotic and muscular.
  • The optimal treatment for these malignant tumors is not yet clear, although, over the years, radiotherapy has been considered the best treatment for spinal PNETs.
  • The described case is that of a 38-year-old man with a primary intra-extramedullary PNET, treated by laminectomy, open biopsy and chemotherapy.
  • The patient, 18 months after the onset of his symptomatology, died without cerebral tumor involvement.

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  • (PMID = 16618339.001).
  • [ISSN] 1351-5101
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 25
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10. Behling E, Birbe R, Veznadaroglu E, Andrews DW, Flanders A, Kenyon LC: Gliosarcoma arising from an anaplastic ependymoma: a case report of a rare entity. Hum Pathol; 2004 Apr;35(4):512-6
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  • We report the first case of a gliosarcoma arising from an anaplastic ependymoma and the second case of gliosarcoma arising from any type of ependymal neoplasm.
  • The tumor recurred despite multiple cycles of postoperative radiation and chemotherapy.
  • After the fourth recurrence, the tumor displayed a biphasic pattern of differentiation.
  • The first pattern was similar to the original anaplastic ependymoma, whereas there was a second new sarcomatous pattern resembling fibrosarcoma that was admixed with and overrunning the ependymal component.
  • The spectrum of gliosarcoma is therefore expanded to include not only astrocytic and oligodendroglial components but ependymal components as well.
  • [MeSH-minor] Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Middle Aged. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology


11. Craver RD, Lipscomb JT, Suskind D, Velez MC: Malignant teratoma of the thyroid with primitive neuroepithelial and mesenchymal sarcomatous components. Ann Diagn Pathol; 2001 Oct;5(5):285-92
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  • A predominant neuroepithelial pattern had ependymal rosettes and mitoses, stained for neuron-specific enolase, neuron-specific B tubulin, and synaptophysin.
  • Loose myxoid tissue resembled primitive cartilage.
  • The tumor from the left and right thyroid lobes exhibited trisomy 8, the right also had hyperdiploid cell lines.
  • She was treated with aggressive combination chemotherapy and radiation.
  • Malignant thyroid teratoma is an aggressive tumor, with 15 of 27 reported patients dying 2 weeks to 3 years after diagnosis.
  • Survivors have been treated with total or subtotal resection, combination chemotherapy with agents effective in the treatment of germ cell tumors as well as sarcomas, and radiation for either recurrent or residual disease.
  • The heterologous elements, lacking MIC2 staining and t(11;22), support the diagnosis of malignant teratoma rather than a neuroepithelial tumor.
  • Therapy should be tailored to the management of all transformed histologies.
  • [MeSH-minor] Adolescent. Aneuploidy. Antineoplastic Combined Chemotherapy Protocols. Biomarkers, Tumor / analysis. Biopsy, Needle. Chemotherapy, Adjuvant. DNA, Neoplasm / analysis. Diagnosis, Differential. Female. Humans. Image Cytometry. Prognosis. Radiotherapy, Adjuvant. Treatment Outcome

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  • [Copyright] Copyright 2001 by W.B. Saunders Company
  • (PMID = 11598856.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
  • [Number-of-references] 34
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12. Nakasu S, Fukami T, Baba K, Matsuda M: Immunohistochemical study for O6-methylguanine-DNA methyltransferase in the non-neoplastic and neoplastic components of gliomas. J Neurooncol; 2004 Dec;70(3):333-40
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although the expression O6-methylguanine-DNA methyltransferase (MGMT) is an important hallmark for decision of nitrosourea chemotherapy for glioma patients, no immunohistochemical method for analysis of MGMT has been standardized yet.
  • Gliomas usually contain non-neoplastic cells even deep in the tumor.
  • High grade gliomas were also studied to find a cut-off point for treatment decision.
  • MGMT immunohistochemistry in the normal brain or brain with non-neoplastic disease revealed nuclear staining in some endothelial cells, inflammatory cells, ependymal cells, astrocytes and oligodendroglias.
  • Although, the endothelial cells were easily distinguished from the neoplastic cells, other cells were often mistaken for tumor cells.
  • In 51 high grade glioma patients, who received both radiotherapy and chemotherapy with nimustine (ACNU), the median overall survival of the MGMT-negative group (23 months) was significantly longer than that of the MGMT-positive group (14 months) (P < 0.009).
  • In the MGMT-positive group, addition of platinum-based chemotherapy did not improve the survival.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain / metabolism. Brain Neoplasms / metabolism. Glioma / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Nimustine / therapeutic use. Prognosis. Radiotherapy. Survival Analysis

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  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
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13. Miyake Y, Okoshi Y, Machino T, Chiba S: Treatment of central nervous system lymphoma in rats with intraventricular rituximab and serum. Int J Hematol; 2010 Oct;92(3):474-80
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of central nervous system lymphoma in rats with intraventricular rituximab and serum.
  • Intraventricularly administered RTX was localized specifically at the lymphoma lesions, indicating that RTX penetrated the ependymal layer of the lateral ventricle to reach the tumor lesion, where it specifically bound to the lymphoma cells.
  • Intraventricular administration of RTX and serum in a rat/human CNS lymphoma model might be a potential novel treatment for CNS lymphomas of B cell origin.
  • [MeSH-major] Antibodies, Monoclonal, Murine-Derived / administration & dosage. Antibodies, Monoclonal, Murine-Derived / therapeutic use. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Central Nervous System Neoplasms / drug therapy. Lymphoma, B-Cell / drug therapy. Serum / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Rats. Rats, Nude. Rituximab

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  • (PMID = 20820968.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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14. Takano T, Akahira J, Moriya T, Murakami T, Tanaka M, Goto M, Niikura H, Ito K, Mikami Y, Okamura K, Yaegashi N: Primary ependymoma of the ovary: a case report and literature review. Int J Gynecol Cancer; 2005 Nov-Dec;15(6):1138-41
MedlinePlus Health Information. consumer health - Ovarian Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ependymoma is a glioma with differentiation toward ependymal cells that usually arises in the central nervous system.
  • Ovarian ependymoma is extremely rare, and the treatment strategies for this disease have not been established.
  • Microscopic examination revealed a highly cellular tumor composed of small cells with hyperchromatic, round-to-oval nuclei and scanty cytoplasm.
  • Perivascular pseudorosettes, ependymal rosettes, and extensive necrosis were observed.
  • Postoperatively, she received adjuvant chemotherapy and underwent secondary cytoreductive surgery that preserved the uterus and right ovary.
  • Her menstrual cycle has resumed, and she is alive without evidence of disease 16 months after the start of treatment.
  • Administration of etoposide-based chemotherapy along with cytoreductive surgery is a potential standard treatment for advanced ovarian ependymoma.
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Female. Gynecologic Surgical Procedures. Humans. Reoperation

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  • (PMID = 16343197.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 16
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15. Takeuchi H, Kubota T, Sato K, Yao Y, Kitai R, Arishima H: Atypical neuronal-glial tumors of cerebral hemispheres in adults with PNET-like component: clinicopathological features of 5 cases. Clin Neuropathol; 2003 Mar-Apr;22(2):47-56
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated 5 cases with brain tumors composed ofneuronal and astrocytic differentiated tumor cells occurring in the cerebral hemispheres of adults.
  • All tumors were surgically resected following radiotherapy and chemotherapy.
  • Histologically, tumor cells were mainly composed of round or oval nucleate cells with scant cytoplasm and compactly arranged with neurocytic features.
  • Immunohistochemically, some tumor cells were immunoreactive for synaptophysin, neurofilament, beta-tubulin, chromogranin A, GFAP and vimentin.
  • Ultrastructurally, tumor cells were variably differentiated as follows: undifferentiated cells having prominent nuclei and scanty cytoplasm with inconspicuous organelles; neuronal cells consisting of neurosecretory granules or vesicles and abortive synapses, and astrocytic cells with cytoplasmic intermediate filaments.
  • However, there was little oligodendrocytic or ependymal differentiation in these tumors.

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  • (PMID = 12670050.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Glial Fibrillary Acidic Protein; 0 / Tubulin; 0 / Vimentin; 9007-49-2 / DNA
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16. Maksoud YA, Hahn YS, Engelhard HH: Intracranial ependymoma. Neurosurg Focus; 2002 Sep 15;13(3):e4
MedlinePlus Health Information. consumer health - Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this paper, the authors compiled a review of the pathological features, imaging characteristics, and treatment strategies related to this brain tumor.
  • The bibliographies of papers obtained were also checked for articles and chapters that could provide additional understanding of this tumor.
  • Most authors recommend resecting as much of the tumor as is safely possible.
  • Microscopically, ependymal tumors show both epithelial and glial features.
  • Because ependymomas often recur despite surgical intervention, radiotherapy and/or radiosurgery may also play an important role in their treatment.
  • The use of chemotherapy in the treatment of these tumors, especially in the very young, is still being studied.

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  • (PMID = 15844876.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 31
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17. Schrot RJ, Ma JH, Greco CM, Arias AD, Angelastro JM: Organotypic distribution of stem cell markers in formalin-fixed brain harboring glioblastoma multiforme. J Neurooncol; 2007 Nov;85(2):149-57
The Lens. Cited by Patents in .

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  • A 41-year-old male with a right posterior temporal glioblastoma had undergone surgery, radiation, and chemotherapy.
  • After formalin fixation, sectioning, and mapping of tumor location in the gross specimen, histologic specimens were prepared from tumor-bearing and grossly normal hemispheres.
  • Both markers co-localized to the ependymal and subependymal zones on the side of the tumor, but not in the normal hemisphere or more rostrally in the affected hemisphere.
  • The robust staining for ATF5 and CD133 in histologically normal ventricular zone suggests that an increase in periventricular stem cell activity occurred in this patient on the side of the tumor, either as a localized response to brain injury or as an integral component of oncogenesis and tumor recurrence.
  • [MeSH-minor] AC133 Antigen. Adult. Biomarkers / metabolism. Cerebral Ventricles / metabolism. Fatal Outcome. Humans. Immunohistochemistry. Male. Tissue Distribution

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  • [CommentIn] J Neurooncol. 2008 Sep;89(2):247-8; author reply 249 [18568293.001]
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  • (PMID = 17516028.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 Antigen; 0 / ATF5 protein, human; 0 / Activating Transcription Factors; 0 / Antigens, CD; 0 / Biomarkers; 0 / Glycoproteins; 0 / PROM1 protein, human; 0 / Peptides
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18. Lou E: Oncolytic viral therapy and immunotherapy of malignant brain tumors: two potential new approaches of translational research. Ann Med; 2004;36(1):2-8
MedlinePlus Health Information. consumer health - Genes and Gene Therapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncolytic viral therapy and immunotherapy of malignant brain tumors: two potential new approaches of translational research.
  • Approximately 60% of all brain tumors are gliomas, which are derived from interstitial tissue of the brain, such as astrocytic or ependymal tissue, or oligodendrocytes.
  • The traditional protocols for treatment of malignant gliomas include diagnostic surgery, followed by regimens of radio- and chemotherapies.
  • In the case of chemotherapy, the treatment protocols have remained nearly unchanged for over 30 years despite high mortality rates, and with little to no improvement in outcome.
  • New advances in the fields of molecular biology and immunology have resulted in new possibilities for treating malignant gliomas by targeting cellular and molecular mechanisms of tumor cells, and stand in contrast to traditional forms of treatment.
  • In the field of gene therapy, the possibility of using oncolytic viruses, such as HSV-1, for glioma therapy--specifically, of high grade astrocytomas--is being explored, and trials have begun using a replication-selective mutant strain known as G207.
  • The two examples mentioned here are discussed in this review and cited as possible improvements in the treatment of high grade astrocytomas.
  • [MeSH-major] Brain Neoplasms / therapy. Genetic Therapy. Glioma / therapy. Immunotherapy
  • [MeSH-minor] Genetic Vectors / therapeutic use. Humans. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / immunology. Transforming Growth Factor beta2. Viruses / genetics. Viruses / immunology

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  • (PMID = 15000342.001).
  • [ISSN] 0785-3890
  • [Journal-full-title] Annals of medicine
  • [ISO-abbreviation] Ann. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / TGFB2 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta2
  • [Number-of-references] 35
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