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1. Brandes AA, Cavallo G, Reni M, Tosoni A, Nicolardi L, Scopece L, Franceschi E, Sotti G, Talacchi A, Turazzi S, Ermani M: A multicenter retrospective study of chemotherapy for recurrent intracranial ependymal tumors in adults by the Gruppo Italiano Cooperativo di Neuro-Oncologia. Cancer; 2005 Jul 1;104(1):143-8
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  • [Title] A multicenter retrospective study of chemotherapy for recurrent intracranial ependymal tumors in adults by the Gruppo Italiano Cooperativo di Neuro-Oncologia.
  • BACKGROUND: No data on the role of chemotherapy in recurrent ependymal tumors are available in adults.
  • The aim of the current study was to investigate outcomes after salvage chemotherapy in this setting.
  • METHODS: A retrospective review was made of the charts of 28 adults (> or = 18 years) with progressive or recurrent ependymal tumors after surgery and radiotherapy, who received chemotherapy between 1993 and 2003 in 3 institutions of the Gruppo Italiano Cooperativo di Neuro-Oncologia network.
  • RESULTS: Thirteen patients (46.3%) received cisplatin-based chemotherapy (Group A) and 15 (53.7%) received regimens without cisplatin (Group B).
  • Platinum-based chemotherapy yielded 2 complete responses (CR) (15.4%) and 2 (15.4%) partial responses (PR), whereas 7 patients (53.8%) remained stable (SD).
  • The overall median time to progression was 9.9 months (95% confidence interval [95% CI], 7.5-21.7 months), 9.9 months (5.2-not reached) for Group A and 10.9 months (95% CI, 7.17-23.9 months) for Group B.
  • CONCLUSIONS: Cisplatin-based chemotherapy achieved a higher response rate, but did not prolong disease progression-free survival or OS.
  • More active regimens for the salvage treatment of ependymal tumors have yet to be found.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Ependymoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Disease-Free Survival. Female. Humans. Italy. Male. Middle Aged. Neoplasm Recurrence, Local. Retrospective Studies. Salvage Therapy

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  • (PMID = 15912507.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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2. 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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  • [Title] Identification of gains on 1q and epidermal growth factor receptor overexpression as independent prognostic markers in intracranial ependymoma.
  • Our aim was to screen for novel genomic imbalances and prognostic markers in ependymal tumors.
  • EXPERIMENTAL DESIGN: We analyzed 68 sporadic tumors by matrix-based comparative genomic hybridization using DNA microarrays containing >6,400 genomic DNA fragments.
  • 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.
  • RESULTS: Chromosomal gain of 1q correlated with pediatric patients (P = 0.004), intracranial ependymomas (P = 0.05), and tumors of grade III (P = 0.002).
  • Gain of 1q21.1-32.1 was associated with tumor recurrence in intracranial ependymomas (P < 0.001).
  • EGFR protein status subdivides intracranial grade II ependymomas into two different risk groups (P = 0.03) as shown by multivariate analysis.
  • CONCLUSIONS: Thus, the states of 1q25 and EGFR represent independent prognostic markers for intracranial ependymomas to identify patient subgroups with different risk profiles in further clinical investigations.
  • 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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3. Maruyama K, Morita A, Shibahara J, Nakazato Y, Kirino T: Multifocal pilocytic astrocytomas with ependymal differentiation in the bilateral medial temporal lobes: case report. Neurol Med Chir (Tokyo); 2005 Aug;45(8):411-4
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  • [Title] Multifocal pilocytic astrocytomas with ependymal differentiation in the bilateral medial temporal lobes: case report.
  • The histological diagnosis was pilocytic astrocytoma with ependymal differentiation and a MIB-1 staining index of up to 8.0%.
  • Adjuvant chemotherapy consisting of carboplatin and vincristine was given followed by radiotherapy.
  • Neuroimaging showed that the bilateral tumors had disappeared and showed no recurrence for 29 months after the diagnosis.
  • Pilocytic astrocytoma usually presents as a solitary mass in the cerebellum or optic pathway with low proliferative activity, but should be included in the differential diagnosis of multifocal tumors arising in the bilateral temporal lobes.
  • Ependymal differentiation with extremely high proliferative activity might be related to this unusual clinical presentation.
  • Intensive treatment is recommended for patients with such specific neuroimaging and histological features.
  • [MeSH-major] Astrocytoma / pathology. Brain Neoplasms / pathology. Temporal Lobe / pathology
  • [MeSH-minor] Antibodies, Antinuclear. Antibodies, Monoclonal. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Proliferation. Child. Diagnosis, Differential. Ependyma / pathology. Hemianopsia / etiology. Hemianopsia / pathology. Hemianopsia / physiopathology. Humans. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Neurosurgical Procedures. Paresis / etiology. Paresis / pathology. Paresis / physiopathology. Radiotherapy. Seizures / etiology. Seizures / pathology. Seizures / physiopathology. Treatment Outcome

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  • (PMID = 16127260.001).
  • [ISSN] 0470-8105
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / MIB-1 antibody
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4. 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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  • BACKGROUND: The epidermal growth factor receptor (EGFR) is over expressed in approximately 50-60% of glioblastoma (GBM) tumors, and the most common EGFR mutant, EGFRvIII, is expressed in 24-67% of cases.
  • 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.
  • There was no significant difference in multifocal disease or gliomatosis cerebri among EGFR expression groups.
  • 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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5. Maksoud YA, Hahn YS, Engelhard HH: Intracranial ependymoma. Neurosurg Focus; 2002 Sep 15;13(3):e4
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  • [Title] Intracranial ependymoma.
  • OBJECT: An intracranial ependymoma is a relatively rare but very interesting variety of glioma.
  • In this paper, the authors compiled a review of the pathological features, imaging characteristics, and treatment strategies related to this brain tumor.
  • METHODS: A Medline search was conducted using the term "ependymoma."
  • The bibliographies of papers obtained were also checked for articles and chapters that could provide additional understanding of this tumor.
  • CONCLUSIONS: The posterior fossa is the most frequent site for an intracranial ependymoma.
  • 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.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / surgery. Ependymoma / pathology. Ependymoma / surgery

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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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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. 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.
  • The median age at diagnosis is 6 years in our patient group; younger children (less than 3 years old) have less favorable outcome.
  • [MeSH-major] Brain Neoplasms. Ependymoma
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Multivariate Analysis. Risk Factors. Survival Rate. Turkey / epidemiology

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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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8. 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.
  • Tumors expressed glial fibrillary acidic protein (87%), S-100 protein (77%), cytokeratin (43%), and epithelial membrane antigen (17%).
  • 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-major] Brain Neoplasms / pathology. Cerebral Ventricle Neoplasms / pathology. Ependymoma / pathology. Glioma, Subependymal / pathology. Supratentorial Neoplasms / pathology
  • [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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9. Dallorso S, Dini G, Ladenstein R, Cama A, Milanaccio C, Barra S, Cappelli B, Garrè ML, EBMT-PDWP: Evolving role of myeloablative chemotherapy in the treatment of childhood brain tumours. Bone Marrow Transplant; 2005 Mar;35 Suppl 1:S31-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evolving role of myeloablative chemotherapy in the treatment of childhood brain tumours.
  • Primary brain tumours, a heterogeneous group of cancer that constitute the second most common cancer in childhood, were historically treated with neurosurgical resection and radiation therapy.
  • Chemotherapy has proven to be beneficial for some histological types, which has since led to exploration of the role of high-dose chemotherapy and haematopoietic stem cell rescue.
  • Children <3 years at diagnosis carry worse prognosis.
  • Rare cancers such as ependymoblastoma, atypical teratoid rhabdoid tumour and choroid plexus carcinoma have a dismal prognosis regardless of the above-mentioned indicators.
  • The use of myeloablative therapy (MAT) has been investigated to improve the rate of long-term DFS, as well as to reduce and delay in the youngest children the use of the craniospinal irradiation associated with unacceptable late effects.
  • Ependymoma and brain stem tumours, for which the available data discourage the use of MAT, are excluded.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebellar Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents. Child. Child, Preschool. Female. Humans. Male. Prognosis. Treatment Outcome

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  • (PMID = 15812527.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 24
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10. 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
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  • [Title] Primary ependymoma of the ovary: a case report and literature review.
  • 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.
  • This is the first report of a patient with advanced ovarian ependymoma who received fertility-sparing surgery and is now alive without disease.
  • 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.
  • After thorough pathologic examination, she was diagnosed as having stage IIIC ovarian ependymoma.
  • 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.
  • Although rare, primary ovarian ependymoma must be kept in mind in the differential diagnosis of ovarian tumors, especially in young women.
  • Administration of etoposide-based chemotherapy along with cytoreductive surgery is a potential standard treatment for advanced ovarian ependymoma.
  • [MeSH-major] Ependymoma / pathology. Ovarian Neoplasms / pathology
  • [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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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.
  • Presently there is no residual disease 16 months after diagnosis.
  • 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-major] Neuroectodermal Tumors, Primitive / diagnosis. Sarcoma / diagnosis. Teratoma / diagnosis. Thyroid Neoplasms / diagnosis
  • [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. 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
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  • [Title] Atypical neuronal-glial tumors of cerebral hemispheres in adults with PNET-like component: clinicopathological features of 5 cases.
  • We investigated 5 cases with brain tumors composed ofneuronal and astrocytic differentiated tumor cells occurring in the cerebral hemispheres of adults.
  • Radiologically, contrast enhancement was demonstrated in these tumors.
  • 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.
  • These tumors were characterized as neuronal and astrocytic differentiated tumors with primitive PNET-like component.
  • However, there was little oligodendrocytic or ependymal differentiation in these tumors.
  • [MeSH-major] Neuroectodermal Tumors, Primitive / pathology. Supratentorial Neoplasms / pathology. Telencephalon / pathology

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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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13. 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.
  • Spinal primitive neuroectodermal tumors (PNET) are very rare tumors, and intramedullary localization is even less common.
  • 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.
  • [MeSH-major] Brain Neoplasms. Laminectomy / methods. Neuroectodermal Tumors, Primitive

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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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14. Garcia-Barriola V, De Gómez MN, Suárez JA, Lara C, González JE, García-Tamayo J: Ovarian ependymoma. A case report. Pathol Res Pract; 2000;196(8):595-9
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  • [Title] Ovarian ependymoma. A case report.
  • We present the case of a 30-year-old woman who was referred to our institution with an erroneous diagnosis of poorly differentiated carcinoma of the ovary.
  • A second laparotomy revealed a bilateral pure ovarian ependymoma that infiltrated the uterus and presented implants on the omentum.
  • Differential diagnosis included mainly endometrioid and small cell carcinoma of the ovary.
  • Presence of typical ependymal rosettes and positivity to GFAP confirmed the diagnosis of ependymoma.
  • Ovarian ependymomas are rare tumors; only eight cases, to our knowledge, have been reported in the literature.
  • They have a favorable prognosis; patients with advanced stage disease are reported alive and well after treatment with surgery and chemotherapy.
  • [MeSH-major] Ependymoma / pathology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adult. Combined Modality Therapy. Diagnosis, Differential. Diagnostic Errors. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Neoplasm Invasiveness

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  • (PMID = 10982025.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein
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15. Johnston DL, Keene D, Bartels U, Carret AS, Crooks B, Eisenstat D, Fryer C, Lafay-Cousin L, Larouche V, Moghrabi A, Wilson B, Zelcer S, Silva M, Brossard J, Bouffet E: Patterns of enrollment of infants with central nervous system tumours on cooperative group studies: a report from the Canadian Pediatric Brain Tumour Consortium. J Neurooncol; 2010 Sep;99(2):243-9
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  • [Title] Patterns of enrollment of infants with central nervous system tumours on cooperative group studies: a report from the Canadian Pediatric Brain Tumour Consortium.
  • In children under the age of 3, the most common solid tumours are brain tumors.
  • Treatment for many of these patients includes surgery, chemotherapy and rarely radiation therapy.
  • Many clinical trials have been performed in an attempt to establish the best treatment for these patients.
  • Patients enrolled on clinical trials contribute to the establishment of the best therapy.
  • We performed a national survey of all children less than the age of three with brain tumours and examined the contribution these patients made to clinical trials.
  • A data bank was established using data collected from Canadian pediatric oncology centers on children less than age 3 diagnosed with brain tumours between 1990 and 2005.
  • Data were collected on the use of adjunctive treatment after surgery, treatment on a protocol, reasons patients were not registered on a protocol, and reasons for discontinuation of therapy.
  • From the 579 cases in the data bank, 302 (52%) patients were treated with further therapy after surgery.
  • The use of further therapy after surgery was significantly higher in patients with cerebellar and brain stem tumors, patients who were over 1 year of age, patients with ependymal and embryonal tumors, and patients with high grade malignant tumors.
  • Only 62 (21%) patients were enrolled on a protocol for therapy.
  • The therapy was stopped because of completion of the protocol in 50% and because of disease progression in 34%.
  • In Canada, about half of children under the age of 36 months with brain tumors are undergoing therapy following surgery for their malignancy but only a small fraction of them are enrolled on a clinical trial.
  • There needs to be improved availability of clinical trials for these patients so that novel therapies can be evaluated and survival improved.
  • [MeSH-major] Brain Neoplasms / epidemiology. Child Health Services / utilization. Glioma / epidemiology. Patient Participation. Patient Selection
  • [MeSH-minor] Canada / epidemiology. Child, Preschool. Combined Modality Therapy. Female. Humans. Infant. Infant, Newborn. Male. Neoplasm Staging. Survival Rate. Treatment Outcome

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  • [Cites] J Pediatr Hematol Oncol. 2007 Dec;29(12):811-4 [18090927.001]
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  • (PMID = 20135195.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. 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.
  • Studies from a plethora of hematologic and solid tumors support the use of histone deacetylase inhibitors (HDACi) as potent anticancer agents.
  • 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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17. 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
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  • [Title] Oncolytic viral therapy and immunotherapy of malignant brain tumors: two potential new approaches of translational research.
  • Brain tumors arise at a rate of nearly 5/100,000 in the general population, with over 17,000 U.S. residents being diagnosed each year.
  • 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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18. Phan TG, O'Neill BP, Kurtin PJ: Posttransplant primary CNS lymphoma. Neuro Oncol; 2000 10;2(4):229-38
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  • The median duration of symptoms before diagnosis was 36 days (range, 5 to 98 days).
  • At diagnosis, the neurologic examination was focally abnormal in 6 of 8 patients.
  • Compared with the initial computed tomographic study, MRI showed 25 additional brain lesions.
  • Ependymal contact occurred in 5 patients.
  • Diagnostic tissue was obtained by stereotactic biopsy from 6 patients and by open biopsy from 2.
  • Slides available for review (7 patients) showed that the tumors were of CD20-positive lineage and were positive for Epstein-Barr virus, using in situ hybridization.
  • In our series, (1) PT-PCNSL presented nonspecifically and progressed rapidly, (2) stereotactic brain biopsy had significant morbidity, and (3) despite multimodal therapy, survival was poor.
  • [MeSH-major] Brain Neoplasms / etiology. Brain Neoplasms / pathology. Immunosuppressive Agents / adverse effects. Lymphoma, Non-Hodgkin / etiology. Lymphoma, Non-Hodgkin / pathology. Organ Transplantation / adverse effects
  • [MeSH-minor] Adult. Brain / drug effects. Brain / pathology. Brain / physiopathology. Cerebrospinal Fluid / chemistry. Cerebrospinal Fluid / cytology. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed

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  • (PMID = 11265232.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA15083
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
  • [Other-IDs] NLM/ PMC1920594
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