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Добірка наукової літератури з теми "Ependymomas"

Автор: Grafiati
Опубліковано: 22 червня 2024

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Статті в журналах з теми "Ependymomas":

1

Romero, Flávio Ramalho, Marco Antônio Zanini, Luis Gustavo Ducati, Roberto Bezerra Vital, Newton Moreira de Lima Neto, and Roberto Colichio Gabarra. "Purely Cortical Anaplastic Ependymoma." Case Reports in Oncological Medicine 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/541431.

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Ependymomas are glial tumors derived from ependymal cells lining the ventricles and the central canal of the spinal cord. It may occur outside the ventricular structures, representing the extraventicular form, or without any relationship of ventricular system, called ectopic ependymona. Less than fifteen cases of ectopic ependymomas were reported and less than five were anaplastic. We report a rare case of pure cortical ectopic anaplastic ependymoma.
2

Neumann, Julia E., Michael Spohn, Denise Obrecht, Martin Mynarek, Christian Thomas, Martin Hasselblatt, Mario M. Dorostkar, et al. "PATH-16. HISTOPATHOLOGICAL EPENDYMOMA VARIANTS ARE ASSOCIATED WITH DISTINCT CLINICAL PARAMETERS AND DNA METHYLATION PATTERNS." Neuro-Oncology 21, Supplement_6 (November 2019): vi146. http://dx.doi.org/10.1093/neuonc/noz175.612.

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Abstract According to the current WHO classification, ependymal tumors are classified as subependymomas, myxopapillary ependymomas, classic ependymomas, anaplastic ependymomas and RELA-fusion positive ependymoma (RELA-EPN). Among classic ependymomas, the WHO defines rare histological variants, i.e. the clear-cell, papillary, and tanycytic ependymoma. In parallel to this WHO classification scheme, DNA methylation patterns can distinguish nine distinct molecular ependymoma subgroups, some of which tightly overlap with certain histopathological subgroups, e.g. subependyomas or myxopapillary ependymomas. Since very little is known about the molecular background of histological classic ependymoma variants, we analyzed histomorphology, clinical parameters and global DNA methylation patterns of diagnosed tanycytic ependymomas (n=12), clear-cell ependymomas (n=14) and papillary ependymomas (n=19). Surprisingly, up to 42% of these variants did not match to ependymomas using a previously published DNA methylation-based classifier for brain tumors. Among the tumors with a match to one of the nine known ependymoma methylation classes, tanycytic ependymomas were predominantly located in the spine, but showed diverse molecular methylation patterns. Most clear-cell ependymomas showed a common histomorphology, were found supratentorially and fell into the methylation class of RELA-EPN. Papillary ependymomas showed a “papillary”, “trabecular” or “pseudo-papillary” growth pattern. Interestingly, a true papillary growth pattern was strongly associated with the molecular class B of posterior fossa ependymoma (PFB), but tumors displayed DNA methylation sites that were significantly different when compared to PFB ependymomas without papillary growth. Our results show that the diagnosis of classic histological ependymoma variants can be challenging. While clear-cell and papillary ependymomas harbor common molecular features, tanycytic ependymoma may not represent a molecularly distinct subgroup.
3

Dimopoulos, Vassilios G., Kostas N. Fountas, and Joe Sam Robinson. "Familial intracranial ependymomas." Neurosurgical Focus 20, no. 1 (January 2006): 1–5. http://dx.doi.org/10.3171/foc.2006.20.1.9.

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Familial cases of intracranial ependymomas have been well documented in the literature. The authors present two cases from a family in which three members harbored intracranial ependymomas. A 54-year-old man with fourth ventricular ependymoma underwent resection of the tumor followed by radiation therapy. His son presented at age 36 years with a fourth ventricular tanycytic ependymoma and underwent total resection of the ependymoma with postoperative radiation therapy. The father's sister had been treated at another institution for a posterior fossa ependymoma. The association of ependymomas with molecular genetic alterations in chromosome 22 has been previously described. Further investigation of the genetic influences may lead to better therapeutic approaches for this relatively rare clinicopathological entity.
4

Ogino, Shuji, Shigeki Kubo, Fadi W. Abdul-Karim, and Mark L. Cohen. "Comparative Immunohistochemical Study of Insulin-like Growth Factor II and Insulin-like Growth Factor Receptor Type 1 in Pediatric Brain Tumors." Pediatric and Developmental Pathology 4, no. 1 (January 2001): 23–31. http://dx.doi.org/10.1007/s100240010112.

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Insulin-like growth factor (IGF)-II is an important growth factor in development of the central nervous system. The purpose of this study was to evaluate expression of IGF-II and IGF receptor type 1 (IGFR1) in various pediatric brain tumors. Immunohistochemistry for IGF-II and IGFR1 was performed on 15 choroid plexus papillomas (CPPs) including 1 atypical CPP, 2 choroid plexus carcinomas (CPCs), 5 anaplastic ependymomas, 7 nonanaplastic ependymomas (simply referred to as “ependymoma”), 5 medulloblastomas, 1 cerebral neuroblastoma, and 1 atypical teratoid/rhabdoid tumor (ATRT) along with 10 non-neoplastic choroid plexus and 3 non-neoplastic ependymal linings. All non-neoplastic choroid plexus, CPPs, CPCs, anaplastic ependymomas, ATRT, 71% of ependymomas, and 67% of non-neoplastic ependymal linings showed cytoplasmic positivity for IGF-II, whereas all medulloblastomas and the cerebral neuroblastoma were negative for IGF-II. In addition to cytoplasmic positivity for IGFR1, membranous positivity was observed in 73% of CPPs, both CPCs, the ATRT, 22% of non-neoplastic choroid plexus, 80% of anaplastic ependymomas, and 29% of ependymomas, but not in any medulloblastoma, cerebral neuroblastoma, or non-neoplastic ependymal lining. IGF-II and IGFR1 may play roles in the pathogeneses of CPP, CPC, anaplastic ependymoma, ependymoma, and ATRT. Immunohistochemical testing for IGF-II and IGFR1 may be useful in differentiating ATRT, CPC, and anaplastic ependymoma from medulloblastoma and cerebral neuroblastoma.
5

Morris, Katrina A., Shazia K. Afridi, D. Gareth Evans, Anke E. Hensiek, Martin G. McCabe, Mark Kellett, Dorothy Halliday, Pieter M. Pretorius, and Allyson Parry. "The response of spinal cord ependymomas to bevacizumab in patients with neurofibromatosis Type 2." Journal of Neurosurgery: Spine 26, no. 4 (April 2017): 474–82. http://dx.doi.org/10.3171/2016.8.spine16589.

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OBJECTIVE People with neurofibromatosis Type 2 (NF2) have a genetic predisposition to nervous system tumors. NF2-associated schwannomas stabilize or decrease in size in over half of the patients while they are receiving bevacizumab. NF2 patients treated with bevacizumab for rapidly growing schwannoma were retrospectively reviewed with regard to ependymoma prevalence and response to treatment. METHODS The records of 95 NF2 patients receiving bevacizumab were retrospectively reviewed with regard to spinal ependymoma prevalence and behavior. The maximum longitudinal extent (MLE) of the ependymoma and associated intratumoral or juxtatumoral cysts were measured on serial images. Neurological changes and patient function were reviewed and correlated with radiological changes. RESULTS Forty-one of 95 patients were found to have ependymomas (median age 26 years; range 11–53 years). Thirty-two patients with a total of 71 ependymomas had scans appropriate for serial assessment with a mean follow-up of 24 months (range 3–57 months). Ependymomas without cystic components showed minimal change in MLE. Twelve patients had ependymomas with cystic components or syringes. In these patients, reductions in MLE were observed, particularly due to decreases in the cystic components of the ependymoma. Clinical improvement was seen in 7 patients, who all had cystic ependymomas. CONCLUSIONS Bevacizumab treatment in NF2 patients with spinal cord ependymomas results in a decrease in the size of intratumoral and juxtatumoral cysts as well as adjacent-cord syringes and a decrease in cord edema. This may provide clinical benefit in some patients, although the changes do not meet the current criteria for radiological tumor response.
6

DiLuna, Michael L., Gillian H. Levy, Shreya Sood, and Charles C. Duncan. "Primary Myxopapillary Ependymoma of the Medulla." Neurosurgery 66, no. 6 (June 1, 2010): E1208—E1209. http://dx.doi.org/10.1227/01.neu.0000369513.84063.a6.

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Abstract OBJECTIVE Myxopapillary ependymoma is a subclassification of ependymoma that is thought to be nearly exclusive to the conus medullaris or filum terminale. Primary intracerebral or brainstem myxopapillary ependymomas are rare. CLINICAL PRESENTATION An 8-year-old child presented with a 5-month history of nausea and vomiting and a 1-week history of headache. Magnetic resonance imaging revealed a nodular mass in the medulla with an associated cyst extending into the fourth ventricle. INTERVENTION A suboccipital craniotomy was performed, and a gross total resection of the lesion and cyst was achieved. Histological examination confirmed the diagnosis of myxopapillary ependymoma. A discussion of other reported cases of extraspinal myxopapillary ependymomas is presented. CONCLUSION This is the first report of a case of myxopapillary ependymoma, confirmed by histology, in the medulla. Although rare, myxopapillary ependymomas outside of the filum terminale do exist.
7

Maksoud, Yaser A., Yoon S. Hahn, and Herbert H. Engelhard. "Intracranial ependymoma." Neurosurgical Focus 13, no. 3 (September 2002): 1–5. http://dx.doi.org/10.3171/foc.2002.13.3.5.

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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. Malignant ependy-momas and ependymomas of the spinal cord (including myxopapillary ependymomas) were excluded from this review. Conclusions The posterior fossa is the most frequent site for an intracranial ependymoma. Children are frequently affected. Most authors recommend resecting as much of the tumor as is safely possible. Microscopically, ependymal tumors show both epithelial and glial features. Glial fibrillary acidic protein immunohistochemistry, therefore, helps in identifying ependymomas. Because ependymomas often recur despite surgical intervention, radiotherapy and/or radio-surgery 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.
8

Hallacq, Paul, François Labrousse, Nathalie Streichenberger, Dan Lisii, and Georges Fischer. "Bifocal myxopapillary ependymoma of the terminal filum: the end of a spectrum?" Journal of Neurosurgery: Spine 98, no. 3 (April 2003): 288–89. http://dx.doi.org/10.3171/spi.2003.98.3.0288.

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✓ Myxopapillary ependymomas represent the most frequent type of ependymomas found at the conus medullaris—cauda equina-terminal filum level. They are neuroectodermal tumors mainly observed during the fourth decade of life. Pediatric cases have been rarely described at an age range of 10 to 13 years. Myxopapillary ependymomas are typically solitary tumors involving the terminal filum. Simultaneous discovery of two tumors located both on the terminal filum has been reported once. The pathogenesis of this focal ependymoma located at the same embryological level, on the terminal filum, is uncertain; it may represent one end of a spectrum, the other end being the giant ependymoma of the terminal filum.
9

Weinstein, Gene M., Knarik Arkun, James Kryzanski, Michael Lanfranchi, Gaurav K. Gupta, and Harprit Bedi. "Spinal Intradural, Extramedullary Ependymoma with Astrocytoma Component: A Case Report and Review of the Literature." Case Reports in Pathology 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/3534791.

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Ependymomas are common spinal lesions, with the vast majority arising in an intramedullary location. Several cases have been described in the literature of ependymomas in an intradural, extramedullary location. The authors present a case of a 56-year-old female who presented with several weeks of lower back pain and weakness. MRI revealed an intradural, extramedullary enhancing mass at L1-L2. The mass was successfully resected surgically. Pathologic evaluation revealed a low grade glioma with components of both ependymoma and pilocytic astrocytoma with MUTYH G382D mutation. Extramedullary ependymomas are very rare tumors. To the authors’ knowledge, this is the first case of ependymoma/astrocytoma collision tumors described in an extramedullary location.
10

Goto, Kazuya, Hiroko Fujii, Gen Honjo, and Satoshi Kore-eda. "GFAP-Negative Subcutaneous Sacrococcygeal Extraspinal Ependymoma." Case Reports in Dermatology 13, no. 2 (June 14, 2021): 293–97. http://dx.doi.org/10.1159/000516618.

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Ependymomas are slowly growing glial tumors derived from the ependymal cells and usually occur in the central nervous system (CNS). Ependymomas rarely occur outside of the CNS and they are called extraspinal ependymomas. In spite of their metastatic potential, extraspinal ependymomas can be misdiagnosed for other benign mass like pilonidal cysts. The diagnosis is confirmed by histopathology and most of the cases are known to show glial fibrillary acidic protein (GFAP), S-100 protein, and keratin (AE1AE3) immunoreactivity. Herein, we present a case of GFAP-negative ependymoma, which presented as asymptomatic subcutaneous tumor of the left buttock and was clinically misdiagnosed as epidermal cyst. Our case indicates that ependymomas cannot be ruled out by lack of GFAP immunoreactivity and an asymptomatic subcutaneous mass could be a malignant tumor like ependymomas, which requires careful examinations.
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Статті в журналах Дисертації Книги

Дисертації з теми "Ependymomas":

1

TIXIER, THIERRY. "Les ependymomes sous-cutanes sacrococcygiens." Clermont-Ferrand 1, 1990. http://www.theses.fr/1990CLF13076.

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2

Eicker, Monika. "Monosomie 22 in Ependymomen." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-58938.

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3

Kilday, John-Paul. "Genomic and epigenetic characterisation of childhood ependymoma." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/12553/.

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Paediatric ependymomas remain a clinical management challenge, with a relatively poor prognosis when compared to other childhood tumours of the central nervous system. An improved understanding of underlying ependymoma biology may identify new correlates of outcome and potential therapeutic targets. To address this, AffymetrixTM 500K SNP arrays were used to establish the nature and range of genomic imbalances in 63 paediatric ependymomas (42 primary and 21 recurrent). Over 80 % of tumours were analysed against patient-matched constitutional DNA. In addition, the Illumina® GoldenGate® Cancer Panel I array was used to identify differences in methylation profile across 98 paediatric ependymomas (73 primary and 25 recurrent). While collective assessment revealed the most common anomalies, specific aberrations were characteristic of certain ependymoma subgroups, particularly those relating to tumour location, patient age, disease recurrence and patient prognosis. The genomic imbalance of 15 selected candidate genes (NSL1, DNAJC25, NAV1, CDKN2A, CHI3L1, HOXA5, TXN, BNIPL, and PRUNE) were confirmed by quantitative Polymerase Chain Reaction. Genomic gain involving regions of chromosome 1q were associated with an unfavourable patient outcome, such as the focal locus on 1q21.3 encompassing PRUNE. The genomic gain of PRUNE correlated with an increased encoded protein expression, as assessed by immunohistochemistry (IHC). This adverse prognostic association with 1q was upheld in the subsequent part of this work. Fluorescent in situ hybridisation and IHC were used to evaluate a panel of six putative prognostic markers (1q25 gain, PRUNE, Tenascin-C, Nucleolin, Ki-67 and NAV1 expression) across a paediatric intracranial ependymoma tissue microarray cohort of 107 primary tumours treated within the confines of two aged defined clinical trials (UK CCLG 1992 04 and SIOP 1999 04). Within the younger UK CCLG 1992 04 cohort, copy number gain of chromosome 1q25 and PRUNE overexpression were independently associated with an increased risk of disease progression, while strong PRUNE expression was also an independent marker of worse overall survival. In addition, increased Tenascin-C expression correlated with a reduced overall survival on univariate analysis. For older children in the SIOP 1999 04 cohort, strong PRUNE expression in ependymomas was again identified as an adverse prognostic marker, correlating with increased mortality on univariate assessment.
4

Tourbez, Arthur. "Développement et caractérisation d'organoïdes de tumeurs cérébrales pédiatriques utilisés en recherche fondamentale et translationnelle." Electronic Thesis or Diss., Lyon 1, 2023. https://n2t.net/ark:/47881/m6416x50.

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Les gliomes de haut grade pédiatriques (pHGG) et les épendymomes de la fosse postérieure de type A (EPN-PFA) représentent l'un des plus grands défis de la neuro-oncologie pédiatrique. Leur singularité se manifeste par une remarquable hétérogénéité inter- et intra-tumorale qui complique le développement de stratégies thérapeutiques efficaces. Afin d'améliorer les perspectives cliniques pour les patients atteints de ces cancers, il est impératif de disposer de modèles pré-cliniques capables de refléter fidèlement les principales caractéristiques de leurs tumeurs d'origine. Au cours de mon doctorat, j'ai élaboré un protocole pour la création et la conservation de tumoroïdes pHGG (pHGG_O) et de tumoroïdes de EPN-PFA (EPN-PFA_O). Ces modèles peuvent être cultivés plusieurs mois/années. De plus, des analyses histologiques et moléculaires approfondies ont permis de montrer que ces modèles préservent l'hétérogénéité inter- et intra-tumorale de leur tumeur d'origine, et ce même après plusieurs passages en culture et cryopréservation. J'ai également démontré que ces modèles peuvent servir à l'évaluation de la réponse aux traitements qui reste comparable à celle observée chez les patients. De plus, ces modèles ont révélé leur potentiel pré-clinique (1) en permettant d'identifier l'ONC201, un inhibiteur de DRD2, comme un agent thérapeutique d'intérêt pour les tumeurs H3K27 nonaltérées, et (2) en contribuant à élaborer des stratégies de combinaison visant à amplifier la réponse thérapeutique à l'ONC201. Ces modèles sont donc des outils pré-cliniques robustes et puissants, en particulier pour l'appréciation des profils de réponses aux traitements et la recherche de nouvelles combinaisons de médicaments efficaces
Pediatric high-grade gliomas (pHGG) and posterior fossa type A ependymomas (EPN-PFA) remain one of the biggest challenges in pediatric oncology. They exhibit vast inter- and intra-tumoral heterogeneity, complicating the development of effective therapeutic strategies. Then to improve their clinical outcome, we absolutely need pre-clinical models that recapitulate key features of their corresponding parental tumors. During my PhD, I developed an optimized protocol for the establishment and biobanking of pHGG organoids (pHGG_O) and EPN-PFA organoids (EPN-PFA_O). These models can be grown long-term and comprehensive histological and molecular analyses showed that they recapitulate inter- and intra-tumoral heterogeneity of their parental tumor even after several passages and cryopreservation as 3D cultures. I further showed that they can be employed to test responses to standard of care therapy as well as new therapeutic options, including drugs from clinical trials as they accurately capture the clinical phenotypes of their respective parental tumors. Moreover, these models led to the identification of the DRD2 inhibitor ONC201 as an unexpected potential therapeutic agent for H3K27M non-altered pediatric brain tumors and helped identify combination strategies to increase the therapeutic response to ONC201. Thus, those models are positioned to support powerful and innovative preclinical studies, particularly those related to personalized assessments of treatment response profiles and identification of novel efficient drug combinations
5

Sabnis, Durgagauri. "An investigation of druggable prognostic markers in paediatric ependymoma." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33243/.

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Background: Paediatric ependymomas are the second most common malignant brain tumours in children. Tumour recurrence, chemoresistance and invasion of surrounding critical structures are the hallmarks of ependymomas. These features are consistent with the cancer stem cell (CSC) hypothesis which states that tumours harbour a sub-population of stem-like cells which underlie therapeutic resistance. This study investigates the role of the radial glial stem cell marker BLBP, the multidrug transporter ABCB1, and the DNA repair enzyme MGMT in therapy failure in ependymomas with particular emphasis on the role of CSCs. Material and Methods: Database analyses were performed to assess the expression of the aforementioned markers in patients from 3 publicly available gene expression datasets. Furthermore, samples from 2 European paediatric ependymoma trial cohorts were screened for ABCB1, BLBP and MGMT expression by immunohistochemistry to elucidate their prognostic value. The expression of these markers was also determined in a panel of 5 ependymoma derived cell lines by QRT-PCR or western blotting analysis. Roles in chemoresistance (clonogenic & cytotoxicity assays) and tumour invasion (wound healing & 3D invasion assay) were then investigated. Results: Poor survival in the chemotherapy-led paediatric ependymoma CNS9204 trial was significantly associated with ABCB1 (P=0.007) and BLBP (P=0.03) expression whilst MGMT (P<0.001) and BLBP (P=0.002) expression predicted poor survival in the radiotherapy-led CNS9904 trial cohort. ABCB1 and BLBP expression was consistent with the CSC hypothesis whilst MGMT was expressed in both CSCs as well as the tumour bulk. Inhibition of ABCB1 and BLBP, with the phosphodiesterase-5 inhibitor vardenafil and PPAR-ϒ antagonist GW9662 respectively, potentiated response to chemotherapy and also inhibited the ability of ependymoma cell lines to migrate and invade. Finally, whilst each of the tested cell lines were resistant to the alkylating agent temozolomide, they were sensitive to the novel N3-propargyl analogue of temozolomide. Conclusion: ABCB1, BLBP and MGMT were not only markers of robust prognostic value but they also contributed functionally to the aggressive behaviour of ependymoma. Inhibition of ABCB1 and BLBP by vardenafil and GW9662 may represent effective approaches to overcome chemoresistance and invasion in ependymoma patients. The N3-propargyl analogue of temozolomide could also represent a novel treatment option for MGMT expressing ependymoma patients.
6

TALIK, ZYGART NATHALIE. "Les ependymomes intracraniens de l'enfant : a propos de 27 observations." Lille 2, 1989. http://www.theses.fr/1989LIL2M382.

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7

Andreiuolo, Felipe. "Target in context : molecular pathology of pediatric ependymoma and high grade glioma." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00913042.

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Biomarkers for the classification, clinical management and prognosis of pediatric brain tumors (ependymoma and high grade glioma, (HGG)) are lacking. To address this, biomarkers were developed and explored in view of classification, prognostication, target identification and prediction of the efficacy of treatment for patients with such tumors.We show that overexpression of neuronal markers distinguishes supratentorial from infratentorial ependymoma, and among the former higher immunoexpression of neurofilament 70 (NEFL) is correlated with better progression free survival (PFS). Tenascin-C (TNC) is significantly overexpressed in infratentorial ependymoma. A multi-institutional European ependymoma collaboration group was established and analyses were performed in a pediatric cohort of 250 patients, where immunohistochemistry (IHC) for TNC showed to be a robust marker of poor overall survival (OS) and PFS, particularly among children under 3 years, this being further validated in an independent cohort. Techniques and scoring performed in different laboratories were highly reproducible. IHC for NEFL and TNC could be used for prognostication of pediatric ependymoma.The analysis of putative predictive markers for the response to targeted therapies in pediatric HGG in the setting of a clinical trial with the anti-EGFR agent erlotinib was performed by IHC and fluorescent in situ hybridization. The frequent loss of PTEN in diffuse intrinsic pontine glioma (DIPG) and the confirmation of the biological singularity of the certain subgroups (expressing EGFR, displaying oligodendroglial differentiation) which seem to be associated with better response to erlotinib have helped our group to establish the design of the next Phase III protocol for this disease at our institution. We report mutations in PI3KCA constituting the first identification of oncogene mutations in some DIPG, which further highlight their biological heterogeneity. Further studies are needed to define the interaction between PTEN loss, EGFR overexpression, oligodendroglial differentiation, PI3KCA mutations and other recent findings such as PDGFRA/MET gains/amplification and TP53 mutations in these heterogeneous lesions and their relationship to the outcome of patients under new targeted therapies for this largely fatal disease.This thesis has allowed us to explore the molecular pathology in the context of biology and clinical setting of pediatric brain tumors.
8

Feuß, Mareike [Verfasser]. "Die mikrochirurgische Therapie des cerebralen und spinalen Ependymoms / Mareike Feuß. Medizinische Fakultät." Bonn : Universitäts- und Landesbibliothek Bonn, 2011. http://d-nb.info/1017916136/34.

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9

LABORIEUX, ANY. "Ependymomes intracraniens de l'enfant : revue de la litterature a propos de deux cas." Nice, 1990. http://www.theses.fr/1990NICE6531.

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10

GENESTIN, ELISABETH. "Ependymome pan-medullaire : etude clinique du 7eme cas de la litterature, et apports des techniques nouvelles." Lille 2, 1989. http://www.theses.fr/1989LIL2M241.

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Книги з теми "Ependymomas":

1

Klimo, Paul, and Nir Shimony. Ependymomas. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0026.

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Pediatric posterior fossa tumors are usually ependymoma, pilocytic astrocytoma, or medulloblastoma. Ependymoma appears well-demarcated with heterogeneous enhancement on magnetic resonance imaging (MRI). Full neural axis MRI is indicated to assess for metastatic disease. Management is typically surgical resection of the tumor, with consideration for cerebrospinal fluid diversion if patients present with severe hydrocephalus. Extent of resection of the tumor is the most important factor in predicting recurrence and overall survival, and gross total resection is ideal. Infratentorial ependymomas have 2 molecular subtypes, which has implications for responsiveness to adjuvant therapy and prognosis. Infratentorial ependymomas are biologically different from supratentorial ependymomas. Postoperative radiation improves local control.
2

Fowler, Raquel. Ependymomas: Prognostic Factors, Treatment Strategies and Clinical Outcomes. Nova Science Publishers, Incorporated, 2016.

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3

Theeler, Brett J., and Mark R. Gilbert. Primary Central Nervous System Tumors. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0129.

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Ependymomas are rare primary central nervous system (CNS) tumors that are thought to arise from ependymal cells lining the ventricular system located throughout the CNS. Ependymomas occur in all age groups but are more common in the pediatric population. Ependymomas typically present as mass lesions within the ventricular system, brain or spinal cord parenchyma. As with most central nervous system tumors, pathologic evaluation is required for definitive diagnosis. Ependymomas are typically treated with a combination of surgery and radiotherapy although this varies depending on tumor location, tumor grade, patient age, extent of tumor resection, and other pretreatment factors. Recent molecular studies demonstrate molecularly defined tumor heterogeneity that appears to have a region-specific pattern. Translating the emerging molecular profiles of ependymomas into improved treatment strategies is the primary goal of ongoing research efforts.
4

Gilbert, Mark R., and Roberta Rudà. Ependymal tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0005.

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Ependymomas are uncommon central nervous system cancers that can arise in the supratentorial, infratentorial, or spinal cord region. Recently, there have been several seminal findings regarding the molecular profiles of ependymomas that have led to marked changes in the classification of this disease. In addition to the World Health Organization grading system that designates ependymomas based on histological appearance into grade I, II, or III, a new molecular classification with distinct entities within the three anatomical regions provides additional subtyping that has prognostic significance and may ultimately provide therapeutic targets. Ependymomas are typically treated with maximum safe tumour resection. Grade III tumours always require radiation treatment even with extensive resection. Radiation is also often administered to patients with grade II ependymomas. Grade I tumours typically receive radiation if there is extensive residual disease, but complete resection may be curative. Local radiation is optimal unless there is imaging or cytological evidence of dissemination in the cerebrospinal fluid. Chemotherapy is less well established although recent molecular findings may lead to subtype specific treatments.
5

Elwell, Christine, and Kufre Sampson. Neurological tumours. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0237.

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Neurological tumours are categorized by the WHO as follows: neuroepithelial tumours (gliomas, oligodendrogliomas, ependymomas, pineal parenchymal tumours, medulloblastoma, neuronal and neuroglial tumours); cranial and paraspinal nerve tumours (schwannoma, neurofibromas); meningeal tumours (meningiomas); lymphomas; germ cell tumours (germinoma, teratoma); sellar region tumours (cranipharyngioma); and metastases. The tumours are classified according to grade. The WHO histological grading scheme used for astrocytomas is based on mitoses, nuclear pleomorphism, necrosis, and endothelial proliferation. WHO Grade I and Grade II tumours are low-grade tumours, and WHO Grade III and Grade IV tumours are high-grade tumours.
6

Haranhalli, Neil, and Jerome J. Graber. Pineal Region Neoplasms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0131.

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Pineal region tumors include a diverse array of neoplasms arising from various components of the pineal gland, including germ cell tumors, germinomas, teratomas, pineocytomas, pineoblastomas, and tumors derived from glial tissues including gliomas, astrocytomas, oligodendrogliomas, and ependymomas. Benign lesions of the pineal gland can include pineal cysts, calcifications and meningiomas. Metastatic tumors can also be found in the pineal region. Numerous infectious and inflammatory conditions can mimic pineal tumors. Most patients present with symptoms of hydrocephalus or Parinaud’s syndrome. Diagnosis often requires biopsy, though some germinomas may be diagnosed based solely on serum and cerebrospinal fluid biomarkers.
7

Hayat, M. A. Tumors of the Central Nervous System, Volume 9: Lymphoma, Supratentorial Tumors, Glioneuronal Tumors, Gangliogliomas, Neuroblastoma in Adults, Astrocytomas, Ependymomas, Hemangiomas, and Craniopharyngiomas. Springer Netherlands, 2016.

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8

Hayat, M. A. Tumors of the Central Nervous System, Volume 9: Lymphoma, Supratentorial Tumors, Glioneuronal Tumors, Gangliogliomas, Neuroblastoma in Adults, Astrocytomas, Ependymomas, Hemangiomas, and Craniopharyngiomas. Springer London, Limited, 2012.

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9

Taylor, Jennie W., and Scott R. Plotkin. Familial CNS Tumor Syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0135.

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Neurofibromatosis type 2 (NF2) is a genetic disorder caused by constitutional mutations in the NF2 tumor-suppressor gene. Bilateral vestibular schwannomas are the hallmark of the syndrome, though meningiomas, ependymomas, and other peripheral schwannomas are common. Inheritance is autosomal dominant and de novo mutations are found in about 50% of patients. Standard treatment for symptomatic tumors is surgery. Radiation therapy may be considered for progressive tumors that are not surgically accessible, but secondary cancers after radiation have been reported. Retrospective studies suggest that bevacizumab may be active for progressive vestibular schwannomas and trials of chemotherapy for NF2-related tumors are in progress. This chapter reviews the epidemiology, genetic features, clinical characteristics, and current treatments for patients with NF2.
10

Ernestus, Ralf-Ingo. Klinik und Prognose der Intrakraniellen Ependymome. Lang AG International Academic Publishers, Peter, 1989.

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Частини книг з теми "Ependymomas":

1

Dragun, Anthony E., Paul J. Schilling, Tod W. Speer, Feng-Ming Kong, Jingbo Wang, Hedvig Hricak, Oguz Akin, et al. "Ependymomas." In Encyclopedia of Radiation Oncology, 222. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1102.

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2

Raghav, Kanwal P. S., and Mark R. Gilbert. "Ependymomas." In Neuro-oncology, 86–94. Oxford, UK: Blackwell Publishing Ltd., 2012. http://dx.doi.org/10.1002/9781118321478.ch8.

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3

Myseros, John S. "Ependymomas." In Textbook of Pediatric Neurosurgery, 1–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-31512-6_92-1.

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4

Gilbert, Mark R., Roberta Ruda, and Riccardo Soffietti. "Ependymomas." In Primary Central Nervous System Tumors, 249–62. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-166-0_11.

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5

Rudà, Roberta, Mark R. Gilbert, and Riccardo Soffietti. "Ependymomas." In Textbook of Uncommon Cancer, 907–16. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119196235.ch64.

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6

Wetjen, Nicholas, and Corey Raffel. "Ependymomas." In Oncology of CNS Tumors, 503–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02874-8_35.

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7

Myseros, John S. "Ependymomas." In Textbook of Pediatric Neurosurgery, 2017–37. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-72168-2_92.

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8

Silverman, Craig L., Patrick R. M. Thomas, and William Cox. "Ependymomas." In Management of Childhood Brain Tumors, 369–82. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1501-8_15.

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9

Omerhodžić, Ibrahim, Mirza Pojskić, and Kenan I. Arnautović. "Myxopapillary Ependymomas." In Spinal Cord Tumors, 273–300. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99438-3_15.

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10

Patel, Nisha R., Michael L. Wong, Anthony E. Dragun, Stephan Mose, Bernadine R. Donahue, Jay S. Cooper, Filip T. Troicki, et al. "Myxopapillary Ependymomas." In Encyclopedia of Radiation Oncology, 522. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1188.

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Тези доповідей конференцій з теми "Ependymomas":

1

Sun, Yang. "Microsurgical management of multiple intramedullary spinal core ependymomas." In INTERNATIONAL SYMPOSIUM ON THE FRONTIERS OF BIOTECHNOLOGY AND BIOENGINEERING (FBB 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5110858.

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2

Mack, Stephen C., and Michael D. Taylor. "Abstract PR03: Myxopapillary spinal ependymomas demonstrate a Warburg phenotype." In Abstracts: AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.brain15-pr03.

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3

Bischof, Jared M., Denise Scholtens, Kelly Arndt, Min Wang, Deli Wang, Chiang-Ching Huang, Maria de Fatima Bonaldo, Richard J. Gilbertson, and Marcelo Bento Soares. "Abstract 3002: Identification of frequently altered protein networks in ependymomas." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3002.

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4

Dantas‐Barbosa, Carmela, Heike Blockus, Birgit Geoerger, Felipe Andreiuolo, Matthieu Peyre, Frederic Commo, Stephanie Puget, Christian Sainte‐Rose, Gilles Vassal, and Jacques Grill. "Abstract A193: From MT3 modulation to HDACi treatment in ependymomas." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a193.

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5

Costa, Fabricio F., Jared M. Bischof, Chris Hamm, Elio F. Vanin, Maria F. Bonaldo, Stephen Iannaccone, Veena Rajaram, Tadanori Tomita, Stewart Goldman, and Marcelo B. Soares. "Abstract 794: RNA-Seq and whole transcriptome analyses in ependymomas." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-794.

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6

Andrade, Fernanda G., Suely K. N. Marie, Hamilton Matushita, Sergio Rosemberg, and Sueli M. Oba-Shinjo. "Abstract 5594: Cyclin D1 expression correlates with supratentorial location of ependymomas." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5594.

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7

Witt, Hendrik, Steve C. Mack, Stefan M. Pfister, Andrey Korshunov, and Michael D. Taylor. "Abstract LB-198: Epigenomic alterations define lethal CIMP-positive ependymomas of infancy." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-198.

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8

Xi, Guifa, Nitin Wadhwani, Rintaro Hashizume, Barbara Mania-Farnell, Marcelo Bento Soares, Charles D. James, and Tadanori Tomita. "Abstract 2871: Global reduction of H3K4me3 improves chemotherapeutic efficacy for pediatric ependymomas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2871.

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9

Xi, Guifa, Nitin Wadhwani, Rintaro Hashizume, Barbara Mania-Farnell, Marcelo Bento Soares, Charles D. James, and Tadanori Tomita. "Abstract 2871: Global reduction of H3K4me3 improves chemotherapeutic efficacy for pediatric ependymomas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2871.

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10

Lammers, J., F. Calkoen, M. Kranendonk, A. Federico, M. Kool, L. Kester, and J. van der Lugt. "P02.07 Characterization of the tumor immune microenvironment of pediatric posterior fossa A ependymomas." In iTOC8 – the 8th Leading International Cancer Immunotherapy Conference in Europe, 8–9 October 2021, Virtual Conference. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jitc-2021-itoc8.19.

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Звіти організацій з теми "Ependymomas":

1

Feria, Alejandro. A novel c.885+1G>A splicing variant in exon 9 of the NF2 gene shows a delayed mild presentation with a predilection for spinal ependymomas. Science Repository OU, April 2019. http://dx.doi.org/10.31487/j.scr.2019.02.010.

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