Relevant bibliographies by topics / Gliomes Chordoides

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  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Gliomes Chordoides'

Author: Grafiati
Published: 16 November 2024

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Journal articles on the topic "Gliomes Chordoides"

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Leeds, Norman E., Frederick F. Lang, Teresa Ribalta, Raymond Sawaya, and Gregory N. Fuller. "Origin of Chordoid Glioma of the Third Ventricle." Archives of Pathology & Laboratory Medicine 130, no. 4 (April 1, 2006): 460–64. http://dx.doi.org/10.5858/2006-130-460-oocgot.

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Abstract Context.—Chordoid glioma is a relatively recently described unique glial neoplasm that has been formally codified by the World Health Organization in Pathology and Genetics of Tumours of the Nervous System, in which it is included along with astroblastoma and gliomatosis cerebri under the rubric “Tumors of Uncertain Origin.” Many examples of chordoid glioma come to clinical attention only at a relatively large size and occupy a large portion of the third ventricle. Accordingly, the anatomic origin of chordoid glioma has been unclear and debated. Objective.—To examine the regional anatomic origin of chordoid glioma. Data Sources.—The clinical, imaging, histologic, immunophenotypic, and ultrastructural data in previously published case series and individual case reports of chordoid glioma were reviewed in conjunction with the study of a new case of chordoid glioma that presented at a relatively small size, thereby facilitating neuroanatomic localization. Conclusions.—Chordoid glioma exhibits features of specialized ependymal differentiation on ultrastructural examination, and all examples reported in the literature to date have displayed a highly stereotypical suprasellar anatomic localization and an ovoid shape, as seen on neuroimaging studies and gross anatomy. Neuroanatomic, radiologic, and clinical evidence supports an anatomic origin for chordoid glioma from the vicinity of the lamina terminalis.
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Thavaratnam, LK, ST Loy, A. Gupta, I. Ng, and JF Cullen. "Chordoid glioma." Singapore Medical Journal 56, no. 11 (November 2015): 641–43. http://dx.doi.org/10.11622/smedj.2015175.

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Liu, Wei-ping, Jin-xiang Cheng, Xi-cai Yi, Hai-ning Zhen, Zhou Fei, Qing Li, and Xiang Zhang. "Chordoid Glioma." Neurologist 17, no. 1 (January 2011): 52–56. http://dx.doi.org/10.1097/nrl.0b013e3181e7db67.

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Ricoy, J. R., R. D. Lobato, B. Báez, A. Cabello, M. A. Martínez, and G. Rodríguez. "Suprasellar chordoid glioma." Acta Neuropathologica 99, no. 6 (June 9, 2000): 699–703. http://dx.doi.org/10.1007/s004010051183.

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Konovalov, A. N., I. V. Chernov, M. V. Ryzhova, D. I. Pitskhelauri, Yu V. Kushel, L. I. Astafieva, O. I. Sharipov, et al. "Chordoid gliomas of the third ventricle." Voprosy neirokhirurgii imeni N.N. Burdenko 87, no. 6 (2023): 14. http://dx.doi.org/10.17116/neiro20238706114.

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Brat, D. J., B. W. Scheithauer, S. C. Cortez, K. Brecher, and P. C. Burger. "THIRD VENTRICULAR “CHORDOID GLIOMA”." Journal of Neuropathology and Experimental Neurology 56, no. 5 (May 1997): 586. http://dx.doi.org/10.1097/00005072-199705000-00072.

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Brat, Daniel J. "Chordoid glioma further defined." Advances in Anatomic Pathology 9, no. 1 (January 2002): 77. http://dx.doi.org/10.1097/00125480-200201000-00016.

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Suetens, Kristin, Jeroen Swinnen, Linde Stessens, Sofie Van Cauter, and Geert Gelin. "Chordoid Glioma as a Differential Diagnosis of Anterior Third Ventricle Tumours: A Rare Case Report and Five-Year Follow-Up." Case Reports in Radiology 2019 (December 4, 2019): 1–6. http://dx.doi.org/10.1155/2019/3584837.

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Chordoid glioma is a rare and relatively recently defined tumour entity. Worldwide there have only been around 90 cases described until now. A chordoid glioma comprises a low-grade suprasellar neuroepithelial neoplasm originating in the anterior part of the third ventricle, with consistent radiological features on MRI. This lesion should be considered as a differential of third ventricle tumours. The patient described in this paper is quite unique in the sense that despite only partial tumour resection was obtained, the residual tumour was not progressive during several years of follow-up. Preoperative recognition of this disease entity is crucial to modify the treatment approach and improve patient outcome.
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Bellamy, Charlotte, Hannah Tovell, Florent Dingli, Damarys Loew, Stephane Liva, Selina Schwaighofer, Eduard Stefan, Alexandra Newton, Marc Sanson, and Franck Bielle. "Abstract 4370: Functional characterisation of a novel mutation in PRKCA, a major driver of chordoid gliomas." Cancer Research 84, no. 6_Supplement (March 22, 2024): 4370. http://dx.doi.org/10.1158/1538-7445.am2024-4370.

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Abstract Chordoid gliomas (ChG) are a rare low-grade brain tumor, believed to be derived from tanycytes. An analysis by the team identified a novel mutation present in all ChGs: PRKCA p.D463H. This mutation involves a D463H substitution at the kinase domain of the Protein kinase C alpha (PKCα), it is not found in any other cancer, and represents the hallmark of ChG. The aim of the project is to identify novel and biologically relevant PKCαD463H signaling pathways, which will demonstrate the involvement and the role of this mutated kinase in cellular functions implicated in the development of ChGs. The D463H mutation affects a critical residue of the kinase domain of PKCα, suggesting that such a change modifies substrate affinity. Following the purification of PKCαD463H, we have shown its inactivation via in vitro kinase assays and peptide array. In cellulo fret-based activity reporter assays have shown that PKCαD463H has a dominant negative effect over PKCαWT. Through co-immunoprecipitation we have shown that the mutant protein can bind the WT form and also colocalizes in the cell. Our results also show that the mutation affects the tertiary structure of the protein, resulting in a more open, unstable protein compared to the WT. Phosphoproteomic analysis of HEK cells overexpressing PKC⍺D463H show a decrease of phosphorylation specifically on proteins involved with cell-cell adhesion, including functionally relevant phosphosites. This is in line with our Co-IP mass spectrometry data which shows a decrease in interaction of PKC⍺D463H with proteins involved in cell junctions. The cell of origin, tanycytes, are highly specialized cells that contain important cell-cell junctions and therefore their perturbation could be a potential route of tumorigenesis. By understanding these changes integrated with our snRNAseq and bulk RNAseq of ChGs, and exploration in cellular models, we hope to elucidate the mechanism by which the mutation leads to the development of Chordoid Glioma. Citation Format: Charlotte Bellamy, Hannah Tovell, Florent Dingli, Damarys Loew, Stephane Liva, Selina Schwaighofer, Eduard Stefan, Alexandra Newton, Marc Sanson, Franck Bielle. Functional characterisation of a novel mutation in PRKCA, a major driver of chordoid gliomas [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4370.
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Sanda, Nicolae, Claudiu-Nicolae Mircea, Michèle Bernier, Avinoam B. Safran, and Sorin Aldea. "Chordoid Glioma Infiltrating Optic Structures." Journal of Neuro-Ophthalmology 39, no. 3 (September 2019): 408–10. http://dx.doi.org/10.1097/wno.0000000000000757.

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Dissertations / Theses on the topic "Gliomes Chordoides"

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Bellamy, Charlotte. "Functional characterization of a novel mutation in PRKCA, the major driver of Chordoid glioma." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL052.

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Le gliome chordoïde (ChG) est une tumeur cérébrale rare de bas grade, caractérisée par une nouvelle mutation ponctuelle récurrente PRKCA p.D463H, une substitution dans le domaine kinase de la protéine kinase C alpha (PKCα). Cette étude démontre le rôle de cette kinase mutée dans le développement des ChG. Ici, nous montrons l'inactivation et l'effet négatif dominant de PKCαD463H via des tests d'activité in vitro et in cellulo. Nos résultats montrent que la mutation affecte la structure tertiaire, ce qui entraîne une protéine ouverte et instable. Les données de spectrométrie de masse phosphoprotéomique et de co-immunoprécipitation des cellules HEK surexprimant PKC⍺D463H montrent une diminution de phosphorylation et interaction avec les protéines impliquées dans l'adhésion cellulaire. Nous confirmons génétiquement par le RNAseq à noyau unique que les ChG dérivent de tanycytes spécialisés. En comprenant le contexte cellulaire de la tumorigenèse ainsi que les changements fonctionnels de cette mutation sur l'activité et l'interactome de PKCα, nous avons élaboré un modèle de développement des ChGs parallèlement à l'identification d'une approche thérapeutique
Chordoid glioma (ChG) is a rare low-grade brain tumor, characterised by a novel recurrent point mutation PRKCA p.D463H, a substitution in the kinase domain of Protein kinase C alpha (PKCα). This study demonstrates the role of this mutated kinase in the development of ChGs. Here we show the inactivation and dominant negative effect of PKCαD463H via in vitro and In cellulo activity assays. Our results show the mutation affects the tertiary structure, resulting in an open, unstable protein. Phosphoproteomic and Co-Immunoprecipitation mass spectrometry data from HEK cells overexpressing PKC⍺D463H show decreased phosphorylation and interaction with proteins involved in cell adhesion. We confirm genetically through single nuclei RNAseq that ChGs derive from specialised tanycytes. By understanding the cell context of tumorigenesis alongside the functional changes of this mutation on the activity and interactome of PKCα, we elaborated a model of the development of ChGs alongside the identification of a therapeutic approach
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Books on the topic "Gliomes Chordoides"

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van den Bent, Martin J., Frederic Dhermain, and Walter Stummer. Other neuroepithelial tumours: astroblastoma, angiocentric glioma, and chordoid glioma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0007.

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This chapter contains a description of three rare entities: astroblastoma, angiocentric glioma, and chordoid glioma. Because these tumours are so rare, the evidence on how to best treat them is anecdotal and essentially consists of case series, but it is the best guidance available and the presentation of larger series with new cases remain unlikely. If one is confronted with such a case, a meticulous review of the clinical, radiological, and pathological characteristics of the case is indicated, to minimize the risk of an erroneous diagnosis. If the case does not fit in with the descriptions of previous cases, alternative diagnoses should be considered.
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Book chapters on the topic "Gliomes Chordoides"

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Liu, Dongyou. "Chordoid Glioma, Angiocentric Glioma, and Diffuse Midline Glioma." In Tumors and Cancers, 31–36. Boca Raton : Taylor & Francis, 2018. | Series: Pocket guides to biomedical sciences | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120522-6.

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"Chordoid Glioma of 3rd Ventricle." In Diagnostic Pathology: Neuropathology, 150–53. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-44592-4.50027-5.

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"Chordoid Glioma of the Third Ventricle." In Diagnostic Imaging: Brain, 478–79. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-37754-6.50140-8.

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Gallia, Gary L., Martin G. Pomper, and Alessandro Olivi. "Chordoid Glioma of the Third Ventricle." In Textbook of Neuro-Oncology, 218–21. Elsevier, 2005. http://dx.doi.org/10.1016/b978-0-7216-8148-1.50032-2.

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Brat, Daniel. "Chordoid glioma of the third ventricle." In Russell & Rubinstein's Pathology of Tumors of the Nervous System 7Ed, 229–33. CRC Press, 2006. http://dx.doi.org/10.1201/b13439-17.

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You might also be interested in the extended bibliographies on the topic 'Gliomes Chordoides' for particular source types:
Journal articles
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