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Astroblastoma
Published in Dongyou Liu, Tumors and Cancers, 2017
Astroblastoma is a rare glial tumor of uncertain origin. It is classified as either low or high grade (well differentiated or anaplastic/malignant). This classification is based on the cellularity, presence of necrosis, and mitotic figures [1]. Astroblastoma constitutes up to 3% of all neuroglial tumors such as astrocytomas, oligodendrogliomas, glioblastomas, and others.
A rare case of intracranial extra-axial ependymoma
Published in Ultrastructural Pathology, 2019
Viscardo Paolo Fabbri, Valentina Papa, Antonio Fioravanti, Monica Messia, Giovanni Tallini, Sofia Asioli, Giovanna Cenacchi
Ependymomas are primary tumors of the central nervous system traditionally characterized by the presence of perivascular pseudorsettes and circumscribed non-infiltrative growth. They represent 2% to 9% of all intracranial tumors and they can arise from the ventricular system or extra-ventricular tissue: in adults, they are mostly spinal cord-located while in children they could be found especially in posterior fossa.2 Intracranial extra-axial ependymomas (IEAEs) are extremely rare: to date, only 20 cases have been described in the literature (Table 1). Probably they result from heterotopic ependymal cell rests during the fetal development.3 Ependymomas have been also reported in extra-cranial sites, as mediastinum, lung and in pelvic, perianal and sacrococcygeal subcutaneous tissues.4 As shown in Table 1 IEAEs have a slightly male predominance and their median age is 38 years (ranged from 13 days to 81 years). Preoperative IEAEs diagnosis is very difficult as they simulate meningiomas or schwannomas (especially when they arise near a cranial nerve). On histology differential diagnosis includes meningiomas, low-grade glioneuronal tumors (as papillary glioneuronal tumor), oligodendrogliomas, neurocytomas and other rare glial entities (astroblastoma or angiocentric glioma) that sometimes can arise in the extra-assial site.5 IEAEs present not only the same morphological spectrum observed in intra-axial tumors but also the same ultrastructural features described in ependymal cells as junctional apparatus, microvilli, and cilia. It is not yet clear if IEAEs have a greater tendency to recur than the intra-parenchymal ependymomas because in the few cases described treatments are not always standardized or available (Table 1).
Brain tumors and circulating micrornas: a systematic review and diagnostic meta-analysis
Published in Expert Review of Molecular Diagnostics, 2022
Amir Hossein Aalami, Hossein Abdeahad, Ali Shoghi, Mohammad Mesgari, Amir Amirabadi, Amirhossein Sahebkar
The keywords applied for literature retrieval included: (‘glioma,’ ‘glioblastoma,’ ‘glioblastoma multiforme,’ ‘brain tumors,’ ‘neurospongioma,’ ‘Malignant glioma,’ ‘Astroblastoma,’ ‘oligo-astrocytoma,’ ‘ependymoma,’ ‘medulloblastoma’) and (‘microRNA,’ ‘miRNA,’ ‘miRs,’) and (‘circulating,’ ‘blood,’ ‘serum,’ ‘plasma’) and (‘diagnosis,’ ‘sensitivity,’ ‘specificity,’ ‘ROC curve’). Besides, reference lists of identified articles were individually searched manually to identify supplementary sources.
Pediatric embryonal brain tumors in the molecular era
Published in Expert Review of Molecular Diagnostics, 2020
Bryan K. Li, Salma Al-Karmi, Annie Huang, Eric Bouffet
The increasing heterogeneity in this umbrella entity and recognition of candidate molecular signatures was shown in two previous molecular studies. Among 254 institutionally diagnosed CNS-PNETs analyzed by Picard et al., nearly half (44%) were excluded after central pathology review, including cases that were reclassified at ATRT, ependymoma, and GBMs [72]. Of the remaining cases, transcriptional profiling and copy number analysis revealed three molecular groups. Group 1 consisted of C19MC-altered tumors with high LIN28 expression. Groups 2 and 3 lacked recurrent copy number alterations but were enriched for oligoneural (OLIG1/2, BCAN, SOX8/10) and mesenchymal differentiation (COL1A2, COL5A, FOXJ1, MSX1) genes, respectively. Indeed, group 2 were associated with nuclear OLIG2 immunostaining, suggesting that some of these tumors were malignant gliomas. Median survival in groups 1–3 in those age <4 years were 1.0, 0.8, and 2.7 years, while those >4 years were 0.5, 1.8 and 4.8 years. A later study by Sturm et al. analyzed 323 institutionally diagnosed CNS-PNET tumors using DNA methylation profiling [122]. Similarly, 196 (61%) tumors were re-classified as other tumor entities based on clustering analyses. Among the remaining cases, 77 (24%) formed four distinct clusters separate from other recognized tumors, which they proposed as new entities: CNS neuroblastoma with FOXR2 activation (CNS-NB-FOXR2 or embryonal tumor with FOXR2 activation), CNS high-grade neuroepithelial tumor with MN1 alteration (CNS-HGNET-MN1) or BCOR alteration (CNS-HGNET-BCOR or embryonal tumor with BCOR alteration), and CNS-Ewing’s family of tumors with CIC gene fusions (CNS-EFT-CIC). The CNS-NB-FOXR2 group closely mirrors the Group 2 CNS-PNETs described by Picard et al. [72,122,123]. While FOXR2 fusion events were observed in three of six samples, unpublished data by Ho et al. have found similar FOXR2 fusions in a subset of HGG with MYCN activation [124]. The subgroup CNS-HGNET-MN1 largely corresponds to tumors with a histological diagnosis of astroblastoma, a less aggressive glial tumor. CNS-HGNET-BCOR and CNS-EFT-CIC tumors share gene alterations previously seen in extra-cranial malignant sarcomas and may represent local variants of the same entity [125–127]. Indeed, subsequent DNA methylation-based clustering show that CNS-EFT-CIC tumors cluster together with their extra-cranial counterparts [124].