ライフサイエンスコーパス: ependymoma

1 alignancies, including glial cell neoplasms (ependymomas).

2 s), meninges (meningiomas), and spinal cord (ependymomas).

3 tential therapeutic target in supratentorial ependymoma.

4 ous deletions of genes not yet implicated in ependymoma.

5 el polyomaviruses were found in nonrecurrent ependymoma.

6 with longer time to progression in recurrent ependymoma.

7 ty for rational therapy for infants with PFA ependymoma.

8 ldren younger than 3 years with intracranial ependymoma.

9 ent of very young children with intracranial ependymoma.

10 rities to YAP1-fusion induced supratentorial ependymoma.

11 the mesenchymal phenotype of posterior fossa ependymoma.

12 aration for YAP fusion oncogenic activity in ependymoma.

13 th gliosarcoma, and one (6%) with anaplastic ependymoma.

14 and ultrastructural characteristics of human ependymoma.

15 response assessment criteria for paediatric ependymoma.

16 llum from tumors such as medulloblastoma and ependymoma.

17 thin 28 recurrent chromosomal alterations in ependymoma.

18 ion of multiple schwannomas, meningiomas and ependymomas.

19 ilocytic astrocytomas, medulloblastomas, and ependymomas.

20 set of CpG sites gain or lose methylation in ependymomas.

21 e aggressive primary tumors and the relapsed ependymomas.

22 ration of CD4(+) T cells in the nonrecurrent ependymomas.

23 ors, including schwannomas, meningiomas, and ependymomas.

24 uld be an effective treatment option for PFA ependymomas.

25 ly all schwannomas, and many meningiomas and ependymomas.

26 rocytomas, 10 pediatric astrocytomas, and 13 ependymomas.

27 olved in the pathogenesis of meningiomas and ependymomas.

28 nonvestibular schwannomas, meningiomas, and ependymomas.

29 vestibular schwannomas (VS), meningiomas and ependymomas.

30 therapeutic strategy for treating childhood ependymomas.

31 FOP), diffuse intrinsic pontine gliomas, and ependymomas.

32 have been observed in a subset of paediatric ependymomas.

33 plifications in CTU1 in 25% of myxopapillary ependymomas.

34 are histo-molecular characteristics of human ependymomas.

35 system such as schwannomas, meningiomas and ependymomas.

36 es and increased survival in mouse models of ependymomas.

37 eripheral nerves, as well as meningiomas and ependymomas.

38 not other astrocytomas, medulloblastomas, or ependymomas.

39 were choroid plexus carcinoma (2 children), ependymoma (1 child), desmoplastic infantile ganglioglio

40 ge: 8-70 years), diagnosed with intracranial ependymoma (1 WHO I, 11 WHO II, 9 WHO III) were treated

41 nodular, two large cell, one anaplastic), 17 ependymomas (13 World Health Organization [WHO] grade II

42 8.9 months, respectively; P = .0006) but not ependymoma (19.5 v 13.3 months, respectively; P = .19).

43 m (CNS) lymphoma (7%) and malignant forms of ependymomas (3%) and meningiomas (2%).

44 ood brain cancer: low-grade glioma (n = 93), ependymoma (32), high-grade glioma (25), medulloblastoma

45 First, we identified subgroups of human ependymoma, a form of neural tumour that arises througho

46 (2020) demonstrate that posterior fossa A ependymoma, a lethal pediatric brain tumor with a silent

47 apply single-cell RNA sequencing to analyze ependymomas across molecular groups and anatomic locatio

48 ry and radiation therapy for posterior fossa ependymoma after accounting for molecular subgroup is no

49 prostate, and squamous cell skin tumors and ependymoma, although there was significant but not overw

50 ognostic factor for outcome in patients with ependymomas, although in infants the use of post-surgica

51 absent tuberin was observed in 2 of 6 (33%) ependymomas analyzed.

52 Using pediatric ependymoma and adult glioblastoma as examples, the 3D br

53 resembles unipolar brush cells, and PFA/PFB ependymoma and cerebellar pilocytic astrocytoma resemble

54 detected in specific types of human tumors: ependymoma and choroid plexus tumors, mesothelioma, oste

55 urther investigational studies are needed in ependymoma and diffuse pontine gliomas because current t

56 Our data indicate that PFA ependymoma and DIPG are driven in part by the action of

57 ontology associated with a good prognosis in ependymoma and it provides preliminary evidence of a ben

58 type gliomas (pediatric high-grade gliomas), ependymoma and medulloblastoma, which commonly occur in

59 f disease control in pediatric patients with ependymoma and results in stable neurocognitive outcomes

60 In this study, a recurrent anaplastic ependymoma and seven glioblastoma biopsy samples, four c

61 The majority of them are ependymomas and astrocytomas, the third commonest is hae

62 social vulnerability, ranging from 11.3% for ependymomas and choroid plexus tumors (mean [SD] surviva

63 relative-difference magnitudes (eg, SES for ependymomas and choroid plexus tumors: mean [SD] duratio

64 een of 42 primary and 11 recurrent pediatric ependymomas and correlated the genetic findings with cli

65 Ependymomas and medulloblastomas also occur in the AYA p

66 A cut off value for mean ADC between Ependymomas and Medulloblastomas was found to be of 0.98

67 tumor types including radial glial cells in ependymomas and oligodendrocyte precursor cells in astro

68 ciated with significantly increased rates of ependymomas and other brain cancers, osteosarcomas, or m

69 mline DNA, including twenty-nine spinal cord ependymomas and sixteen astrocytomas.

70 ssociated with schwannomas, meningiomas, and ependymomas and that is caused by inactivation of the tu

71 iomas, diffuse intrinsic pontine glioma, and ependymoma) and some selected rare tumors (ie, atypical

72 aplastic oligodendroglioma, 1 had anaplastic ependymoma, and 1 had anaplastic astrocytoma.

73 y brain tumors, including craniopharyngioma, ependymoma, and juvenile pilocytic astrocytoma.

74 o high-grade and four low-grade gliomas, one ependymoma, and one sarcoma) were noted, and seven patie

75 ratentorial primitive neuroectodermal tumor, ependymoma, and rhabdoid tumors, 5-year EFS rates were 3

76 ultiforme, gliomatosis cerebri, gliosarcoma, ependymoma, and subependymoma, for their possible associ

77 ofibroma, 1 of 2 neuronoglial tumors, 2 of 3 ependymomas, and 1 of 1 pineoblastoma tested positive.

78 tumors, including schwannomas, meningiomas, ependymomas, and astrocytomas.

79 All medulloblastomas, ependymomas, and high-grade gliomas that abutted a CSF s

80 nd osteosarcoma), and brain tumors (gliomas, ependymomas, and medulloblastomas).

81 f formalin-fixed paraffin-embedded pediatric ependymoma archives.

82 he hallmarks of poor prognosis in paediatric ependymoma are drug resistance, local invasion and recur

83 st common and aggressive molecular groups of ependymoma are the supratentorial ZFTA-fusion associated

84 Recurrent medulloblastoma and ependymoma are universally lethal, with no approved targ

85 Ependymomas are aggressive central nervous system tumors

86 Ependymomas are chemotherapy-resistant brain tumours, wh

87 Ependymomas are common childhood brain tumours that occu

88 Ependymomas are composed of a cellular hierarchy initiat

89 More than 70% of supratentorial ependymomas are defined by highly recurrent gene fusions

90 Ependymomas are generally refractory to chemotherapies a

91 Posterior fossa A (PFA) ependymomas are lethal malignancies of the hindbrain in

92 oblastomas and posterior fossa group A (PFA) ependymomas are located adjacent to and bathed by the ce

93 Here we demonstrate that PFA ependymomas are maintained under hypoxia, associated wit

94 king highly recurrent somatic mutations, PFA ependymomas are proposed to be epigenetically driven tum

95 n, the CpG sites that are hypermethylated in ependymomas are proximal to CpG islands, whereas those t

96 Grade III spinal ependymomas are rare central nervous system tumors with

97 land methylator phenotype-positive hindbrain ependymomas are responsive to clinical drugs that target

98 Intracranial ependymomas are segregated on the basis of anatomical lo

99 e at diagnosis (P < 0.0001), suggesting that ependymomas arising in infants are biologically distinct

100 d between PAs and another human glial tumor (ependymoma) arising supratentorially compared with those

101 th translocation involving LCR-B, a balanced ependymoma-associated t(1;22), were characterized not on

102 us system tumours (schwannomas, meningiomas, ependymomas, astrocytomas, and neurofibromas), periphera

103 hancer and gene expression data derived from ependymoma brain tumors.

104 or alpha2, expressed on medulloblastomas and ependymomas, but not expressed in the normal developing

105 ession was observed in 4 out of 5 paediatric ependymoma cell lines and increased in stem cell enriche

106 MI ependymoma cell lines created by selection for EGF/FGF2-

107 Recently, approximately 60% of human ependymomas, choroid plexus tumors and mesotheliomas wer

108 rus 40 (SV40) is a monkey virus that induces ependymomas, choroid plexus tumors, mesotheliomas, osteo

109 mian virus 40 (SV40) nucleotide sequences in ependymomas, choroid plexus tumors, osteosarcomas, and m

110 xpression microarray profiles from pediatric ependymoma clinical samples were subject to ontological

111 y ependymomas in two non-overlapping primary ependymoma cohorts, with the goal of identifying essenti

112 Posterior fossa ependymoma comprises two distinct molecular variants ter

113 that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the

114 e midline gliomas and posterior fossa type A ependymomas contain the recurrent histone H3 lysine 27 (

115 ion, by integrating our atlas with pediatric ependymomas data, we identified specific molecular signa

116 Analysis of sporadic astrocytomas and ependymomas demonstrated either increased rap1 or reduce

117 oteins has been implicated in supratentorial ependymoma development.

118 cation of diffuse and circumscribed gliomas, ependymomas, embryonal tumours and meningiomas, and disc

119 nd current clinical trials for children with ependymoma, emphasizing the history and evolution of tre

120 Ependymoma (EPN) is a common form of brain tumor in chil

121 Ependymoma (EPN) is a paediatric brain tumour that relie

122 onsisted of 7 pilocytic astrocytoma (PA), 19 ependymoma (EPN), 5 glioblastoma (GBM), 6 medulloblastom

123 enomic states in high-grade glioma (HGG) and ependymoma (EPN).

124 Recurrence is frequent in pediatric ependymoma (EPN).

125 number aberrations, poor-prognosis hindbrain ependymomas exhibit a CpG island methylator phenotype.

126 Posterior fossa type A (PFA) ependymomas exhibit very low H3K27 methylation and expre

127 transcriptional activator GCN4 also promote ependymoma formation.

128 for patients diagnosed with grade III spinal ependymomas from 2004 to 2017.

129 eningioma, Pituitary, No tumor, Astrocytoma, Ependymoma, Glioblastoma, Oligodendroglioma, Medulloblas

130 Freshly isolated mouse ependymoma, glioma and choroid plexus carcinoma cells ex

131 mon and aggressive subgroup, posterior fossa ependymoma group A (PF-EPN-A), occurs in young children

132 TA-fusion associated and the posterior fossa ependymoma group A.

133 Conversely, posterior fossa ependymoma group B (PF-EPN-B) tumours display frequent l

134 low uptake in less than 50% of the tumor and ependymoma had low uptake throughout the tumor.

135 Incompletely resected EPN_PFA ependymomas have a dismal prognosis, with a 5-year progr

136 Ependymomas have a variable prognosis.

137 s and stem-like cells in medulloblastoma and ependymoma in a SOX2-dependent manner.

138 criptome of a novel model of the brain tumor ependymoma in mice to that of a subtype of the human dis

139 suboccipital craniotomy for resection of an ependymoma in the 4th ventricle.

140 of active chromatin landscapes in 42 primary ependymomas in two non-overlapping primary ependymoma co

141 Therapy for ependymoma includes aggressive surgical intervention and

142 PFA ependymomas initiate from a cell lineage in the first tr

143 Pediatric ependymoma is a devastating brain cancer marked by its r

144 Ependymoma is a heterogeneous entity of central nervous

145 Posterior fossa group A (PFA) ependymoma is a lethal brain cancer diagnosed in infants

146 Posterior fossa type A (PFA) ependymoma is a lethal pediatric brain tumor proposed to

147 Ependymoma is a locally aggressive tumor with metastatic

148 Ependymoma is a tumor of the brain or spinal cord.

149 most impactful biomarker for posterior fossa ependymoma is molecular subgroup affiliation, independen

150 Ependymoma is the third most common pediatric tumor with

151 The outcome of pediatric ependymomas is difficult to predict based on clinical an

152 shows that stereotactic IBT for intracranial ependymomas is safe and can provide a high degree of loc

153 ctivity in neuronal precursor cells leads to ependymoma-like tumours in mice.

154 an attractive alternative to microsurgery in ependymomas located in eloquent areas or as a salvage tr

155 tive therapies and patient stratification in ependymoma mandates better prognostication.

156 We conclude that cytogenetic analysis of ependymomas may help to classify these tumors and provid

157 genetic imbalances in pediatric intracranial ependymomas may help to predict clinical outcome.

158 omas, the majority of meningiomas and 1/3 of ependymomas Merlin loss is causative.

159 ssential for the survival of patient-derived ependymoma models in a group-specific manner.

160 me (n = 21), anaplastic astrocytoma (n = 3), ependymoma (n = 2), meningioma (n = 3), oligodendrogliom

161 glioma (n = 4), medulloblastoma (n = 2), and ependymoma (n = 2).

162 ma/peripheral neuroectodermal tumor (n = 6), ependymoma (n = 3), and pineal germinoma (n = 1).

163 ulloblastoma (n = 29), astrocytoma (n = 10), ependymoma (n = 5), germinoma (n = 3), atypical teratoid

164 with diagnoses of brainstem glioma (n = 6), ependymoma (n = 8), medulloblastoma/primitive neuroectod

165 ing retrospective cohorts of posterior fossa ependymomas (n = 820) were profiled using genome-wide me

166 ma, N = 1), RP1 mutations in 5.9% of tumors (ependymoma, N = 3), and ESX1 mutations in 5.9% of tumors

167 = 3), and ESX1 mutations in 5.9% of tumors (ependymoma, N = 3).

168 identified NF2 mutations in 15.7% of tumors (ependymoma, N = 7; astrocytoma, N = 1), RP1 mutations in

169 formed whole-genome sequencing of 12 tumors (ependymoma, N = 9; astrocytoma, N = 3).

170 Over half of childhood intracranial ependymomas occur in children younger than 5 years.

171 system such as schwannomas, meningiomas and ependymomas occurring spontaneously or as part of a here

172 Ependymoma occurs most frequently within the central ner

173 for molecular and cellular heterogeneity in ependymomas of the central nervous system is not underst

174 eries of mouse models, we validate eight new ependymoma oncogenes and ten new ependymoma TSGs that co

175 two with germinomas (two CRs), and one with ependymoma (one CR).

176 One patient had cerebral and caudal ependymomas, one had severe and progressive emphysema, t

177 dermal tumors, 57.8; germ cell tumors, 63.5; ependymoma or high-grade glioma, 69.8; low-grade glioma,

178 mas, whereas no mutations were identified in ependymomas or low-grade astrocytomas.

179 cted in several rare human tumors, including ependymomas, osteosarcomas, and mesotheliomas.

180 redictive marker of chemotherapy response in ependymoma patients and vardenafil, currently used to tr

181 stance, migration and invasion in paediatric ependymoma patients at non-toxic concentrations.

182 duced progression-free survival of pediatric ependymoma patients treated with such compounds.

183 ic astrocytoma and two molecular subtypes of ependymoma (PF-EPN-A, ST-EPN-RELA) using laser-extracted

184 Childhood posterior fossa group A ependymomas (PFAs) have limited treatment options and be

185 nd bear dismal prognoses compared to group B ependymomas (PFBs).

186 ioma, pituitary adenoma, Hodgkin's lymphoma, ependymoma, pineal neoplasm, rhabdomyosarcoma, and three

187 While prognostically favorable groups of ependymoma predominantly harbor differentiated cells, ag

188 YAP1 fusion-positive supratentorial ependymomas predominantly occur in infants, but the mole

189 ghty-seven pediatric patients diagnosed with ependymoma received CRT in which doses ranging from 54.0

190 estibular schwannomas, 20 meningiomas, and 2 ependymomas) received treatment with brigatinib.

191 reveal a developmental hierarchy underlying ependymomas relevant to biological and clinical behavior

192 atients develop schwannomas, meningiomas and ependymomas resulting from mutations in the tumor suppre

193 ncing analyses of human YAP1-MAMLD1-positive ependymoma reveal enrichment of NFI and TEAD transcripti

194 e and whole-exome sequencing of 47 hindbrain ependymomas reveals an extremely low mutation rate, and

195 RT-PCR sequencing of 16 childhood ependymoma samples identified SEC61G-EGFR chimeric mRNAs

196 ssion was measured in a recurrent anaplastic ependymoma, seven glioblastoma and two normal brain tiss

197 Treatment of ependymoma should include surgery with the aim of gross-

198 ociations were uncovered, including BRCA1 in ependymoma, SPIDR in HGG, SMC5 in MB, and SMARCAL1 in os

199 ZFTA-RELA fusion and EPHB2 in supratentorial ependymoma (ST-EPN).

200 s a critical event in the production of this ependymoma subgroup.

201 ouse models and in human YAP1-fusion induced ependymoma, supporting their similarity.

202 ng frame 67), which frequently occurs in PFA ependymomas, suppresses homologous recombination (HR)-me

203 Over 95% of ependymomas that arise in the cortex are driven by a gen

204 tes were observed in tumors, particularly in ependymomas that displayed prolonged stable disease on l

205 methylation level between normal control and ependymomas, the differentially methylated CpG sites are

206 85 patients had anaplastic ependymoma; the tumours of 122 were located in the infra

207 se models of group 3 medulloblastoma and PFA ependymoma, thereby providing a rationale for clinical t

208 1 fusion functions as an oncogenic driver of ependymoma through recruitment of TEADs and NFIs, indica

209 s down-regulated in the recurrent anaplastic ependymoma tissue control cell lines.

210 G and NHA cells and the recurrent anaplastic ependymoma tissue.

211 nges in assessing the response of paediatric ependymoma to clinical trial therapy.

212 he single cell transcriptional landscapes of ependymoma to define cellular programs that mediate ther

213 iation therapy (CRT) for localized childhood ependymoma to determine whether the irradiated volume co

214 refine treatment regimens for children with ependymoma to reduce the risk of complications associate

215 med neural stem cells--the cell of origin of ependymoma--to form these tumours in mice.

216 Unlike other ependymomas, transient exposure of PFA cells to ambient

217 rall survival for children with intracranial ependymoma treated with surgery, radiation therapy, and-

218 m outcome in patients harboring intracranial ependymomas treated with interstitial brachytherapy (IBT

219 e eight new ependymoma oncogenes and ten new ependymoma TSGs that converge on a small number of cell

220 ncers associated with the differentiation of ependymoma tumor cells into tumor-derived cell lineages

221 olites (163 chemical classes) from pediatric ependymoma tumor tissue microarrays (diameter: <1 mm; th

222 treatments is due to limited knowledge about ependymoma tumorigenic mechanisms.

223 methylation analysis in primary and relapsed ependymoma tumors, to identify chromosomal conformations

224 ions, YAP-MAMLD1 and C11ORF95-YAP, underlies ependymoma tumourigenesis from neural progenitor cells.

225 er and colleagues identify nine subgroups of ependymoma using DNA methylation profiles.

226 ve chromosomal copy-number aberrations in 44 ependymomas using comparative genomic hybridization.

227 esponse criteria for paediatric intracranial ependymoma vary historically and across different intern

228 red with the unexposed, the relative risk of ependymoma was not increased in the cohorts exposed as i

229 nts most likely to give rise to subgroups of ependymoma, we matched the transcriptomes of human tumou

230 entified as a molecular marker of aggressive ependymoma, we propose that the brain vascular ECM promo

231 during progression of pediatric intracranial ependymomas, we exploited a high-throughput bisulfite se

232 Patients with classic supratentorial ependymoma were observed after gross total resection (GT

233 aled that genes associated with nonrecurrent ependymoma were predominantly immune function-related.

234 ears [range 0.9-22.9 months]) with localised ependymoma were treated.

235 The medulloblastomas and ependymomas were subcategorized according to the latest

236 oblastomas, 36 Pilocytic Astrocytomas and 26 Ependymomas) were scanned using diffusion weighted imagi

237 her, NSCs generated the first mouse model of ependymoma, which is highly penetrant and accurately mod

238 a tumours, specifically medulloblastomas and ependymomas, which account for about 30% of all newly di

239 1G-EGFR chimeric mRNAs in one infratentorial ependymoma WHO III, arguing that this fusion occurs in a

240 nd April, 2003, we enrolled 89 children with ependymoma who were aged 3 years or younger at diagnosis

241 IBT were each 90% and 100% at all times for ependymomas WHO I/II, for anaplastic ependymomas WHO III

242 mes for ependymomas WHO I/II, for anaplastic ependymomas WHO III 100%, 100%, 70% and 100%, 100%, 86%,

243 Approximately 50% of children with ependymoma will suffer from tumor recurrences that will

244 investigated whether treatment of childhood ependymoma with CRT would preserve cognitive function.

245 The transcriptome of human supratentorial ependymomas with amplified EPHB2 and deleted INK4A/ARF m

246 nd recurrent group 3 medulloblastoma and PFA ependymoma xenografts in mouse models.

247 The EFS for patients with ependymoma younger than 3 years of age who received imme