ライフサイエンスコーパス: ependymoma

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

2 alignancies, including glial cell neoplasms (ependymomas).

3 ldren younger than 3 years with intracranial ependymoma.

4 ent of very young children with intracranial ependymoma.

5 thin 28 recurrent chromosomal alterations in ependymoma.

6 tential therapeutic target in supratentorial ependymoma.

7 ous deletions of genes not yet implicated in ependymoma.

8 el polyomaviruses were found in nonrecurrent ependymoma.

9 with longer time to progression in recurrent ependymoma.

10 system such as schwannomas, meningiomas and ependymomas.

11 ly all schwannomas, and many meningiomas and ependymomas.

12 es and increased survival in mouse models of ependymomas.

13 rocytomas, 10 pediatric astrocytomas, and 13 ependymomas.

14 olved in the pathogenesis of meningiomas and ependymomas.

15 eripheral nerves, as well as meningiomas and ependymomas.

16 not other astrocytomas, medulloblastomas, or ependymomas.

17 ion of multiple schwannomas, meningiomas and ependymomas.

18 ilocytic astrocytomas, medulloblastomas, and ependymomas.

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

20 e aggressive primary tumors and the relapsed ependymomas.

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

22 ors, including schwannomas, meningiomas, and ependymomas.

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

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

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

26 8.9 months, respectively; P = .0006) but not ependymoma (19.5 v 13.3 months, respectively; P = .19).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Ependymomas are chemotherapy-resistant brain tumours, wh

50 Ependymomas are common childhood brain tumours that occu

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

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

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

54 Intracranial ependymomas are segregated on the basis of anatomical lo

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

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

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

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

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

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

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

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

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

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

65 Posterior fossa ependymoma comprises two distinct molecular variants ter

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

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

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

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

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

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

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

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

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

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

76 Ependymomas have a variable prognosis.

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

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

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

80 Therapy for ependymoma includes aggressive surgical intervention and

81 Ependymoma is a locally aggressive tumor with metastatic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 Ependymoma occurs most frequently within the central ner

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 85 patients had anaplastic ependymoma; the tumours of 122 were located in the infra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 The medulloblastomas and ependymomas were subcategorized according to the latest

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

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

136 1G-EGFR chimeric mRNAs in one infratentorial ependymoma WHO III, arguing that this fusion occurs in a

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

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

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

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

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

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