ライフサイエンスコーパス: meningioma

1 our independent cohort of 140 patients with meningioma.

2 puted tomography (CT) and subsequent risk of meningioma.

3 ed with neurologic sequelae after subsequent meningioma.

4 ons for evaluation of confirmed or suspected meningioma.

5 on of brain tumours describes 15 subtypes of meningioma.

6 SSTR-targeted PRRT for treatment-refractory meningioma.

7 had no impact on patients with unresectable meningioma.

8 n the treatment of neuroendocrine tumors and meningioma.

9 ifepristone in the treatment of unresectable meningioma.

10 pigenomic, and histopathologic signatures in meningioma.

11 ing of novel strategies for aggressive human meningioma.

12 marker for worse recurrence free survival in meningioma.

13 stradiol-progestin users were diagnosed with meningioma.

14 therapy or targeted therapy for intracranial meningioma.

15 hemotherapy or targeted therapy in recurrent meningioma.

16 r between low-grade and high-grade recurrent meningioma.

17 clinical trials for patients with recurrent meningioma.

18 f molecular investigation in pathogenesis of meningioma.

19 ancers, including malignant mesothelioma and meningioma.

20 Little is known about the causes of meningioma.

21 istopathological nature and WHO grade of the meningioma.

22 observational studies to be risk factors for meningioma.

23 y being associated with an increased risk of meningioma.

24 nt for the future diagnosis and treatment of meningioma.

25 ceased, including six deaths attributed to a meningioma.

26 to identify distinct methylation classes of meningiomas.

27 le to cranial radiotherapy (CRT) -associated meningiomas.

28 cell line TRA and in human Merlin-deficient meningiomas.

29 ervous system, most notably schwannomas, and meningiomas.

30 promising approach for treatment-refractory meningiomas.

31 with the activation ratios in metastases and meningiomas.

32 ations in AKT3, PIK3R1, PRKAR1A, and SUFU in meningiomas.

33 eptors are expressed in approximately 70% of meningiomas.

34 might serve as a novel therapeutic target in meningiomas.

35 has recently been introduced for imaging of meningiomas.

36 PRC binding to DNA methylation in malignant meningiomas.

37 extent of epigenetic alteration in malignant meningiomas.

38 ntifiable orthotopic model for NF2-deficient meningiomas.

39 biquitin ligase, in nearly one-fourth of all meningiomas.

40 observed in patients with primary gliomas or meningiomas.

41 ten benign, five atypical and four malignant meningiomas.

42 molecular landscapes of medulloblastomas and meningiomas.

43 central nervous system tumors in adults are meningiomas.

44 uggest that AR-42 is a potential therapy for meningiomas.

45 ng, were identified in ~5% of non-NF2 mutant meningiomas.

46 destly successful in patients with recurrent meningiomas.

47 targeted therapy treatments for intracranial meningiomas.

48 antly higher risk of recurrence and death in meningiomas.

49 and CD45(+) immune infiltrating cells in all meningiomas.

50 suggest that e-HRT may be safe in incidental meningiomas.

51 86 spatially-distinct samples from 13 human meningiomas.

52 haracteristic imaging features described for meningiomas.

53 litate informative radiological reporting of meningiomas.

54 pected shared pathogenesis with intracranial meningiomas.

55 7, the same location for causal mutations of meningiomas.

56 etween patients, especially tumor perfusion (meningioma, 0.1-1 mL.g(-1).min(-1), and NETs, 0.02-1 mL.

57 Meningioma-1 (MN1) overexpression is frequently observed

58 ]), incidental findings were found, of which meningiomas (143 of 5800; 2.5% [95% CI: 2.1%, 2.9%]) and

59 schwannomas (1011 [20.6%] of 4905 patients), meningiomas (1490 [30.4%]), arteriovenous malformations

60 r, population-based US case-control study of meningioma (2006-2009).

61 Most common diagnoses were meningioma (37%) and high-grade glioma (20%).

62 98 and 460.22 voxels +/- 276.83; P = .15) or meningiomas (424.07 voxels +/- 247.58 and 415.18 voxels

63 02-1 mL.g(-1).min(-1)) and receptor density (meningioma, 5-34 nmol.L(-1), and NETs, 7-35 nmol.L(-1)).

64 hemangioma (72.7%) followed by orbital sheet meningioma (9.1%).

65 In the past she had encephalic meningiomas, a tongue schwannoma and bilateral acoustic

66 Meningiomas account for one-third of all primary brain t

67 ittle evidence of an increase in the risk of meningioma, acoustic neuroma, or parotid gland tumors in

68 armacological approaches to treat refractory meningiomas across all WHO grades.

69 stically significant increase in the risk of meningioma after exposure to CT of the head (HR: 1.49; 9

70 fteen patients with recurrent or progressive meningiomas after multimodal pretreatment or unfavorable

71 We retrospectively collected 497 meningiomas along with 309 samples of other extra-axial

72 atients (38%) had a predisposing mutation to meningioma and 27 of 135 patients (20%) to schwannoma, r

73 mol (118 +/- 71 mug) and 4.2 +/- 1.8 GBq for meningioma and 87 +/- 50 nmol (135 +/- 78 mug) and 5.1 +

74 d iterative gene discovery for glioblastoma, meningioma and breast cancer, using a sequentially augme

75 e sought to characterize PD-L1 expression in meningioma and elucidate its regulatory mechanisms.

76 g immune complexes, which were found both in meningioma and healthy blood donor sera.

77 implemented as a routine diagnostic test in meningioma and integrated into the WHO classification.

78 increased proliferation of merlin-deficient meningioma and mesothelioma.

79 ldhood Cancer Survivor Study, a diagnosis of meningioma and onset of neurologic sequelae were ascerta

80 of 111 patients who had treatment-refractory meningioma and received SSTR-targeted PRRT.

81 bpopulation of patients with an unresectable meningioma and refractory to radiotherapy, hormonal chem

82 e develop a human cerebral organoid model of meningioma and validate the high ADC marker genes CDH2 a

83 unotherapy for a large animal model of human meningioma and warrant further development toward human

84 In all schwannomas, the majority of meningiomas and 1/3 of ependymomas Merlin loss is causat

85 s of the nervous system such as schwannomas, meningiomas and ependymomas occurring spontaneously or a

86 matosis type 2 patients develop schwannomas, meningiomas and ependymomas resulting from mutations in

87 s of the nervous system such as schwannomas, meningiomas and ependymomas.

88 er cranial and peripheral nerves, as well as meningiomas and ependymomas.

89 erized by formation of multiple schwannomas, meningiomas and ependymomas.

90 whole-genome or whole-exome sequencing on 17 meningiomas and focused sequencing on an additional 48 t

91 ts a study of the uptake of (90)Y-DOTATOC in meningiomas and high-grade gliomas (HGGs) and a feasibil

92 efine the spectrum of genetic alterations in meningiomas and identify potential therapeutic targets.

93 m measures of CP and CS between fibroblastic meningiomas and other subtypes were observed (P<.01).

94 sh the genomic landscape of primary atypical meningiomas and potential therapeutic targets.

95 Meningiomas and schwannomas are usually sporadic, isolat

96 SWI/SNF complex in the pathogenesis of both meningiomas and tumors with clear-cell histology.

97 The majority of meningiomas and virtually all aneurysms not referred or

98 l nerves (vestibular schwannomas), meninges (meningiomas), and spinal cord (ependymomas).

99 d cancer suggest a decreased risk of glioma, meningioma, and acute lymphoblastic leukemia in patients

100 ly increased risks of oral cancer, melanoma, meningioma, and leukemia.

101 l was created for tumor types (i.e., glioma, meningioma, and pituitary), which were discriminated wit

102 t malignancies, 0.16 (95% CI, 0.06-0.41) for meningiomas, and 1.71 (95% CI, 0.88-3.33) for nonmelanom

103 sms, including 1026 malignancies, 233 benign meningiomas, and 1856 nonmelanoma skin cancers.

104 19 nonmelanoma skin cancers, 21 nonmalignant meningiomas, and 43 other benign neoplasms.

105 plastic disease associated with schwannomas, meningiomas, and ependymomas and that is caused by inact

106 th reduced risk for subsequent malignancies, meningiomas, and nonmelanoma skin cancers.

107 between gray matter, white matter, gliomas, meningiomas, and pituitary tumors, allowing their ready

108 Although typically benign, about 20% of meningiomas are aggressive, and despite the rigor of the

109 Meningiomas are central nervous system tumors that origi

110 Meningiomas are known to express somatostatin receptor 2

111 Multiple schwannomas and/or meningiomas are more frequently associated with a tumor

112 Meningiomas are mostly benign brain tumours, with a pote

113 Most meningiomas are pathologically benign or atypical, but 3

114 Meningiomas are primary tumors of the central nervous sy

115 Malignant and atypical meningiomas are resistant to standard therapies and asso

116 Although meningiomas are the most common intracranial tumours, th

117 Meningiomas are the most common primary brain tumor and

118 Meningiomas are the most common primary intracranial tum

119 Meningiomas are the most common primary nervous system t

120 Meningiomas are the most common primary non-glial intrac

121 Meningiomas are the second most common neoplasm in NF2,

122 e show the clinical significance of PD-L1 in meningioma as a marker that can predict tumor recurrence

123 c inhibitors, may prove useful in refractory meningiomas as recently demonstrated with sunitinib and

124 s, spine tumors, pediatric brain tumors, and meningiomas, as well as other clinical trial end points,

125 on also occur in spontaneous schwannomas and meningiomas, as well as other types of cancer including

126 oredoxin domain containing 16 (TXNDC16) as a meningioma-associated Ag by protein macroarray screening

127 Conclusion When prevalent cases of meningioma at first exposure to CT of the head are exclu

128 sifier was built to discriminate gliomas and meningiomas based on 36 glioma and 19 meningioma samples

129 We treated 11 meningioma-bearing dogs with surgery and vaccine immunot

130 take in HGGs was significantly worse than in meningiomas but was still acceptable for RGS, particular

131 ch as renal cell carcinoma, mesothelioma and meningioma, but not uveal melanoma.

132 F2 is disrupted in approximately half of all meningiomas, but the complete spectrum of genetic change

133 In HGGs, the uptake was lower than in meningiomas, but the tumor-to-nontumor ratio was higher

134 The cumulative incidence of a subsequent meningioma by age 40 years was 5.6% (95% CI, 4.7% to 6.7

135 In addition, meningiomas can occur in a variety of unusual intracrani

136 However, all 12 meningioma cases among men were classified as unexposed

137 and 131,248 estradiol-progestin users), and meningioma cases were identified from the Finnish Cancer

138 Our studies on several meningioma cell lines cultured in hypoxic conditions val

139 hat telomerase-immortalized Ben-Men-1 benign meningioma cells harbored a single nucleotide deletion i

140 ll-cycle progression of normal meningeal and meningioma cells may have implications for why AR-42 is

141 ome screen in NF2-null human arachnoidal and meningioma cells, we showed activation of EPH RTKs, c-KI

142 egulated proteins in miR-200a-overexpressing meningioma cells.

143 d: adenocarcinoma, adenoid cystic carcinoma, meningioma, chondrosarcoma and fibromyxoid sarcoma.

144 INTERPRETATION: DNA methylation-based meningioma classification captures clinically more homog

145 to a better understanding of NF2-associated meningiomas clinical behavior and their genetic underpin

146 In the solitary meningioma cohort, 34 of 63 patients (54%) had a constit

147 These results indicate that men with meningioma commonly react with a serologic antimeningiom

148 2) were associated with an increased risk of meningioma compared with CRT doses of 1.5 to 19.9 Gy ( P

149 f the transosseous extension of intracranial meningiomas compared with CE-MRI.

150 ical and anaplastic meningiomas from typical meningiomas consisted of mean and skewness of SK and kur

151 Meningiomas constitute about 34% of primary intracranial

152 We queried the NorthShore Meningioma Database for patients with >= 6 months of e-H

153 he benign tumors, the atypical and malignant meningiomas demonstrate increased global DNA hypomethyla

154 With a median follow-up of 72 months after meningioma diagnosis (range, 3.8 to 395 months), 22 part

155 The median interval from primary cancer to meningioma diagnosis was 22 years (5 to 37 years).

156 e CE-MRI within 30 d and pathology-confirmed meningioma diagnosis with inclusion or exclusion of tran

157 Within 6 months before or subsequent to a meningioma diagnosis, 20% (30 of 149) reported at least

158 Our findings identify multiple-spinal-meningioma disease as a new discrete entity and establis

159 t the majority of primary (de novo) atypical meningiomas display loss of NF2, which co-occurs either

160 Importantly, these primary atypical meningiomas do not harbour TERT promoter mutations, whic

161 tools for treating progressive unresectable meningioma, especially in cases of high tracer uptake in

162 Consistent with this observation, atypical meningiomas exhibit upregulation of EZH2, the catalytic

163 sed to CRT and subsequently diagnosed with a meningioma experience significant neurologic morbidity.

164 Meningiomas express members of the somatostatin receptor

165 we consider the estimated odds ratio (OR) of meningioma for each genetic instrument.

166 offers high diagnostic accuracy to delineate meningioma from tumor-free tissue even in recurrent tumo

167 DNA methylation data clearly segregated all meningiomas from other skull tumours.

168 best model for differentiating fibroblastic meningiomas from other subtypes consisted of skewness of

169 ated genome-wide DNA methylation patterns of meningiomas from ten European academic neuro-oncology ce

170 for differentiating atypical and anaplastic meningiomas from typical meningiomas consisted of mean a

171 Survivors reporting a meningioma had increased risks of neurologic sequelae >

172 egistry; however, one-third of patients with meningioma had to be excluded because they either had a

173 Most meningiomas had simple genomes, with fewer mutations, re

174 However, several meningiomas harbored more complex patterns of copy-numbe

175 Pharmacotherapy for meningiomas has remained largely experimental.

176 Cystic changes in meningiomas have been divided into five subtypes, and ac

177 summary, our results suggest that malignant meningiomas have distinct DNA methylation patterns compa

178 In most cases, meningiomas have typical imaging appearances and locatio

179 vival rates were above 90% for patients with meningioma, Hodgkin lymphoma, thyroid carcinoma, basal c

180 ARCE1 in six further individuals with spinal meningiomas identified two additional heterozygous loss-

181 Incidental meningiomas (IMs) are the most common intracranial neopl

182 finding suggests a distinctive etiology for meningioma in men.

183 he long arm of chromosome 22 (22q) result in meningiomas in neural-crest cell-derived meninges, while

184 h rates of ten spinal and ten cranial benign meningiomas in seven NF2 patients that concluded with su

185 signaling, TRAF7, KLF4, and POLR2A result in meningiomas in the mesodermal-derived meninges of the mi

186 n between postmenopausal hormone therapy and meningioma incidence in Finland.

187 'Typical' meningiomas include meningothelial, fibrous, and transit

188 ossible variations in imaging appearances of meningiomas including the differential features of commo

189 iochemical analyses revealed that aggressive meningiomas involve loss of the repressor function of th

190 Spontaneous canine meningioma is a clinically meaningful but underutilized

191 Meningioma is an intracranial tumor with few confirmed r

192 The provisional diagnosis of meningioma is mainly made by MRI.

193 icance and regulatory mechanisms of PD-L1 in meningioma is not yet fully characterized.

194 Management of clinically aggressive meningiomas is a considerable challenge.

195 Transosseous extension of intracranial meningiomas is known to be an important risk factor for

196 endations for the diagnosis and treatment of meningiomas is low compared with other tumours such as h

197 hogenesis and the anatomical distribution of meningiomas is presented alongside existing understandin

198 The standard treatment of meningiomas is surgery or radiotherapy.

199 A subset of meningiomas lacking NF2 alterations harbored recurrent o

200 udy other diseases within the CPA, including meningiomas, lipomas, vascular malformations, hemangioma

201 an important role for (68)Ga-DOTATATE PET in meningioma management.

202 edian, 0.79; range, 0.28-1.66; P = .043) and meningiomas (median, 0.91; range, 0.52-2.05; P < .01).

203 Conversely, our data show that benign meningiomas (MENs), which contain less water than brain

204 NF2-associated VSs are often accompanied by meningioma (MN), and the majority of NF2 patients show l

205 Meningiomas (MNs), arising from the arachnoid/meningeal

206 rathyroid, lung, and unknown primary tumors, meningioma, mycosis fungoides, and myeloid leukemia.

207 orme (GBM) (n = 20), metastasis (n = 21), or meningioma (n = 22).

208 mber 31, 2016, on presentation with a single meningioma (n = 42) or schwannoma (n = 135) before age 2

209 s of patients who presented with an isolated meningioma (n = 42; median [range] age, 11 [1-24] years;

210 Patients with transosseous extension of meningioma (n = 67) showed significantly larger lesions

211 with neuroendocrine tumors (NETs; n = 21) or meningioma (n = 8) after the administration of (177)Lu-D

212 ), white matter (n = 66), gliomas (n = 158), meningiomas (n = 111), and pituitary tumors (n = 154) fr

213 ; P = 0.011) than patients with extraosseous meningiomas (n = 15).

214 Rarely, meningiomas occur at multiple sites, usually occurring i

215 Meningiomas often express estrogen receptors, which were

216 a has been implicated in the pathogenesis of meningiomas, one of the most common central nervous syst

217 d from time of exposure to the occurrence of meningioma or death or until December 31, 2010, with log

218 urements ((111)In-DOTATATE) of patients with meningioma or neuroendocrine tumors (NETs).

219 excluded because they either had a prevalent meningioma or other brain tumor at the first CT examinat

220 people with an apparently sporadic solitary meningioma or schwannoma had a causative predisposition

221 Young patients presenting with a solitary meningioma or schwannoma should be referred for genetic

222 and young adults presenting with a solitary meningioma or schwannoma.

223 termine the frequency of the known heritable meningioma- or schwannoma-predisposing mutations in chil

224 yielded comparable results for extraosseous meningiomas (P = 0.132) and the extraosseous part of tra

225 2) and the extraosseous part of transosseous meningiomas (P = 0.636), whereas the volume of the intra

226 l and anaplastic meningiomas than in typical meningiomas (P<.01).

227 esis of the human meninges in the context of meningioma pathogenesis and anatomical distribution.

228 To identify how miR-200a contributes to meningioma pathogenesis at the molecular level, we used

229 estimated on (68)Ga-DOTATOC PET scans of 11 meningioma patients and 12 HGG patients.

230 nome-wide association study comprising 1,606 meningioma patients and 9,823 controls.

231 All meningioma patients but one with an atypical extracrania

232 e is potentially very useful for stratifying meningioma patients to observation-only or adjuvant trea

233 ta-analysis, including all published data on meningioma patients treated with SSTR-targeted PRRT.

234 utoantibodies against TXNDC16 exclusively in meningioma patients' sera and not in sera of healthy con

235 In meningioma patients, TBR was higher in rCBV maps than in

236 f somatostatin-based radiopeptide therapy in meningioma patients.

237 Petroclival meningiomas (PCMs) are regarded as one of the most formi

238 lar or other benign schwannomas, WHO grade 1 meningiomas, pituitary adenomas, and haemangioblastoma.

239 th rate of NF2-associated spinal and cranial meningiomas point to the differences in timing of tumor

240 s or other features of known schwannoma- and meningioma-predisposing syndromes.

241 4%) had a constitutional mutation in a known meningioma predisposition gene.

242 nt diffusion coefficient (ADC) distinguishes meningioma regions with proliferating cells enriched for

243 lmic findings after pterional craniotomy for meningioma removal or aneurysm clipping.

244 been linked to uveal melanoma, mesothelioma, meningioma, renal cell carcinoma and basal cell carcinom

245 4.7%, 7.9% and 15.4% of WHO-I/WHO-II/WHO-III meningiomas, respectively.

246 abnormality in metastases (rho = -0.50) and meningiomas (rho = -0.55).

247 Recent research points to an impact on meningioma risk from factors related to immune function

248 Lead exposure was positively associated with meningioma risk in women only (n = 38 unexposed and 9 ex

249 factors, and assessed their association with meningioma risk using data from a genome-wide associatio

250 lated traits to assess the relationship with meningioma risk using Mendelian randomization (MR), an a

251 = 1.28, 95% CI = 1.01-1.63, P = 0.042) with meningioma risk, albeit non-significant after correction

252 nship between the obesity-related traits and meningioma risk, we consider the estimated odds ratio (O

253 We determined the cellular composition of 51 meningioma samples by multiparameter flow cytometric (MF

254 of different cell populations coexisting in meningioma samples, with a more accurate measure of gene

255 e-wide DNA methylation profiles from all 497 meningioma samples.

256 as and meningiomas based on 36 glioma and 19 meningioma samples.

257 dy reactivity, we achieved discrimination of meningioma sera from healthy controls with an accuracy o

258 Some specific entities such as JNA and meningioma showed distinctive diffusion characteristics.

259 istochemical staining of PD-L1 expression in meningiomas showed 43% positivity in both tumor and immu

260 antibodies bound allogeneic canine and human meningiomas, showing common antigens across breed and sp

261 Among typical meningiomas, significant differences in histogram measur

262 apy was associated with an increased risk of meningioma (standardized incidence ratio = 1.29, 95% con

263 tumorigenesis and define mutually exclusive meningioma subgroups with distinct clinical and patholog

264 llectively, these findings identify distinct meningioma subtypes, suggesting avenues for targeted the

265 ith hypermethylated CpG islands in malignant meningiomas (such as HOXA6 and HOXA9) tend to coincide w

266 oters are suppressed in malignant and benign meningiomas, suggesting the switching of gene silencing

267 The meningioma task force of the European Association of Neu

268 nificantly higher in atypical and anaplastic meningiomas than in typical meningiomas (P<.01).

269 pite previous studies on benign and atypical meningiomas, the key molecular pathways involved in mali

270 We report genomic analysis of 300 meningiomas, the most common primary brain tumors, leadi

271 nes CDH2 and PTPRZ1 as potential targets for meningioma therapy using live imaging, single cell RNA s

272 (68)Ga-DOTATATE PET/CT enables detection of meningioma tissue based on somatostatin receptor 2 expre

273 of the entire molecular genetic landscape of meningioma to identify biologically and clinically relev

274 and epigenomic analyses, we compared benign meningiomas to atypical ones.

275 ation phenotype in these cells and inhibited meningioma tumor growth in mice.

276 uthors assessed individual seroreactivity to meningioma tumor-associated antigens among participants

277 cranial tumors, but the molecular drivers of meningioma tumorigenesis are poorly understood.

278 included oligodendroglioma, astrocytoma, and meningioma tumors of different histological grades and t

279 kull tumours that might histologically mimic meningioma variants.

280 Tracer uptake values and meningioma volumes were determined.

281 The risk of meningioma was assessed by using data from the Swedish C

282 tatistically significant increase in risk of meningioma was found among exposed subjects compared wit

283 NA) showed distinctly high ADC values, while meningioma was the only benign lesion with restricted di

284 Uptake of (90)Y-DOTATOC in meningiomas was high in all studied patients.

285 To understand the function of these genes in meningioma, we develop a human cerebral organoid model o

286 n of next-generation genomic analyses of 775 meningiomas, we report that recurrent somatic p.Gln403Ly

287 cerides and waist circumference with risk of meningioma were non-significant.

288 nd LZTR1 gene mutations, while patients with meningioma were screened for NF2, SMARCB1, SMARCE1, and

289 Patients with progressive unresectable meningioma were treated with (90)Y-DOTATOC and (177)Lu-D

290 These non-NF2 meningiomas were clinically distinctive-nearly always be

291 Results One hundred ninety-nine meningiomas were identified among 169 participants.

292 For comparison, 8 patients with meningiomas were included.

293 s with primary (n = 12) or recurrent (n = 9) meningiomas were prospectively enrolled.

294 e atypical, three anaplastic, and 39 typical meningiomas were retrospectively studied.

295 en linked to increased risk of recurrence in meningiomas, whereas the association to mortality largel

296 ing second- or third-line option for complex meningiomas, which are progressive or otherwise not trea

297 sequent high-grade gliomas and 57.3-100% for meningiomas, which are similar rates to those observed i

298 In contrast, meningiomas with mutant NF2 and/or chromosome 22 loss we

299 ed individuals with familial multiple spinal meningiomas without NF2 mutations.

300 T examination were not excluded, the risk of meningioma would have been falsely increased (HR: 2.28;

301 at investigating intratumor heterogeneity in meningiomas would elucidate biologic drivers and reveal