ライフサイエンスコーパス: meningioma

1 nt for the future diagnosis and treatment of meningioma.

2 had no impact on patients with unresectable meningioma.

3 ifepristone in the treatment of unresectable meningioma.

4 ing of novel strategies for aggressive human meningioma.

5 ceased, including six deaths attributed to a meningioma.

6 stradiol-progestin users were diagnosed with meningioma.

7 therapy or targeted therapy for intracranial meningioma.

8 hemotherapy or targeted therapy in recurrent meningioma.

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

10 clinical trials for patients with recurrent meningioma.

11 ccompanied with a slightly increased risk of meningioma.

12 risk (P = .03) for rate of mortality after a meningioma.

13 r incidentally discovered, clinically silent meningioma.

14 our independent cohort of 140 patients with meningioma.

15 therefore, HRT use may be a risk factor for meningioma.

16 therapy (HRT) as a possible risk factor for meningioma.

17 herbicide exposures and risk for glioma and meningioma.

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

19 ed with neurologic sequelae after subsequent meningioma.

20 ons for evaluation of confirmed or suspected meningioma.

21 on of brain tumours describes 15 subtypes of meningioma.

22 eptors are expressed in approximately 70% of meningiomas.

23 might serve as a novel therapeutic target in meningiomas.

24 has recently been introduced for imaging of meningiomas.

25 PRC binding to DNA methylation in malignant meningiomas.

26 extent of epigenetic alteration in malignant meningiomas.

27 ntifiable orthotopic model for NF2-deficient meningiomas.

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

29 observed in patients with primary gliomas or meningiomas.

30 ten benign, five atypical and four malignant meningiomas.

31 molecular landscapes of medulloblastomas and meningiomas.

32 central nervous system tumors in adults are meningiomas.

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

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

35 destly successful in patients with recurrent meningiomas.

36 targeted therapy treatments for intracranial meningiomas.

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

38 onal, 14 meningothelial, and two angiomatous meningiomas.

39 he imprinting control region of MEG3 gene in meningiomas.

40 7, the same location for causal mutations of meningiomas.

41 providing insights into novel therapies for meningiomas.

42 r SNs, including nonmelanoma skin cancer and meningiomas.

43 identified within metastatic lung tumors and meningiomas.

44 been identified as the initial event in many meningiomas.

45 pected shared pathogenesis with intracranial meningiomas.

46 to identify distinct methylation classes of meningiomas.

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

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

49 ervous system, most notably schwannomas, and meningiomas.

50 with the activation ratios in metastases and meningiomas.

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

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

53 o determine the prognostic importance of the meningioma 1 (MN1) gene expression levels in the context

54 We showed previously that meningioma 1 (MN1) is a novel target of 1,25(OH)(2)D(3)

55 Meningioma-1 (MN1) overexpression is frequently observed

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

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

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

59 98 and 460.22 voxels +/- 276.83; P = .15) or meningiomas (424.07 voxels +/- 247.58 and 415.18 voxels

60 02-1 mL.g(-1).min(-1)) and receptor density (meningioma, 5-34 nmol.L(-1), and NETs, 7-35 nmol.L(-1)).

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

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

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

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

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

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

67 In addition, 66 cases of meningioma and 1,007 cases of nonmelanoma skin cancer we

68 9 typical meningiomas included one secretory meningioma and 11 fibroblastic, 11 transitional, 14 meni

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

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

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

72 er syndrome seem to be at increased risk for meningioma and childhood brain tumours, and possibly bla

73 ere is an association between a diagnosis of meningioma and either current or past HRT use in women.

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

75 There was no association between meningioma and herbicide or insecticide exposure among m

76 positive association between a diagnosis of meningioma and HRT use, with an odds ratio of 2.2 (95% C

77 increased proliferation of merlin-deficient meningioma and mesothelioma.

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

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

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

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

82 rain or spinal cord neoplasms, including 137 meningiomas and 73 gliomas in a young adult population.

83 Downregulation of miR-200a in meningiomas and arachnoidal cells resulted in increased

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

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

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

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

90 factors affecting survival in second primary meningiomas and gliomas that developed in survivors incl

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 association between HRT use and diagnosis of meningioma, and therefore, HRT use may be a risk factor

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

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

105 19 nonmelanoma skin cancers, 21 nonmalignant meningiomas, and 43 other benign neoplasms.

106 ervous system tumors, including schwannomas, meningiomas, and ependymomas.

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

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

109 Malignant meningiomas are associated with less than 2 years median

110 Meningiomas are central nervous system tumors that origi

111 Meningiomas are common tumors, representing 15% to 25% o

112 Meningiomas are known to express somatostatin receptor 2

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

114 Meningiomas are mostly benign brain tumours, with a pote

115 Most meningiomas are pathologically benign or atypical, but 3

116 Meningiomas are primary tumors of the central nervous sy

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

118 Although meningiomas are the most common intracranial tumours, th

119 Meningiomas are the most common primary nervous system t

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

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

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

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

124 We identified a new susceptibility locus for meningioma at 10p12.31 (MLLT10, rs11012732, odds ratio =

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

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

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

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

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

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

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

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

133 o data exist that examine gene expression in meningioma by hormone receptor status.

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

135 are the first to examine gene expression for meningioma cases by hormone receptor status and indicate

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

137 Elevated levels of miR-200a inhibited meningioma cell growth in culture and in a tumor model i

138 e majority of human meningiomas or the human meningioma cell lines IOMM-Lee and CH157-MN.

139 2 missense mutations into NF2 gene-deficient meningioma cell lines revealed that merlin loss of funct

140 Merlin-deficient human meningioma cells and merlin knockdown arachnoidal cells,

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

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

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

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

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

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 cides had a significantly increased risk for meningioma compared with women who never used herbicides

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

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

152 Meningiomas constitute about 34% of primary intracranial

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

154 es our understanding of the genetic basis of meningioma development.

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

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

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

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

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

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

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

162 ervous system tumors, including schwannomas, meningiomas, ependymomas, and astrocytomas.

163 develop nervous system tumours (schwannomas, meningiomas, ependymomas, astrocytomas, and neurofibroma

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

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

166 ells, the nonneoplastic cell counterparts of meningiomas, exhibit rapamycin-sensitive constitutive mT

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

168 Meningiomas express members of the somatostatin receptor

169 iforme (GBM), metastatic lung carcinoma, and meningioma for markers known to be expressed on immunore

170 Five recurrent and progressive meningiomas for which surgical specimens were available

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

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

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

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

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

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

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

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

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

180 An association between hormones and meningioma has been postulated.

181 Pharmacotherapy for meningiomas has remained largely experimental.

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

183 and tested against nonprogressive high-grade meningiomas, high-grade gliomas, and nontumor brain spec

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

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

186 or machine showed the ability to distinguish meningioma image spectra from the nontumor brain and fro

187 finding suggests a distinctive etiology for meningioma in men.

188 The frequency of meningioma in women with either current or past HRT use

189 was 865 in 100,000, whereas the frequency of meningioma in women without the history of HRT use was 3

190 benign neurological tumors, schwannomas and meningiomas, in humans; however, mutations in murine Nf2

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

192 The 39 typical meningiomas included one secretory meningioma and 11 fib

193 ity to predict recurrence and progression of meningiomas induces significant anxiety for patients and

194 Spontaneous canine meningioma is a clinically meaningful but underutilized

195 Meningioma is an intracranial tumor with few confirmed r

196 tion, although survival after second primary meningioma is good.

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

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

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

200 The standard treatment of meningiomas is surgery or radiotherapy.

201 A subset of meningiomas lacking NF2 alterations harbored recurrent o

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

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

204 Here, we define a typical human meningioma microRNA (miRNA) profile and characterize the

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

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

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

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

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

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

211 he CNS (n=13; 4.3 [2.3-7.4]), especially for meningioma (n=7; 12.0 [4.8-24.8]) and childhood brain tu

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 o defined role for adjuvant chemotherapy for meningioma of any grade following initial diagnosis.

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

217 Meningiomas, one of the most common human brain tumors,

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

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

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

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

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

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

224 G3 is not expressed in the majority of human meningiomas or the human meningioma cell lines IOMM-Lee

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

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

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

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

229 rmalities of 14q32 are often associated with meningioma pathogenesis and progression; therefore, it h

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

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

232 All meningioma patients but one with an atypical extracrania

233 Cases were 462 glioma and 195 meningioma patients diagnosed between 1994 and 1998 in t

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

235 The data are surgical specimens from 31 meningioma patients undergoing neurosurgical resection a

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

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

238 f somatostatin-based radiopeptide therapy in meningioma patients.

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

240 4%) had a constitutional mutation in a known meningioma predisposition gene.

241 pressor gene at chromosome 14q32 involved in meningioma progression via a novel mechanism.

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

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

244 Often considered benign, meningiomas represent 32% of intracranial tumors with th

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

246 The authors examined incident glioma and meningioma risk associated with occupational exposure to

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

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

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

252 nd the upregulation of beta-catenin in human meningioma samples.

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

254 ALT in medulloblastomas, oligodendrogliomas, meningiomas, schwannomas, and pediatric glioblastoma mul

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

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

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

258 Among typical meningiomas, significant differences in histogram measur

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

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

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

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

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

264 The meningioma task force of the European Association of Neu

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

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

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

268 a multifunctional tumor suppressor miRNA in meningiomas through effects on the E-cadherin and Wnt/be

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

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

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

272 y unrecognized signaling cascade involved in meningioma tumor development and highlights a novel mole

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

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

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

276 kull tumours that might histologically mimic meningioma variants.

277 Tracer uptake values and meningioma volumes were determined.

278 erapy for at least 3 years, the incidence of meningioma was 1.40-fold higher (95% confidence interval

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

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

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

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

283 Five-year relative survival after meningiomas was similar for males (84.0%; 95% CI, 72.6%

284 To identify susceptibility loci for meningioma, we conducted a genome-wide association study

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

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

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

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

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

290 ry of symptomatic or incidentally discovered meningiomas were identified, 156 (11%) of whom were eith

291 For comparison, 8 patients with meningiomas were included.

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

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

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

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

296 an help determine the grades and subtypes of meningiomas, which can better assist in surgical plannin

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

298 c loss at the MEG3 locus is also observed in meningiomas, with increasing prevalence in higher grade

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;