ライフサイエンスコーパス: schwannoma

1 resection for acoustic neuromas (vestibular schwannomas).

2 ongly overexpressed and basally activated in schwannoma.

3 with the cellular features of her plexiform schwannoma.

4 lts presenting with a solitary meningioma or schwannoma.

5 e, 8 leiomyosarcoma, 1 hepatoblastoma, and 1 schwannoma.

6 , occurring in one out of every six men with schwannoma.

7 l, cell-matrix adhesion and proliferation of schwannoma.

8 wannomas (VS) and 38 schwannomatosis-related schwannomas.

9 ciatic nerve to mimic central and peripheral schwannomas.

10 on of the NF2 gene occurs in the majority of schwannomas.

11 endothelial growth factor (VEGF) therapy in schwannomas.

12 n 28 out of 34 (82%) schwannomatosis-related schwannomas.

13 ion in the volume of most growing vestibular schwannomas.

14 eurofibromatosis type 2 and from 22 sporadic schwannomas.

15 nd the cardinal sign is bilateral vestibular schwannomas.

16 lling Rac activity as a possible therapy for schwannomas.

17 entation, myxomatosis, endocrine tumors, and schwannomas.

18 alignant peripheral nerve sheath tumours and schwannomas.

19 endocrine tumours and psammomatous melanotic schwannomas.

20 ytoma, 8 glioblastomas, 6 meningiomas, and 2 schwannomas.

21 , showed expression of these proteins in all schwannomas.

22 (3.0%) and not at all in gangliogliomas and schwannomas.

23 zed by the occurrence of multiple peripheral schwannomas.

24 d by the development of bilateral vestibular schwannomas.

25 rmine genomic aberrations common to sporadic schwannomas.

26 of tested patients with hybrid neurofibromas/schwannomas.

27 ic and therapeutic studies of NF2-associated schwannomas.

28 e performed in nine patients with vestibular schwannomas.

29 rve tumors histologically identical to human schwannomas.

30 including desmoid fibromatosis (0 of 17) and Schwannoma (0 of 3), were immunonegative for DOG1.

31 s: 97 neurofibromatosis type 2 (NF2)-related schwannomas, 104 sporadic vestibular schwannomas (VS) an

32 Of 109 cranial schwannomas, 106 (97.2%) were vestibular.

33 f 8 astrocytomas, 2 of 2 meningiomas, 3 of 3 schwannomas, 2 of 2 medulloblastomas, 1 of 1 neurofibrom

34 A mouse model with a murine schwannoma allograft was also used to examine the antitu

35 Furthermore, schwannomas also commonly develop in other cranial nerve

36 ast she had encephalic meningiomas, a tongue schwannoma and bilateral acoustic neurinomas.

37 ch is known to be under merlin regulation in schwannoma and is involved in increased proliferation of

38 neurofibromatosis 2 (NF2) gene are linked to schwannoma and meningioma tumorigenesis.

39 The most common types include schwannoma and neurofibroma.

40 rs and is a potential therapeutic target for schwannoma and other merlin-deficient tumours.

41 oma had an LZTR1 mutation (3 were vestibular schwannomas and 1 was a nonvestibular schwannoma), and 9

42 angliogliomas, 41 meningiomas, 10 vestibular schwannomas and 31 pituitary adenomas.

43 ominant cause in the development of sporadic schwannomas and are also involved in the pathogenesis of

44 Prkar1a(+/-) mice developed nonpigmented schwannomas and fibro-osseous bone lesions beginning at

45 opment induces a high incidence of malignant schwannomas and gliomas in rats.

46 the specific loss of merlin is universal to schwannomas and is not linked to loss of ezrin, radixin,

47 degree of tumor-brain adhesion of vestibular schwannomas and may provide a method to improve preopera

48 hese gliomas, compared to 30-33% of sporadic schwannomas and meningiomas and none of eight oligodendr

49 or whose inactivation underlies the familial schwannomas and meningiomas of neurofibromatosis 2 and t

50 erlin inactivation also occur in spontaneous schwannomas and meningiomas, as well as other types of c

51 predominantly in benign neurological tumors, schwannomas and meningiomas, in humans; however, mutatio

52 sorder characterized by bilateral vestibular schwannomas and meningiomas.

53 elopment of nervous system tumors, including schwannomas and meningiomas.

54 uses of benign human brain tumors, including schwannomas and meningiomas.

55 in schwannomin/merlin is commonly mutated in schwannomas and meningiomas.

56 in the development of familial and sporadic schwannomas and meningiomas.

57 rized by the formation of bilateral acoustic schwannomas and other benign tumors associated with the

58 ne have frequently been detected not only in schwannomas and other central nervous system tumors of N

59 ction has been observed not only in familial schwannomas and other central nervous system tumors, but

60 , could be potential therapeutic targets for schwannomas and other Merlin-deficient tumours.

61 isease characterized by bilateral vestibular schwannomas and other nonmalignant tumors of the brain,

62 r characterized by the development of benign schwannomas and other Schwann-cell-derived tumors associ

63 matosis type 2 (NF2) gene cause formation of schwannomas and other tumors in the nervous system.

64 which is characterized by the development of schwannomas and other tumors of the nervous system.

65 sults represent the first miRNA profiling of schwannomas and the first report of a tumor suppressor f

66 om neurofibromatosis type 2, all spontaneous schwannomas and the majority of meningiomas.

67 ular endothelial growth factor by vestibular schwannomas and the role of Notch signaling in malignant

68 VEGF was expressed in 100% of vestibular schwannomas and VEGFR-2 in 32% of tumor vessels on immun

69 Multiple schwannomas and/or meningiomas are more frequently assoc

70 ibular schwannomas and 1 was a nonvestibular schwannoma), and 9 (8.5%) had an NF2 mutation.

71 ad multiple tumors in addition to vestibular schwannoma, and none had a positive family history.

72 icance in differentiating normal tissue from schwannomas, and 9 showed statistical significance in di

73 nervous system tumors such as neurofibromas, schwannomas, and malignant peripheral nerve sheath tumor

74 nnomin or merlin, is absent in virtually all schwannomas, and many meningiomas and ependymomas.

75 in the central nervous system, most notably schwannomas, and meningiomas.

76 oblastomas, oligodendrogliomas, meningiomas, schwannomas, and pediatric glioblastoma multiformes.

77 MK was induced in human neurofibromas, schwannomas, and various nervous system tumors associate

78 additional tumors or other features of known schwannoma- and meningioma-predisposing syndromes.

79 Neurofibromas and schwannomas are benign peripheral nerve sheath tumours t

80 Neurofibromas and schwannomas are benign Schwann cell-derived peripheral n

81 Schwannomas are common peripheral nerve sheath tumors th

82 m multiple genetically well-defined tumours, schwannomas are most frequent among those.

83 Schwannomas are peripheral nerve sheath tumors that ofte

84 Schwannomas are peripheral nerve tumors that typically h

85 Segmental schwannomatosis is diagnosed when schwannomas are restricted to 1 extremity and is thought

86 Schwannomas are slow-growing typically encapsulated tumo

87 tations predispose to rhabdoid tumors versus schwannomas are still unknown.

88 Meningiomas and schwannomas are usually sporadic, isolated tumors occurr

89 Patients with bilateral vestibular schwannomas associated with neurofibromatosis type 2 (NF

90 paraffin-embedded samples from 21 vestibular schwannomas associated with neurofibromatosis type 2 and

91 system tumours and strongly overexpressed in schwannoma at the mRNA level.

92 Mechanisms underlying schwannomas basal proliferation and cell-matrix adhesion

93 wider role than MEK1/2 in the development of schwannomas because adhesion is more dependent on KSR1 t

94 the cohort of those who developed a solitary schwannoma before age 25 years, 44 of 153 patients (29%)

95 ndition associated with bilateral vestibular schwannomas, benign tumors that arise from the eighth cr

96 ic mutation of the other NF2 allele in every schwannoma but no mutation of the remaining SMARCB1 alle

97 mutations predispose to rhabdoid tumors and schwannomas but the mechanisms underlying the tumor type

98 the majority of sporadic and NF2-associated schwannomas, but many schwannomas fail to demonstrate ge

99 rlin is found in most sporadic and inherited schwannomas, but the molecular mechanisms underlying neo

100 prior studies, we generated a mouse model of schwannomas by performing tissue-specific knockout (KO)

101 RNA expression profiling of human vestibular schwannomas by using an array representing 407 known miR

102 found that overexpression of miR-7 inhibited schwannoma cell growth both in culture and in xenograft

103 uppression of PI3-kinase activity as well as schwannoma cell growth is abrogated by a single PIKE-L p

104 B and on the cell cycle in a human malignant schwannoma cell line (STS-26T).

105 d by primary denervated Schwann cells or the Schwannoma cell line RN22 produces chemotactic activity

106 ation in regulating cell survival in the rat schwannoma cell line RN22, which expresses p75, but not

107 s Stat3 and Stat5 phosphorylation in the rat schwannoma cell line RT4.

108 ion mediated by IGF-I treatment in the human schwannoma cell line STS26T.

109 atients with sporadic VS, and an established schwannoma cell line were screened.

110 We examined this possibility in rat schwannoma cell lines overexpressing wild-type merlin is

111 ty, we generated doxycycline-regulatable RT4 schwannoma cell lines that inducibly express full-length

112 Dominant negative Rac inhibited schwannoma cell ruffling but had no apparent effect on N

113 Schwannoma cell stress fibers were inhibited by C3 trans

114 We show that Gas6 is mitogenic and increases schwannoma cell-matrix adhesion and survival acting via

115 ration, cell-matrix adhesion and survival in schwannoma cells acting via 37/67 kDa non-integrin lamin

116 Schwannoma cells also showed spread areas 5-7-fold great

117 ession of cellular prion protein (PrP(C)) in schwannoma cells and tissues.

118 vation of ERK and the proliferation of human schwannoma cells bearing a loss-of-function mutation in

119 NF2 gene product, merlin, were unchanged in schwannoma cells compared to NHSC.

120 n suppression of Rac signaling, and cultured schwannoma cells contain elevated, GTP-bound, active Rac

121 ro model for human schwannoma, we found that schwannoma cells display enhanced proliferation because

122 c activity in normal human Schwann cells and schwannoma cells during interaction with neurons.

123 Schwannoma cells frequently had elevated basal prolifera

124 of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients and suppresses the on

125 t regulated overexpression of HRS in RT4 rat schwannoma cells had the same functional consequences as

126 Importantly, we show that human schwannoma cells have reduced expression of SOX10 protei

127 the NF2 protein, merlin, into primary human schwannoma cells in an attempt to reverse the cytoskelet

128 inhibits the proliferation of NF2-deficient schwannoma cells in culture and displayed potent anti-tu

129 aches, impairs the proliferation of NF2-null schwannoma cells in culture and inhibits their ability t

130 ed significant antiproliferative activity in schwannoma cells in vitro, via the inhibition of HDAC ac

131 sed expression of wild-type merlin in Tr6BC1 schwannoma cells inhibits HA binding to CD44.

132 suppressor phosphatase and tensin homolog in schwannoma cells leading to increased activity of anti-a

133 mechanisms underlying neoplastic changes in schwannoma cells remain unclear.

134 nhibitor, the chemical compound NSC23766, to schwannoma cells restored neuronal interaction.

135 that regulated overexpression of HRS in rat schwannoma cells results in similar effects as overexpre

136 Schwannoma cells showed high Rac activity at distal regi

137 t merlin and HRS may regulate cell growth in schwannoma cells through interacting pathways.

138 rP(C) protein is also strongly released from schwannoma cells via exosomes and as a free peptide sugg

139 Treatment of RN22 Schwannoma cells with IL-6 or LIF enhanced the secretion

140 We compared cultured schwannoma cells with Schwann cells from normal human pe

141 Human primary VS cells, HEI-193 schwannoma cells, and SC4 Nf2(-/-) Schwann cells were us

142 We found that schwannoma cells, containing merlin mutations and consti

143 dditionally, we report that in RT4-D6P2T rat schwannoma cells, Cx32 is differentially phosphorylated

144 and recombinant IGFBP-1, we demonstrate that schwannoma cells, in contrast to Schwann cells, release

145 display many of the characteristics of human schwannoma cells, including increased expression of plat

146 d an in vitro model comprising human primary schwannoma cells, the most common Merlin-deficient tumou

147 Using a regulatable expression system in rat schwannoma cells, we analyzed proliferation, actin cytos

148 lly, while attempting to silence Pak1 in rat schwannoma cells, we found that these cells were unable

149 degradation endogenously expressed in D6P2T-schwannoma cells.

150 12nnr cells, C6 glioblastoma cells, and RN22 schwannoma cells.

151 and Rac pathways are abnormally activated in schwannoma cells.

152 ation and actin organization are aberrant in schwannoma cells.

153 trix adhesion and survival acting via Axl in schwannoma cells.

154 ll development is disrupted in primary human schwannoma cells.

155 ated forms were elevated in human vestibular schwannomas compared with normal human Schwann cells (SC

156 2 (NF2) develop bilateral cochleovestibular schwannomas (CVSs) that cause binaural deafness in most

157 sue, as compared to primary Schwann cells or schwannoma-derived cells.

158 We previously showed that schwannoma-derived Schwann cells exhibit membrane ruffli

159 Schwannomas develop from proliferation of dedifferentiat

160 otent anti-tumor activity in vivo, impairing schwannoma development in an orthotopic model of NF2.

161 Ras 1 (KSR1), has a vital role in promoting schwannomas development.

162 ment strategies for patients with vestibular schwannomas dominated the field.

163 dic and NF2-associated schwannomas, but many schwannomas fail to demonstrate genetic evidence of bial

164 To assess the requirement for Rac1 in schwannoma formation, we generated a double KO (DKO) of

165 understanding inherited predispositions for schwannoma formation.

166 at KSR1 and DCAF1 may co-operate to regulate schwannomas formation.

167 SFN also significantly inhibited schwannoma growth in vivo.

168 1, previously shown to be a key regulator in schwannoma growth we hypothesized that Axl is a good tar

169 n apparently sporadic solitary meningioma or schwannoma had a causative predisposition mutation.

170 Twenty-four patients (55%) with a spinal schwannoma had a constitutional mutation, while only 20

171 mutation, while only 20 (18%) with a cranial schwannoma had a constitutional predisposition (P < .001

172 Four of 106 people (3.8%) with a cranial schwannoma had an LZTR1 mutation (3 were vestibular schw

173 on for certain tumor types (e.g. meningioma, schwannoma) has permitted nonoperative therapy for some

174 with multiple schwannomas without vestibular schwannomas have been postulated to compose a distinct s

175 Most schwannomas have biallelic mutations in the NF2 tumor su

176 Neurofibromatosis 2-associated vestibular schwannomas have variable growth rates that tend to decl

177 e first description of a pigmented choroidal schwannoma in the context of a PHTS.

178 The presence of multiple schwannomas in a single patient suggests possible associ

179 omal dominant inherited disorder of multiple schwannomas in approximately 80% of 22q-related schwanno

180 Neurofibromas in NF1 and schwannomas in NF2 or schwannomatosis are defined by dis

181 istics and pathogenesis of neurofibromas and schwannomas in the neurofibromatoses.

182 order characterized by tumors, predominantly schwannomas, in the nervous system.

183 ted loss of merlin expression in all studied schwannomas, including 12 tumors lacking genetic evidenc

184 ull anatomical spectrum of human NF2-related schwannomas, including the characteristic functional def

185 eight individuals with schwannomatosis whose schwannomas involved somatic loss of one copy of 22q, en

186 The genomic landscape of schwannoma is complex and many of the molecules implicat

187 tion and the abnormal cellular morphology of schwannoma is unknown.

188 proliferation, increased focal adhesions and schwannoma-like morphology.

189 itro promoter dissection was undertaken in a Schwannoma line.

190 ons lead to increased risk of neurofibromas, schwannomas, low grade, pilocytic optic pathway gliomas,

191 Among these, multiple hybrid neurofibromas/schwannomas may also appear, not yet being defined by a

192 ave symptoms until much later and vestibular schwannomas may be the only tumors.

193 ors affecting the cranial nerves (vestibular schwannomas), meninges (meningiomas), and spinal cord (e

194 ltiple tumours of the nervous system such as schwannomas, meningiomas and ependymomas occurring spont

195 Neurofibromatosis type 2 patients develop schwannomas, meningiomas and ependymomas resulting from

196 ltiple tumours of the nervous system such as schwannomas, meningiomas and ependymomas.

197 F2 is characterized by formation of multiple schwannomas, meningiomas and ependymomas.

198 als develop nervous system tumors, including schwannomas, meningiomas, and ependymomas.

199 of central nervous system tumors, including schwannomas, meningiomas, ependymomas, and astrocytomas.

200 Patients develop nervous system tumours (schwannomas, meningiomas, ependymomas, astrocytomas, and

201 prominent radial recurrent vessels (n = 1), schwannoma (n = 1), or bicipitoradial bursa (n = 1).

202 ntation with a single meningioma (n = 42) or schwannoma (n = 135) before age 25 years.

203 [range] age, 11 [1-24] years; 22 female) or schwannoma (n = 135; median [range] age, 18 [0.2-24] yea

204 Vestibular schwannomas, neurogenetic syndromes such as schwannomato

205 and SMARCB1-negative schwannomatosis-related schwannomas, occurring less frequently in sporadic VS.

206 eatures consistent with a pigmented cellular schwannoma of the choroid.

207 half of all cases with hybrid neurofibromas/schwannomas of patients with multiple peripheral nerve s

208 genetic disorder characterized by bilateral schwannomas of the eighth cranial nerve.

209 Patients with NF2 can also develop schwannomas on other cranial and peripheral nerves, as w

210 the study of choice to exclude a vestibular schwannoma or other neoplasm of the cerebellopontine ang

211 atosis 2 (NF2) features bilateral vestibular schwannomas, other benign neural tumors, and cataracts.

212 quency of the known heritable meningioma- or schwannoma-predisposing mutations in children and young

213 receptor as well as its ligand Gas6 in human schwannoma primary cells compared to normal Schwann cell

214 viously shown that Prkar1a(+/-) mice develop schwannomas reminiscent of those seen in CNC and that si

215 of tinnitus that may arise after vestibular schwannoma removal.

216 zation in the brainstem following vestibular schwannoma removal.

217 o meningioma and 27 of 135 patients (20%) to schwannoma, respectively.

218 AK pathway, via integrin beta1, potentiating schwannoma's proliferation and cell-matrix adhesion.

219 First, analysis of primary schwannoma samples derived from NF2 patients showed that

220 and Ack1 being inversely correlated in human schwannoma samples.

221 sis type 2 (NF2) gene is commonly mutated in schwannomas, Schwann cell tumors that contain cells lack

222 nts presenting with a solitary meningioma or schwannoma should be referred for genetic testing.

223 n of an LZTR1 mutation was present in all 25 schwannomas studied.

224 ortion of cells from schwannomatosis-related schwannomas, suggest that these tumors develop through a

225 NF2 gene is observed in nearly all sporadic schwannomas, suggesting that the NF2 gene is a critical

226 ther tumours, such as psammomatous melanotic schwannoma, testicular Sertoli-cell tumours, and pituita

227 ision is the treatment of choice for orbital schwannomas that cause pain, disfigurement, diplopia, or

228 , and moesin in 22 vestibular and peripheral schwannomas that had been evaluated for NF2 mutations an

229 g identified distinct molecular subgroups of schwannomas that were associated with anatomical locatio

230 In all schwannomas, the majority of meningiomas and 1/3 of epen

231 he driver mutations in ENU-induced malignant schwannomas, the molecular basis of ENU-induced gliomas

232 and Mer) are significantly overexpressed in schwannoma tissues.

233 iR-7 as a potential therapeutic molecule for schwannoma treatment, and they prompt clinical evaluatio

234 Schwannoma tumors, which occur sporadically and in patie

235 Bilateral vestibular schwannomas, tumors on cranial nerve VIII, are pathognom

236 liferation of Schwann cells and formation of schwannoma tumours in patients with neurofibromatosis ty

237 is also key to the pathology of Merlin-null schwannoma tumours.

238 e analysis of the NF2 gene in a panel of 239 schwannoma tumours: 97 neurofibromatosis type 2 (NF2)-re

239 mpared with control nerve tissue, defining a schwannoma-typical signature.

240 olecular analysis of 22 hybrid neurofibromas/schwannomas using array comparative genomic hybridizatio

241 Vestibular schwannoma (VS) is an intracranial tumor that causes sig

242 Vestibular schwannoma (VS) is the most common tumor of the cerebell

243 related schwannomas, 104 sporadic vestibular schwannomas (VS) and 38 schwannomatosis-related schwanno

244 Vestibular schwannomas (VSs) are the most common tumours of the cer

245 ndrome characterized by bilateral vestibular schwannomas (VSs) resulting in deafness and brainstem co

246 The survival of mice bearing intracranial schwannomas was extended by at least 50%.

247 Using our in vitro model for human schwannoma, we found that schwannoma cells display enhan

248 Because NF2 is mutant in most or all human schwannomas, we postulate that loss of NF2 contributes t

249 Patients with schwannoma were screened for NF2, SMARCB1, and LZTR1 gen

250 neurofibromatosis with bilateral vestibular schwannomas were analyzed for mutations in the NF2 gene.

251 common tumor in individuals with NF2 is the schwannoma, which is composed of neoplastic Schwann cell

252 deletion of exon 2 in Schwann cells develop schwannomas, which confirms the crucial nature of exon 2

253 bromatosis type 2 and progressive vestibular schwannomas who were not candidates for standard treatme

254 l neural crest cells caused the formation of schwannomas with divergent differentiation.

255 e generated the first mouse model developing schwannomas with the same underlying gene mutations foun

256 2 patients who experienced recurrent orbital schwannoma without evidence for neurofibromatosis.

257 Patients with multiple schwannomas without vestibular schwannomas have been pos

258 i-VEGF therapy normalizes the vasculature of schwannoma xenografts in nude mice and successfully cont