ライフサイエンスコーパス: schwannoma

1 resection for acoustic neuromas (vestibular schwannomas).

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

3 ongly overexpressed and basally activated in schwannoma.

4 with the cellular features of her plexiform schwannoma.

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

6 lts presenting with a solitary meningioma or schwannoma.

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

8 d by the development of bilateral vestibular schwannomas.

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

10 ciatic nerve to mimic central and peripheral schwannomas.

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

12 endothelial growth factor (VEGF) therapy in schwannomas.

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

14 ion in the volume of most growing vestibular schwannomas.

15 eurofibromatosis type 2 and from 22 sporadic schwannomas.

16 nd the cardinal sign is bilateral vestibular schwannomas.

17 lling Rac activity as a possible therapy for schwannomas.

18 entation, myxomatosis, endocrine tumors, and schwannomas.

19 alignant peripheral nerve sheath tumours and schwannomas.

20 endocrine tumours and psammomatous melanotic schwannomas.

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

22 , showed expression of these proteins in all schwannomas.

23 (3.0%) and not at all in gangliogliomas and schwannomas.

24 condensates were evident in human vestibular schwannomas.

25 strains as immunotherapies for benign murine schwannomas.

26 zed by the occurrence of multiple peripheral schwannomas.

27 d by the development of bilateral vestibular schwannomas.

28 rmine genomic aberrations common to sporadic schwannomas.

29 of tested patients with hybrid neurofibromas/schwannomas.

30 ic and therapeutic studies of NF2-associated schwannomas.

31 e performed in nine patients with vestibular schwannomas.

32 rve tumors histologically identical to human schwannomas.

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

34 a (1.80, 1.41-2.30, p<0.0001) and vestibular schwannoma (1.49, 1.10-2.04, p=0.011).

35 Diagnostic entities included vestibular schwannomas (1011 [20.6%] of 4905 patients), meningiomas

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

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

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

39 (10 vestibular schwannomas, 8 nonvestibular schwannomas, 20 meningiomas, and 2 ependymomas) received

40 coma, 1 astrocytoma, 1 unspecified type) and schwannomas (3 of 12, 25%) were the most common malignan

41 RNA, and mRNA was performed in a subset of 9 schwannomas, 4 of which harbor DGCR8-E518K.RESULTSWe ide

42 ith progressive target tumors (10 vestibular schwannomas, 8 nonvestibular schwannomas, 20 meningiomas

43 ]), haemangioblastoma (29 [0.6%]), and other schwannomas (80 [1.6%]).

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

45 Furthermore, schwannomas also commonly develop in other cranial nerve

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

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

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

49 The most common types include schwannoma and neurofibroma.

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

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

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

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

54 ns, particularly in patients with vestibular schwannomas and candidates for cochlear implantation.

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

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

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

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

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

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

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

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

63 sorder characterized by bilateral vestibular schwannomas and meningiomas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Multiple schwannomas and/or meningiomas are more frequently assoc

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

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

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

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

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

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

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

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

89 miRNA profiling of PTCs, MNG, schwannomas, and Wilms tumors revealed a common profile

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

91 Neurofibromas and schwannomas are benign peripheral nerve sheath tumours t

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

93 Schwannomas are common peripheral nerve sheath tumors th

94 Schwannomas are common, highly morbid and medically untr

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

96 Schwannomas are peripheral nerve sheath tumors that ofte

97 Schwannomas are peripheral nerve tumors that typically h

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

99 Schwannomas are slow-growing typically encapsulated tumo

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

101 Meningiomas and schwannomas are usually sporadic, isolated tumors occurr

102 anatomic structures, evaluate for vestibular schwannomas, assess for inflammatory and/or infectious p

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

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

105 glioblastoma, pituitary adenoma, vestibular schwannoma, astrocytoma, and oligodendroglioma, with inf

106 o underwent surgical resection of vestibular schwannoma at 66 reporting facilities, the median length

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

108 Mechanisms underlying schwannomas basal proliferation and cell-matrix adhesion

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

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

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

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

113 evelopment not only for the treatment of NF2 schwannomas but also other tumors in which peroxynitrite

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 A panel of normal and NF2-null Schwann and schwannoma cell lines were used to characterize the effe

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

131 Schwannoma cell stress fibers were inhibited by C3 trans

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

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

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

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

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

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

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

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

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

141 Schwannoma cells frequently had elevated basal prolifera

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

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

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

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

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

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

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

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

150 In this protocol, we describe how to inject schwannoma cells into the mouse brain cerebellopontine a

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

152 mechanisms underlying neoplastic changes in schwannoma cells remain unclear.

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

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

155 Schwannoma cells showed high Rac activity at distal regi

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

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

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

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

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

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

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

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

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

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

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

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

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

169 ll development is disrupted in primary human schwannoma cells.

170 degradation endogenously expressed in D6P2T-schwannoma cells.

171 12nnr cells, C6 glioblastoma cells, and RN22 schwannoma cells.

172 and Rac pathways are abnormally activated in schwannoma cells.

173 ation and actin organization are aberrant in schwannoma cells.

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

175 2 (NF2) develop bilateral cochleovestibular schwannomas (CVSs) that cause binaural deafness in most

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

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

178 Schwannomas develop from proliferation of dedifferentiat

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

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

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

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

183 ation, survival, and adhesion while inducing schwannoma formation in a novel in vivo orthotopic trans

184 s identify a novel signaling axis underlying schwannoma formation, revealing new and potentially drug

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

186 understanding inherited predispositions for schwannoma formation.

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

188 Here, we show that vestibular schwannomas from NF2 patients and human, merlin-deficien

189 ing NF-kappaB signaling and Merlin-deficient schwannoma genesis.

190 SFN also significantly inhibited schwannoma growth in vivo.

191 1, previously shown to be a key regulator in schwannoma growth we hypothesized that Axl is a good tar

192 rapies had an additive effect on suppressing schwannoma growth.

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

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

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

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

197 or all tumors; meningiomas and nonvestibular schwannomas had the greatest benefit.

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

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

200 Most schwannomas have biallelic mutations in the NF2 tumor su

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

202 BACKGROUNDNeurofibroma/schwannoma hybrid nerve sheath tumors (N/S HNSTs) are ne

203 r immunity in that the growth of rechallenge schwannomas implanted following primary bacterial treatm

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

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

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

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

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

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

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

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

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

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

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

215 appaB signaling elements in human and murine schwannomas, leading us to identify a caspase-cleaved, p

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

217 itro promoter dissection was undertaken in a Schwannoma line.

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

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

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

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

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

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

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

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

226 nherited, neoplastic disease associated with schwannomas, meningiomas, and ependymomas and that is ca

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

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

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

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

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

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

233 Vestibular schwannomas, neurogenetic syndromes such as schwannomato

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

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

236 A case of primary pericardial schwannoma of the posterior pericardium with concerns fo

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

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

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

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

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

242 DGCR8-E518K-positive tumors, including MNG, schwannomas, papillary thyroid cancers (PTCs), and Wilms

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

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

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

246 of tinnitus that may arise after vestibular schwannoma removal.

247 zation in the brainstem following vestibular schwannoma removal.

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

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

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

251 and Ack1 being inversely correlated in human schwannoma samples.

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

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

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

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

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

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

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

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

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

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

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

263 and Mer) are significantly overexpressed in schwannoma tissues.

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

265 beta1 resulted in a significant reduction in schwannoma tumor growth.

266 Schwannoma tumors, which occur sporadically and in patie

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

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

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

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

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

272 diagnosed small- and medium-sized vestibular schwannoma, upfront radiosurgery demonstrated a signific

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

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

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

276 ge on surgical outcomes following vestibular schwannoma (VS) resection, few if any large-scale invest

277 d occupational noise exposure and vestibular schwannoma (VS), found in several studies, represents re

278 for small-sized (Koos I up to II) vestibular schwannoma (VS).

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

280 sorder characterized by bilateral vestibular schwannomas (VS) that arise from neoplastic Schwann cell

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

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

283 NF2 is characterized by bilateral vestibular schwannomas (VSs) that cause progressive and debilitatin

284 osis type 2 (NF2) and progressive vestibular schwannomas (VSs).

285 ion, revealing new and potentially druggable schwannoma vulnerabilities with future therapeutic poten

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

287 uman VS cells and a mouse allograft model of schwannoma, we evaluated the dual mTORC1/2 inhibitor AZD

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

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

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

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

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

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

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

295 s, which included vestibular or other benign schwannomas, WHO grade 1 meningiomas, pituitary adenomas

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

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

298 2 patients who experienced recurrent orbital schwannoma without evidence for neurofibromatosis.

299 Patients with multiple schwannomas without vestibular schwannomas have been pos

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