ライフサイエンスコーパス: astrocytoma

1 and was absent in 25 samples (3 controls, 22 astrocytomas).

2 e in the pathobiology of pediatric low-grade astrocytoma.

3 anaplastic ependymoma, and 1 had anaplastic astrocytoma.

4 ressive glioblastoma but not less aggressive astrocytoma.

5 or other therapy for subependymal giant-cell astrocytoma.

6 a multiforme, and 18 patients had anaplastic astrocytoma.

7 d responsible for tumorigenesis of pilocytic astrocytoma.

8 dary glioblastoma" evolving from a low-grade astrocytoma.

9 oma multiforme (GBM) is the highest grade of astrocytoma.

10 ymphoblastic leukemia, Hodgkin lymphoma, and astrocytoma.

11 l cancer, gastric cancer, and an early-onset astrocytoma.

12 ryngioma, ependymoma, and juvenile pilocytic astrocytoma.

13 aplastic oligodendroglioma, and 1 anaplastic astrocytoma.

14 ere SSEA-4(+) and correlated with high-grade astrocytoma.

15 olon, lung, pancreas, thyroid, prostate, and astrocytoma.

16 A) cell line from a WHO grade III anaplastic astrocytoma.

17 rentially expressed genes in the majority of astrocytoma.

18 e associated with an underlying infiltrative astrocytoma.

19 ative to baseline in subependymal giant cell astrocytomas.

20 educed the volume of subependymal giant cell astrocytomas.

21 are found to be active--but dysregulated--in astrocytomas.

22 tes to injury and the malignant phenotype of astrocytomas.

23 16Ink4a) deletions in pediatric infiltrative astrocytomas.

24 and induction of the malignant phenotype of astrocytomas.

25 g schwannomas, meningiomas, ependymomas, and astrocytomas.

26 mphoma, pancreatic neuroendocrine tumors and astrocytomas.

27 eoplastic tissue with features of high-grade astrocytomas.

28 l importance to the development of pilocytic astrocytomas.

29 pment of low-grade to high-grade progressive astrocytomas.

30 survival, and full penetrance of high-grade astrocytomas.

31 atment, and emerging therapies for recurrent astrocytomas.

32 ace of malignant glioblastomas or high-grade astrocytomas.

33 nt phenotype via comparison with lower-grade astrocytomas.

34 angiomyolipomas and subependymal giant cell astrocytomas.

35 e Raf/MEK/ERK and PI3K/AKT cascades in human astrocytomas.

36 y, the ZM fusion was found only in grade III astrocytomas (1/13; 7.7%) or secondary GBMs (sGBMs, 3/20

37 denocarcinomas, 1 osteosarcoma, 1 sarcoma, 1 astrocytoma, 1 low-grade glioma, and 2 preinvasive breas

38 Among 165 primary high-grade astrocytomas, 13% of grade IV tumors and 2% of grade III

39 cytoma (6q), and two subependymal giant cell astrocytomas (16p and 21q).

40 8 boys and 5 girls) were included (5 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 gliomatosis c

41 p36 were frequently identified in anaplastic astrocytomas (22%) and glioblastomas (34%).

42 in 16 samples, 7/10 controls (70%) and 9/35 astrocytomas (26%).

43 There were 37 pilocytic astrocytomas, 34 medulloblastomas (23 classic, eight des

44 inal features was associated with giant cell astrocytoma (37.1% vs. 14.6%; P = 0.018), renal angiomyo

45 The most common histology was pilocytic astrocytoma (46.3%).

46 cluded (5 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 gliomatosis cerebri, and 1 glioblastoma

47 There were 21 low-grade astrocytomas, 64 oligodendrogliomas, and 16 mixed oligoa

48 ons were two gangliogliomas (3q and 9p), one astrocytoma (6q), and two subependymal giant cell astroc

49 r serial growth of a subependymal giant cell astrocytoma, a new lesion of 1 cm or greater, or new or

50 ing, the microvascular network of pilomyxoid astrocytoma, a subtype of optic glioma with abundant myx

51 cluster of gliomas identified the pilocytic astrocytomas, a second grouped the 1p/19q codeleted olig

52 specific perturbations that yield high-grade astrocytomas (anaplastic astrocytomas and GBMs).

53 astoma, glioma, malignant glioma, anaplastic astrocytoma, anaplastic oligodendroglioma, anaplastic ol

54 Thirty-five samples of pilocytic astrocytoma and 10 control samples of cerebellum from pa

55 ression of miR-3189-3p was down-regulated in astrocytoma and glioblastoma clinical samples compared w

56 ggressive histologic subtype among malignant astrocytoma and is associated with poor outcomes because

57 use model of spontaneous multifocal invasive astrocytoma and its derived neuroprogenitors, human glio

58 tissue from mouse models of both high-grade astrocytoma and medulloblastoma display hypersensitivity

59 ferences in bulk profiles between IDH-mutant astrocytoma and oligodendroglioma can be primarily expla

60 se data are supported by the fact that human astrocytoma and oligodendroglioma display a high degree

61 lesions with IDH-mutated genotypes, between astrocytoma and oligodendroglioma histologies, as well a

62 ficant overexpression of glypican-1 in human astrocytoma and oligodendroglioma samples compared with

63 observed (one in thalamic juvenile pilocytic astrocytoma and one in optic pathway glioma) at dose lev

64 ontribute to de novo formation of high-grade astrocytoma and progression into glioblastoma, respectiv

65 oma showed molecular similarity to pilocytic astrocytoma and relatively favorable survival.

66 AA1549-BRAF fusion genes typifying low-grade astrocytomas and (V600E)BRAF alterations characterizing

67 ly diagnosed low-grade gliomas (21 low-grade astrocytomas and 14 low-grade oligodendrogliomas and low

68 eatment paradigms for BRAF-altered pediatric astrocytomas and also demonstrate that therapies must be

69 than TSC1, with more subependymal giant cell astrocytomas and angiomyolipomas, higher incidence of ph

70 protein (TSPO) is upregulated in high-grade astrocytomas and can be imaged by PET using the selectiv

71 at yield high-grade astrocytomas (anaplastic astrocytomas and GBMs).

72 cate that 1p deletions are common anaplastic astrocytomas and glioblastomas but are distinct from the

73 as, ductal breast carcinomas, and anaplastic astrocytomas and glioblastomas.

74 ratify patients with IAs, especially diffuse astrocytomas and gliomatosis cerebri, for diagnostic, th

75 h recent studies on the genesis of low-grade astrocytomas and highlight neuronal support functions of

76 mas (67.5%), but was unmethylated in grade I astrocytomas and in DNA from age matched control brain s

77 ions have been discovered in adult low-grade astrocytomas and in glioblastomas.

78 on transcripts expressed in 10 of 10 grade 1 astrocytomas and in none of the grade 2 to 4 tumors.

79 or greater were restricted to grade 3 and 4 astrocytomas and included the MDM4 (1q32), PDGFRA (4q12)

80 s was significantly higher than in low-grade astrocytomas and low-grade oligodendrogliomas.

81 ndrogliomas and with a slower time course in astrocytomas and mixed gliomas.

82 DH1 in more than 70% of WHO grade II and III astrocytomas and oligodendrogliomas and in glioblastomas

83 The expression of Tax1 in primary human astrocytomas and oligodendrogliomas resulted in signific

84 be frequent and early genetic alterations in astrocytomas and oligodendrogliomas.

85 exchange factor ECT2 is elevated in primary astrocytomas and predicts both survival and malignancy.

86 echanism associated with the pathogenesis of astrocytomas and provide a model for the loss of contact

87 ion in the volume of subependymal giant-cell astrocytomas and seizure frequency and may be a potentia

88 as frequently methylated in WHO grade II-III astrocytomas and WHO grade IV primary glioblastomas (67.

89 Both radiographic response (one anaplastic astrocytoma) and stable disease (one medulloblastoma, tw

90 op glial neoplasms (optic gliomas, malignant astrocytomas) and neuronal dysfunction (learning disabil

91 found present in 20 samples (7 controls, 13 astrocytomas) and was absent in 25 samples (3 controls,

92 core, cytological type (oligodendroglioma vs astrocytoma), and, potentially, the extent of resection.

93 e development of brain cancer (most commonly astrocytomas), and Tpmt status has been associated with

94 samples analyzed included oligodendroglioma, astrocytoma, and meningioma tumors of different histolog

95 glioma samples, including oligodendroglioma, astrocytoma, and oligoastrocytoma, all of different hist

96 uantitative RT-PCR in 41 GBMs, 43 anaplastic astrocytomas, and 7 adjacent normal tissues.

97 oth astrocytoma cell lines and primary human astrocytomas, and colocalizes with RAC1 and CDC42 at the

98 cluding carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas.

99 ours (schwannomas, meningiomas, ependymomas, astrocytomas, and neurofibromas), peripheral neuropathy,

100 Malignant astrocytomas are a deadly solid tumor in children.

101 Although malignant astrocytomas are a leading cause of cancer-related death

102 Astrocytomas are common and lethal human brain tumors.

103 Malignant astrocytomas are highly invasive brain tumors.

104 In contrast, astrocytomas are readily generated from NPs with additio

105 Pediatric low-grade astrocytomas are the most common brain tumors in childre

106 Astrocytomas are the most common type of brain tumors in

107 nt gliomas (MG), including grades III and IV astrocytomas, are the most common adult brain tumors.

108 Low-grade brain tumors (pilocytic astrocytomas) arising in the neurofibromatosis type 1 (N

109 olume of the primary subependymal giant-cell astrocytoma, as assessed on independent central review (

110 d cortical tubers or subependymal giant cell astrocytomas, as well as tissue microarrays of six types

111 l rapamycin therapy can induce regression of astrocytomas associated with TSC and may offer an altern

112 could affect growth or induce regression in astrocytomas associated with TSC.

113 mus in patients with subependymal giant cell astrocytomas associated with tuberous sclerosis complex.

114 se of everolimus for subependymal giant cell astrocytomas associated with tuberous sclerosis.

115 se of everolimus for subependymal giant cell astrocytomas associated with tuberous sclerosis.

116 ertional mutagenesis can identify high-grade astrocytoma-associated genes and they imply an important

117 ytoma (PPP1CB-ALK), novel BRAF fusions in an astrocytoma (BCAS1-BRAF) and a ganglioglioma (TMEM106B-B

118 primitive neuroectodermal tumor (PNET), and astrocytoma before 6 years of age diagnosed in 1990-2007

119 change in volume of subependymal giant-cell astrocytomas between baseline and 6 months.

120 and growth of pilocytic and other low-grade astrocytomas beyond the association of a minority of cas

121 the most frequent HHV detected in pilocytic astrocytoma, but at very low levels.

122 year of life were positively associated with astrocytoma, but the confidence intervals included the n

123 ious PKC isoforms are increased in malignant astrocytomas, but not in non-neoplastic astrocytes.

124 h fetal growth appeared to involve pilocytic astrocytomas, but not other astrocytomas, medulloblastom

125 the brain, growth of subependymal giant cell astrocytomas can cause life-threatening symptoms--eg, hy

126 ncy for 43 PNET, 34 medulloblastoma, and 106 astrocytoma cases and 30,569 controls living within 5 mi

127 ced HIV replication by threefold in both the astrocytoma cell line U87MG and primary fetal astrocytes

128 In studies with a murine astrocytoma cell line, heat shock dramatically reduces t

129 from altered localization of beta-TrCP1; in astrocytoma cell lines and in normal brain tissue the E3

130 berrantly localized to the cytoplasm in both astrocytoma cell lines and primary human astrocytomas, a

131 Overexpression of ADAR3 in astrocyte and astrocytoma cell lines inhibits RNA editing at the Q/R s

132 Here, we demonstrate that the human astrocytoma cell lines U-118, U-87, CCF-STTG1, and SW108

133 membranes obtained from the 1321N1 and A172 astrocytoma cell lines were immobilized on a chromatogra

134 ated in 9L and SF188 tumor cells (glioma and astrocytoma cell lines).

135 In contrast, in three metastatic astrocytoma cell lines, S268 was under phosphorylated, s

136 t a novel role for the ghrelin/GHS-R axis in astrocytoma cell migration and invasiveness of cancers o

137 Human astrocytoma cell stress granules contain mRNAs that are

138 nhancer activity by 40% in neuroblastoma and astrocytoma cells (pBonferroni < .0001).

139 e Rac1 with GHS-R on the leading edge of the astrocytoma cells and imparting the tumor cells with a m

140 the use of genetically modified 1321N1 human astrocytoma cells and of spinal cord astrocytes derived

141 n is important for the malignant behavior of astrocytoma cells and that it contributes to the high mo

142 no effect on cell proliferation of human CCF astrocytoma cells but stimulated nerve growth factor (NG

143 ly stimulated phospholipase C stimulation in astrocytoma cells expressing G protein-coupled human (h)

144 -sensitive Ca(2+) transients in human 1321N1 astrocytoma cells expressing human P2Y1R.

145 Cytoplasmic fractionation of astrocytoma cells followed by ECT2 immunoprecipitation a

146 Diminished integrin expression in astrocytoma cells leads to reduced activation of latent

147 that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of highly angio

148 that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of highly invas

149 These data reveal that astrocytoma cells manipulate their angiogenic balance by

150 ECT2 overexpression in astrocytoma cells resulted in a transition to an amoeboi

151 inhibit ATP-induced calcium influx in 1321N1 astrocytoma cells stably transfected with the human P2X4

152 uced intracellular calcium release in 1321N1 astrocytoma cells stably transfected with the human P2Y4

153 ease of UDP-Gal was observed in 1321N1 human astrocytoma cells stimulated with the protease-activated

154 h migratory potential, as shown by comparing astrocytoma cells to carcinoma cells without synemin at

155 increase in intracellular calcium in 1321N1 astrocytoma cells transiently expressing full-length P2X

156 nculin in focal contacts of synemin-silenced astrocytoma cells were similar to those of controls.

157 Synemin-silenced astrocytoma cells were smaller and spread more slowly th

158 Mice bearing orthotopically implanted astrocytoma cells with diminished ECT2 levels following

159 e aggregates TIAR and G3BP1 was performed on astrocytoma cells, and subsequent analysis revealed that

160 We have shown previously that, in astrocytoma cells, synemin is present at the leading edg

161 n (AP-1) -mediated gene expression in 1321N1 astrocytoma cells, whereas the nonmitogenic agonist carb

162 are a novel form of epigenetic regulation in astrocytoma cells, which may be targetable by chemical i

163 1 and CDC42 at the leading edge of migrating astrocytoma cells.

164 in mesenchymal-amoeboid transition in human astrocytoma cells.

165 cting protein that regulates RHO activity in astrocytoma cells.

166 lant of genetically relevant murine or human astrocytoma cells.

167 (shRNAs) sharply decreased the migration of astrocytoma cells.

168 s at human P2Y receptors expressed in 1321N1 astrocytoma cells.

169 r distribution and signaling in human 1321N1 astrocytoma cells.

170 B) are localized to stress granules in human astrocytoma cells.

171 ogenitor/stem cells and U-251MG glioblastoma/astrocytoma cells.

172 umors with molecular similarity to pilocytic astrocytomas, class II tumors are similar to 1p/19q code

173 her than that of the fusogenic strain A59 in astrocytoma DBT cells.

174 RC GFAP expression lowered plectin levels in astrocytoma-derived stable transfectants and plectin-pos

175 on is necessary for NF1-associated low-grade astrocytoma development, additional genetic changes may

176 xamined the role of AMPK in a mouse model of astrocytoma driven by oncogenic H-Ras(V12) and/or with P

177 Hodgkin's lymphomas, non-Hodgkin lymphomas, astrocytomas, Ewing's sarcomas, and rhabdomyosarcomas (p

178 as signaling in neurons promotes gliosis and astrocytoma formation in a cell nonautonomous manner.

179 d in high-grade as compared with lower-grade astrocytomas, further suggesting that MCT4 is a clinical

180 of cell lysate solutions obtained from human astrocytoma (glioblastoma) U-87MG cell line, with the ex

181 ntial to development of the highest grade of astrocytoma, Glioblastoma multiforme were: COL4A1, EGFR,

182 Astrocytoma (glioma) formation in neurofibromatosis type

183 ome sequencing of a MYBL1-rearranged diffuse astrocytoma grade II demonstrated MYBL1 tandem duplicati

184 8q13.1 gain, was observed in 28% of diffuse astrocytoma grade IIs and resulted in partial duplicatio

185 Glioblastoma multiforme (GBM)/astrocytoma grade IV is a malignant and lethal brain can

186 is produced a gene network for each grade of astrocytoma (Grade I-IV), and 'key genes' within each gr

187 The 1p status of astrocytomas has not yet been thoroughly examined.

188 elatively common in subtypes of sarcomas and astrocytomas, has rarely been reported in epithelial mal

189 of glioblastoma multiforme (GBM), a grade IV astrocytoma, have been enriched by the expressed marker

190 Survival in the majority of high-grade astrocytoma (HGA) patients is very poor, with only a rar

191 DP-43 was detected in RFs of human pilocytic astrocytomas; however, involvement of TDP-43 in AxD has

192 sk for glioma (HR, 0.50; 95% CI, 0.44-0.58), astrocytoma (HR, 0.43; 95% CI, 0.36-0.51), neuroblastoma

193 Infiltrative astrocytomas (IAs) represent a group of astrocytic gliom

194 19q differentiating oligodendrogliomas from astrocytomas; (iii) IDH1/2 mutations; and (iv) select pa

195 G production, we established an IDH1-mutated astrocytoma (IMA) cell line from a WHO grade III anaplas

196 with limited support for increased risks for astrocytoma in children up to age 6.

197 tation seems to define a subset of malignant astrocytomas in children, in which there is frequent con

198 ulted in regrowth of subependymal giant cell astrocytomas in one patient.

199 andard treatment for subependymal giant-cell astrocytomas in patients with the tuberous sclerosis com

200 risk of brain tumors (particularly pilocytic astrocytomas) independently of gestational age, not only

201 cs seen in oligodendrogliomas and small-cell astrocytomas, indicating a contribution of cell-of-origi

202 GFBP2 or Akt with K-Ras was required to form astrocytomas, indicating that activation of two separate

203 g pathways in the regulation of LRP-mediated astrocytoma invasion.

204 t and 1p/19q co-deletion, whereas anaplastic astrocytoma is divided into IDH wild-type ( IDH-wt) and

205 ed enteric neurons and cells derived from an astrocytoma is reversible, as the protein's distribution

206 Glioblastoma multiforme (GBM), the grade IV astrocytoma, is the most common and aggressive brain tum

207 different cells yielded benign infiltrative astrocytomas, malignant astrocytomas, or tumors with cha

208 ADC metrics and cellularity of the pilocytic astrocytomas, medulloblastomas, and ependymomas.

209 nvolve pilocytic astrocytomas, but not other astrocytomas, medulloblastomas, or ependymomas.

210 Pediatric midline high-grade astrocytomas (mHGAs) are incurable with few treatment ta

211 ed with PKCe inhibitors, while metastasis of astrocytomas might be blocked by PKCe stimulators.

212 f cytoskeletal GTPases are key regulators of astrocytoma migration and invasion; expression of the gu

213 s or genetic deletion in a murine high-grade astrocytoma model markedly promotes tumour growth and th

214 n this study, we used the spontaneous murine astrocytoma model SMA560 injected intracranially into sy

215 CNS heterozygosity of Pten into the Nf1/p53 astrocytoma model.

216 on, matrix metalloproteinase-2 activity, and astrocytoma motility.

217 ant cell astrocytomas (n = 4) or a pilocytic astrocytoma (n = 1) were treated with oral rapamycin at

218 Initial diagnoses were grade 2 astrocytoma (n = 6) and other grade 1/2 gliomas (n = 5).

219 mor types included supratentorial high-grade astrocytoma (n = 7), low-grade glioma (n = 9), brain ste

220 inite TSC and either subependymal giant cell astrocytomas (n = 4) or a pilocytic astrocytoma (n = 1)

221 an tumor cell lines, including glioblastoma, astrocytoma, neuroblastoma, lung adenocarcinoma, and bre

222 Glioblastoma multiforme (GBM) is a malignant astrocytoma of the central nervous system associated wit

223 8,000 promoters in normal human brain and in astrocytomas of various grades using the methylated CpG

224 We included patients with grade 2 astrocytoma, oligoastrocytoma, or oligodendroglioma who

225 r who had a low-grade (WHO grade II) glioma (astrocytoma, oligoastrocytoma, or oligodendroglioma) wit

226 r who had a low-grade (WHO grade II) glioma (astrocytoma, oligoastrocytoma, or oligodendroglioma) wit

227 in long-term survivors of WHO grade I or II astrocytoma, oligodendroglioma, or oligoastrocytoma with

228 covery on a population of low-grade gliomas (astrocytomas, oligodendrogliomas, and mixed gliomas) to

229 nfiltrating low-grade gliomas (LGGs) include astrocytomas, oligodendrogliomas, and mixed oligoastrocy

230 f remaining 1p/19q intact gliomas, including astrocytomas, oligodendrogliomas, and oligoastrocytomas,

231 ion, causing rapid development of high-grade astrocytoma on intracranial transplantation.

232 In culture medium from epsilon3/4 human astrocytoma or epsilon3/3, epsilon4/4 and epsilon3/4 pri

233 ion of oncogenes delivered, resembling human astrocytoma or glioblastoma in the majority of cases.

234 utional histologic diagnosis (eg, anaplastic astrocytoma or glioblastoma multiforme), as well as age,

235 astoma multiforme, and those with anaplastic astrocytoma or oligodendroglioma were 54, 52, and 116 wk

236 and laboratory HCMV strains, HCMV-permissive astrocytoma, or dendritic cells, as well as "naive" and

237 benign infiltrative astrocytomas, malignant astrocytomas, or tumors with characteristics seen in oli

238 tly in AYAs only for CNS tumours (p=0.0046), astrocytomas (p=0.040), and malignant melanomas (p<0.000

239 Pilocytic astrocytoma (PA) is the most common glial cell tumor ari

240 ) analysis of three NF1-associated pilocytic astrocytoma (PA) tumors.

241 nitial study cohort consisted of 7 pilocytic astrocytoma (PA), 19 ependymoma (EPN), 5 glioblastoma (G

242 Pilocytic astrocytomas (PAs) are the most common glioma in childre

243 Pilocytic astrocytomas (PAs), WHO malignancy grade I, are the most

244 Pilocytic astrocytomas (PAs, WHO grade I) are the most common brai

245 rated into clinical evaluation of anaplastic astrocytoma patients.

246 usions in a neuroblastoma (BEND5-ALK) and an astrocytoma (PPP1CB-ALK), novel BRAF fusions in an astro

247 to have concomitant subependymal giant cell astrocytomas, renal angiomyolipomas, cognitive impairmen

248 Low-grade glial neoplasms (astrocytomas) represent one of the most common brain tum

249 odendrogliomas, mixed oligoastrocytomas, and astrocytomas, respectively.

250 rray studies which compared normal tissue to astrocytoma revealed a set of 646 differentially express

251 rofiles with those of Grade II and Grade III astrocytoma samples and determined that the observed upr

252 Anaplastic astrocytoma samples with mutated IDH1 display lower leve

253 35% of patients with subependymal giant cell astrocytoma (SEGA) associated with tuberous sclerosis co

254 roteins in tuber and subependymal giant cell astrocytoma (SEGA) specimens in TSC.

255 l nodules (SENs) and subependymal giant cell astrocytomas (SEGAs) are common brain lesions found in p

256 In astrocytomas, several hundred CpG islands undergo specif

257 lated with TF expression in human high-grade astrocytoma specimens.

258 udopalisades in surgically removed malignant astrocytoma specimens.

259 cells, and subsequent analysis revealed that astrocytoma stress granules harbor unique mRNAs for vari

260 argetable by chemical inhibitors and enhance astrocytoma susceptibility to conventional therapy, such

261 terations seen in GBM but not in lower-grade astrocytomas that could be responsible for TF up-regulat

262 covery of aberrant KAP splicing in malignant astrocytomas that leads to increased expression of KAP-r

263 Genomic DNA from SB-induced astrocytoma tissue was extracted and transposon insertio

264 re significantly higher in GB and anaplastic astrocytoma tissues than in grade II glioma and normal c

265 and decelerates the progression of low-grade astrocytoma to GBM in a spontaneous transgenic glioma mo

266 tion and progression of low-grade fibrillary astrocytoma to high-grade anaplastic gliomas.

267 expression uniquely sensitized primary human astrocytomas to apoptosis.

268 alth Organization (WHO) grade III anaplastic astrocytomas to WHO grade IV glioblastomas.

269 or TCF/LEF members in primary astrocytes and astrocytomas transiently transfected with an HIV long te

270 were determined for 65 patients with grade 2 astrocytoma treated at our institution during the study

271 s of high infiltration/migration in grade IV astrocytoma tumor tissue.

272 can help identify highly aggressive WHO III astrocytoma tumors and may help in adjusting standard tr

273 Y) and murine (N1E-115) neuroblastoma, human astrocytoma (U-87 MG and 1321 N1), and rat glioma (C6)).

274 -60), IC(50) = 9 muM, and human glioblastoma-astrocytoma (U373), IC(50) = 25 muM), but not toxic (up

275 amics of VEEV Trinidad donkey-infected human astrocytoma U87MG cells were determined by carrying out

276 ion in the volume of subependymal giant cell astrocytomas versus none in the placebo group (differenc

277 stimate of MT among 65 patients with grade 2 astrocytoma was 6.7% +/- 3.9%; no risk factor analyzed,

278 = 0.0007), and EGFR expression in anaplastic astrocytoma was associated with nearly 3-fold poorer sur

279 mouse models of the malignant brain cancer, astrocytoma, we report that tumor cells induce pathologi

280 ith serial growth of subependymal giant-cell astrocytomas were eligible for this open-label study.

281 ts from a natural history study of low-grade astrocytomas were tested an average of 111 days after su

282 trial, 60 patients with recurrent malignant astrocytomas were treated with bevacizumab and irinoteca

283 everse correlation increased after excluding astrocytomas, whereas it became insignificant after excl

284 ncy of Pten accelerated formation of grade 3 astrocytomas, whereas loss of Pten heterozygosity and Ak

285 individuals display subependymal giant cell astrocytomas, which can lead to substantial neurological

286 Pilocytic astrocytomas, which contain abnormal glial cells, have h

287 d increased KAP mRNA expression in malignant astrocytomas, which correlates with increasing histologi

288 ard proliferative glial programs, initiating astrocytomas, while at moderate RAS/ERK levels, Ascl1 pr

289 e applied our method to detect HS from human astrocytoma (WHO grade II) and glioblastoma (GBM, WHO gr

290 stoma (GBM, WHO grade IV) slides compared to astrocytoma (WHO grade II) slides.

291 multiforme (GBM) is an aggressive, Grade IV astrocytoma with a poor survival rate, primarily due to

292 The prognosis of WHO III astrocytoma with an early TTP(min) of 12.5 min or less d

293 strategy for treating a subset of pediatric astrocytomas with BRAF(V600E) mutation and CDKN2A defici

294 se mutations are characteristic of pediatric astrocytomas with KIAA1549-BRAF fusion genes typifying l

295 Strong associations were observed for astrocytomas with mutated IDH1 or IDH2 (grades 2-4) (OR=

296 ation of transposon-terminated Csf1 mRNAs in astrocytomas with SB insertions in intron 8.

297 the brains of nude mice generated high-grade astrocytomas with short latency and 100% penetrance.

298 66, P=4.7x10(-12) to 2.2x10(-8)) but not for astrocytomas with wild-type IDH1 and IDH2 (smallest P=0.

299 oblastoma multiforme and one with anaplastic astrocytoma) with histologically documented recurrent gl

300 F as a frequent mutation target in pediatric astrocytomas, with distinct types of BRAF alteration occ