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

3 rentially expressed genes in the majority of astrocytoma.

4 e associated with an underlying infiltrative astrocytoma.

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

6 a subtotal excision of a brainstem pilocytic astrocytoma.

7 n tumors in children and adults is glioma or astrocytoma.

8 anaplastic ependymoma, and 1 had anaplastic astrocytoma.

9 ressive glioblastoma but not less aggressive astrocytoma.

10 or other therapy for subependymal giant-cell astrocytoma.

11 ymphoblastic leukemia, Hodgkin lymphoma, and astrocytoma.

12 a multiforme, and 18 patients had anaplastic astrocytoma.

13 d responsible for tumorigenesis of pilocytic astrocytoma.

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

15 ryngioma, ependymoma, and juvenile pilocytic astrocytoma.

16 aplastic oligodendroglioma, and 1 anaplastic astrocytoma.

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

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

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

20 ative to baseline in subependymal giant cell astrocytomas.

21 educed the volume of subependymal giant cell astrocytomas.

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

23 tes to injury and the malignant phenotype of astrocytomas.

24 16Ink4a) deletions in pediatric infiltrative astrocytomas.

25 and induction of the malignant phenotype of astrocytomas.

26 g schwannomas, meningiomas, ependymomas, and astrocytomas.

27 mphoma, pancreatic neuroendocrine tumors and astrocytomas.

28 eoplastic tissue with features of high-grade astrocytomas.

29 l importance to the development of pilocytic astrocytomas.

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

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

32 atment, and emerging therapies for recurrent astrocytomas.

33 angiomyolipomas and subependymal giant cell astrocytomas.

34 nty-nine spinal cord ependymomas and sixteen astrocytomas.

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

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

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

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

39 8 boys and 5 girls) were included (5 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 gliomatosis c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 TP3 exhibit increased NOTCH signaling, are astrocytoma and IDHmut-non-codel.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 less appropriate for modelling more diffuse astrocytomas and oligodendrogliomas, but could be tuned

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

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

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

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

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

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

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

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

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

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

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

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

93 riteria, including 19 oligodendrogliomas, 26 astrocytomas, and 11 mixed gliomas in 30 males and 26 fe

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

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

96 s, hemangiomas, epidermoid cysts, cerebellar astrocytomas, and metastatic lesions.

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

98 Malignant astrocytomas are a deadly solid tumor in children.

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

100 Astrocytomas are common and lethal human brain tumors.

101 Malignant astrocytomas are highly invasive brain tumors.

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

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

104 Astrocytomas are the most common type of brain tumors in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 Human astrocytoma cell stress granules contain mRNAs that are

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

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

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

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

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

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

139 Cytoplasmic fractionation of astrocytoma cells followed by ECT2 immunoprecipitation a

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

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

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

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

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

145 antagonistic potency was assessed in 1321N1 astrocytoma cells stably transfected with the human P2X1

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

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

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

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

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

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

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

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

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

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

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

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

158 1 and CDC42 at the leading edge of migrating astrocytoma cells.

159 in mesenchymal-amoeboid transition in human astrocytoma cells.

160 cting protein that regulates RHO activity in astrocytoma cells.

161 lant of genetically relevant murine or human astrocytoma cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 Astrocytoma (glioma) formation in neurofibromatosis type

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

179 8q13.1 gain, was observed in 28% of diffuse astrocytoma grade IIs and resulted in partial duplicatio

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

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

182 urrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-a

183 omprised patients with WHO grade I pilocytic astrocytoma harbouring either one of the two most common

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

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

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

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

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

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

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

191 DH-mutant and 1p19q co-deleted (n = 81); (2) astrocytoma, IDH-mutant and 1p19q non-codeleted (n = 54)

192 mutant and 1p19q non-codeleted (n = 54); (3) astrocytoma, IDH-wildtype (n = 20).

193 , a similar association was only retained in astrocytoma, IDH-wildtype.

194 markers and added prognostic information in astrocytoma, IDH-wildtype.

195 19q differentiating oligodendrogliomas from astrocytomas; (iii) IDH1/2 mutations; and (iv) select pa

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

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

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

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

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

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

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

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

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

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

206 Glioblastoma (GBM), or grade IV astrocytoma, is a malignant brain cancer that contains s

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

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

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

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

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

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

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

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

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

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

217 ll characterized cohorts of human high-grade astrocytomas, mostly glioblastomas, compared to healthy

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

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

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

221 tions in 15.7% of tumors (ependymoma, N = 7; astrocytoma, N = 1), RP1 mutations in 5.9% of tumors (ep

222 sequencing of 12 tumors (ependymoma, N = 9; astrocytoma, N = 3).

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

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

225 8,000 promoters in normal human brain and in astrocytomas of various grades using the methylated CpG

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

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

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

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

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

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

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

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

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

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 astrocytoma (PA), the most common childhood brain tumor,

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

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

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

246 rated into clinical evaluation of anaplastic astrocytoma patients.

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

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

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

250 PFA/PFB ependymoma and cerebellar pilocytic astrocytoma resemble the prenatal gliogenic progenitor c

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

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

253 Anaplastic astrocytoma samples with mutated IDH1 display lower leve

254 35% of patients with subependymal giant cell astrocytoma (SEGA) associated with tuberous sclerosis co

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

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

257 In astrocytomas, several hundred CpG islands undergo specif

258 t acute myeloid leukemia, oligodendroglioma, astrocytoma, solid papillary breast carcinoma with rever

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

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

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

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

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

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

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

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

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

268 expression uniquely sensitized primary human astrocytomas to apoptosis.

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

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

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

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

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

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

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

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

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

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

279 = 0.0007), and EGFR expression in anaplastic astrocytoma was associated with nearly 3-fold poorer sur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

299 66, P=4.7x10(-12) to 2.2x10(-8)) but not for astrocytomas with wild-type IDH1 and IDH2 (smallest P=0.

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