ライフサイエンスコーパス: glioblastoma multiforme

1 c astrocytomas, 5 gliomatosis cerebri, and 1 glioblastoma multiforme).

2 ar degeneration, or certain cancers, such as glioblastoma multiforme.

3 the recently described proneural subtype of glioblastoma multiforme.

4 y driver and candidate therapeutic target in glioblastoma multiforme.

5 eatable brain cancer in children and adults: glioblastoma multiforme.

6 amyotrophic lateral sclerosis, dementia and glioblastoma multiforme.

7 on regarding life expectancy to survivors of glioblastoma multiforme.

8 uman brain, but it is frequently silenced in glioblastoma multiforme.

9 redicts survival after surgery for recurrent glioblastoma multiforme.

10 iver cancer, soft tissue leiomyosarcoma, and glioblastoma multiforme.

11 , spinal cord injury, multiple sclerosis and glioblastoma multiforme.

12 al trials with selected kinase inhibitors in glioblastoma multiforme.

13 rectly correlates with that of CBX7 in human glioblastoma multiforme.

14 mas, meningiomas, schwannomas, and pediatric glioblastoma multiformes.

15 Twenty-two patients had glioblastoma multiforme, 2 had anaplastic oligodendrogli

16 sion was assessed in lung adenocarcinoma and glioblastoma multiforme and documented in several other

17 The EphA2 receptor is overexpressed in glioblastoma multiforme and has been to shown to contrib

18 motherapy failure, and patients with primary glioblastoma multiforme and high tumor CcO activity have

19 On average, glioblastoma multiforme and medulloblastoma had uniform,

20 ng brain cancer cell lines: primary cancers (glioblastoma multiforme and neuroblastoma), human brain

21 er types in the Cancer Genome Atlas project: glioblastoma multiforme and ovarian serous cystadenocarc

22 ld have a significant impact on treatment of glioblastoma multiforme and suggests previously undescri

23 ssive cancer entities like neuroblastoma and glioblastoma multiforme are still difficult to treat and

24 alpha mRNA was detected in highly aggressive glioblastoma multiforme as compared with Grade II/III gl

25 isogenic cell lines representing the cancer glioblastoma multiforme, at the basal level, under EGF s

26 nized as a widespread oncogenic signature in glioblastoma multiforme, but the complexity of its contr

27 Here, we exploit this characteristic of glioblastoma multiforme by engineering aligned polycapro

28 s known to drive the aggressive character of glioblastoma multiforme by promoting aerobic glycolysis

29 Tested on colorectal carcinoma and glioblastoma multiforme cancer stem cells (CSCs) from pa

30 on of SEC61gamma serves significant roles in glioblastoma multiforme cell survival likely via a mecha

31 (fibroblast), H23 (lung cancer), and A-172 (glioblastoma multiforme) cell lines and knocked out in H

32 ER stress modulates DR5 expression in human glioblastoma multiforme cells and can enhance TRAIL effi

33 Human glioblastoma multiforme cells demonstrate varying levels

34 oma multiforme cells inhibited growth of the glioblastoma multiforme cells in mouse brain in vivo.

35 ced cell proliferation and survival in human glioblastoma multiforme cells in vitro and in vivo.

36 unfolded protein responses in CypB-depleted glioblastoma multiforme cells indicated that CypB allevi

37 rexpression of transfected miR-25 and -32 in glioblastoma multiforme cells inhibited growth of the gl

38 r results were obtained in U87MG and primary glioblastoma multiforme cells maintained in primary cult

39 uidic mixing tool is reported to encapsulate glioblastoma multiforme cells within miniaturized gelati

40 p amino acids were transfected into U-251 MG glioblastoma multiforme cells, and functional activity o

41 R), provides an essential survival signal in glioblastoma multiforme cells.

42 ypoxia-inducing factor (HIF)-1alpha in human glioblastoma multiforme cells.

43 G cells compared with bevacizumab-responsive glioblastoma multiforme cells.

44 closporine, greatly reduced the viability of glioblastoma multiforme cells.

45 is in acute myeloid leukemia, breast cancer, glioblastoma multiforme, colon, skin and lung cancer.

46 Malignant gliomas, including glioblastoma multiforme, constitute the most common and

47 Glioblastoma multiforme contains a subpopulation of canc

48 itor AGK-2 showed the highest effect against glioblastoma multiforme CSCs.

49 tients with brain tumors, such as aggressive glioblastoma multiforme, CTC assays are needed that do n

50 est the proposed method on breast cancer and glioblastoma multiforme data obtained from TCGA.

51 rough simulation studies, and application to glioblastoma multiforme data resulted in informative can

52 expression data from the Cancer Genome Atlas Glioblastoma multiforme dataset and show that survival i

53 on three colorectal cancer datasets and two glioblastoma multiforme datasets and show that our multi

54 Here, we report that human glioblastoma multiforme-derived LN-18 cells do not hydro

55 port that global DNA methylation patterns in glioblastoma multiforme divide adult and pediatric tumor

56 ilico screening, we then found that the anti-glioblastoma multiforme drug lead vacquinol is an inhibi

57 sis, LGG (Brain lower grade glioma) and GBM (Glioblastoma multiforme), due to the possible progressio

58 In clinical specimens of glioblastoma multiforme, elevated levels of CCL2 express

59 of human pulmonary arterial hypertension and glioblastoma multiforme exhibited a markedly increased a

60 High grade gliomas such as glioblastoma multiforme express multiple members of the

61 In human glioblastoma multiforme, expression of CD44 correlated w

62 The patients had glioblastoma multiforme (GBM) (n = 20), metastasis (n =

63 26% (95% CI: 17-35%, P = 1.05 x 10(-8)) for glioblastoma multiforme (GBM) and 25% (95% CI: 17-32%, P

64 o a proinvasive phenotype in mouse models of glioblastoma multiforme (GBM) and in a subset of GBM pat

65 gene-1 (AEG-1; MTDH) is highly expressed in glioblastoma multiforme (GBM) and many other types of ca

66 ed in normal tissues but widely expressed in glioblastoma multiforme (GBM) and other neoplasms.

67 Glioblastoma multiforme (GBM) and the mesenchymal GBM su

68 orted CD133(+) and CD133(-) cells from human glioblastoma multiforme (GBM) and, by subtractive analys

69 Using glioblastoma multiforme (GBM) as a model system, we soug

70 selectively expressed at a high frequency by glioblastoma multiforme (GBM) as well as several other t

71 or to (18)F-FET in predicting progression of glioblastoma multiforme (GBM) at follow-up.

72 tantly, human primary and recurrent pairs of glioblastoma multiforme (GBM) biopsies as well as primar

73 F207, from an RNAi viability screen in human glioblastoma multiforme (GBM) brain tumor stem cells.

74 rain tumors such as medulloblastoma (MB) and glioblastoma multiforme (GBM) can derive from neural pre

75 In a glioblastoma multiforme (GBM) cancer cell model, we exam

76 xpression of lipid metabolism genes in human glioblastoma multiforme (GBM) cancer cells.

77 Glioblastoma multiforme (GBM) cell line, highly malignan

78 egrating metabolic and functional studies in glioblastoma multiforme (GBM) cell lines, preclinical mo

79 Glioblastoma Multiforme (GBM) cells are highly invasive,

80 might increase the susceptibility of U-87 MG glioblastoma multiforme (GBM) cells to subsequent treatm

81 deletion mutant (EGFRvIII) present on human glioblastoma multiforme (GBM) cells were used for therap

82 e interleukin-13 (IL-13) effectively targets glioblastoma multiforme (GBM) cells, which are known to

83 n 24 (mda-7/IL-24) in invasive primary human glioblastoma multiforme (GBM) cells.

84 ng ligand (TRAIL)-induced apoptosis in human glioblastoma multiforme (GBM) cells.

85 ns of NDRG4 in the context of astrocytes and glioblastoma multiforme (GBM) cells.

86 Glioblastoma multiforme (GBM) comprises several molecula

87 ression network (WGCN) analysis algorithm on glioblastoma multiforme (GBM) data obtained from the TCG

88 te the power of RCytoscape, a portion of the Glioblastoma multiforme (GBM) data set from the Cancer G

89 Glioblastoma multiforme (GBM) displays cellular hierarch

90 The malignant brain cancer glioblastoma multiforme (GBM) displays invasive growth b

91 s and circulating monocytes in patients with glioblastoma multiforme (GBM) express ligands for activa

92 n profiles of 202 tumors of the brain cancer glioblastoma multiforme (GBM) given at the Cancer Genome

93 otypes with a bias for amino acid changes in glioblastoma multiforme (GBM) in comparison to the low-g

94 Glioblastoma multiforme (GBM) is a deadly primary brain

95 Glioblastoma multiforme (GBM) is a devastating brain tum

96 e most common malignant primary brain tumor, glioblastoma multiforme (GBM) is a devastating disease w

97 Glioblastoma multiforme (GBM) is a fatal brain tumor cha

98 Glioblastoma multiforme (GBM) is a fatal primary brain t

99 Glioblastoma multiforme (GBM) is a highly invasive and v

100 Glioblastoma multiforme (GBM) is a highly invasive brain

101 Glioblastoma multiforme (GBM) is a highly invasive brain

102 Glioblastoma multiforme (GBM) is a highly malignant prim

103 Glioblastoma multiforme (GBM) is a highly malignant prim

104 Glioblastoma multiforme (GBM) is a lethal brain tumor ch

105 Glioblastoma multiforme (GBM) is a lethal cancer charact

106 Glioblastoma multiforme (GBM) is a lethal, therapy-resis

107 Real-time monitoring of drug efficacy in glioblastoma multiforme (GBM) is a major clinical proble

108 Glioblastoma multiforme (GBM) is a malignant astrocytoma

109 Glioblastoma multiforme (GBM) is a severe brain malignan

110 Glioblastoma Multiforme (GBM) is a tumor with high morta

111 The brain tumor glioblastoma multiforme (GBM) is among the most lethal f

112 Glioblastoma multiforme (GBM) is among the most lethal o

113 Glioblastoma multiforme (GBM) is an aggressive brain tum

114 Glioblastoma multiforme (GBM) is an aggressive brain tum

115 Glioblastoma multiforme (GBM) is an aggressive brain tum

116 Glioblastoma multiforme (GBM) is an aggressive, Grade IV

117 Glioblastoma multiforme (GBM) is an intractable tumor de

118 Glioblastoma multiforme (GBM) is characterized by a path

119 Glioblastoma multiforme (GBM) is characterized by overex

120 The aggressiveness of glioblastoma multiforme (GBM) is defined by local invasi

121 Glioblastoma multiforme (GBM) is highly invasive and uni

122 Recurrent glioblastoma multiforme (GBM) is incurable with current

123 The dismal prognosis of glioblastoma multiforme (GBM) is mainly due to the poor

124 Glioblastoma multiforme (GBM) is one of the most aggress

125 Glioblastoma multiforme (GBM) is one of the most aggress

126 Glioblastoma multiforme (GBM) is one of the most intract

127 e high frequency of abnormal PI3K signaling, glioblastoma multiforme (GBM) is particularly relevant b

128 Glioblastoma multiforme (GBM) is the most aggressive and

129 Glioblastoma multiforme (GBM) is the most aggressive bra

130 Glioblastoma multiforme (GBM) is the most aggressive for

131 Glioblastoma multiforme (GBM) is the most aggressive of

132 Glioblastoma multiforme (GBM) is the most common and agg

133 Glioblastoma multiforme (GBM) is the most common and agg

134 Glioblastoma multiforme (GBM) is the most common and let

135 Glioblastoma multiforme (GBM) is the most common and let

136 Glioblastoma multiforme (GBM) is the most common and let

137 Glioblastoma multiforme (GBM) is the most common and let

138 Glioblastoma multiforme (GBM) is the most common and mal

139 Glioblastoma multiforme (GBM) is the most common form of

140 Glioblastoma multiforme (GBM) is the most common primary

141 Glioblastoma multiforme (GBM) is the most common type of

142 Glioblastoma multiforme (GBM) is the most frequent and a

143 Glioblastoma multiforme (GBM) is the most frequent and i

144 e important function of endothelial cells in glioblastoma multiforme (GBM) is to create a niche that

145 The lack of innovative drug targets for glioblastoma multiforme (GBM) limits patient survival to

146 Neoplastic cells of Glioblastoma multiforme (GBM) may or may not show sustai

147 detection sensitivity and can differentiate glioblastoma multiforme (GBM) microvesicles from nontumo

148 se hallmark features, we developed a de novo glioblastoma multiforme (GBM) model derived from immorta

149 Volumetric change in glioblastoma multiforme (GBM) over time is a critical fa

150 reatment is the major cause of mortality for glioblastoma multiforme (GBM) patients.

151 oxM1B-expressing immortalized NHAs displayed glioblastoma multiforme (GBM) phenotypes, suggesting tha

152 Macrophages accumulate with glioblastoma multiforme (GBM) progression and can be tar

153 n, outcomes for patients diagnosed as having glioblastoma multiforme (GBM) remain poor.

154 Glioblastoma multiforme (GBM) remains a mainly incurable

155 Importance: Glioblastoma multiforme (GBM) remains almost invariably

156 Glioblastoma multiforme (GBM) remains the deadliest brai

157 A central question in glioblastoma multiforme (GBM) research is the identity o

158 The lethality of the aggressive brain tumor glioblastoma multiforme (GBM) results in part from its s

159 We show that in glioblastoma multiforme (GBM) specimens, death-domain ad

160 ozygously lost in approximately 20% of human glioblastoma multiforme (GBM) specimens, primarily of th

161 d primary cultures, whereas remaining low in glioblastoma multiforme (GBM) stable cell lines, low-gra

162 genome-wide RNAi screens in patient-derived glioblastoma multiforme (GBM) stem cells (GSCs).

163 engineered stem cells have shown promise for glioblastoma multiforme (GBM) therapy; however, key prec

164 has shown that patients newly diagnosed with glioblastoma multiforme (GBM) treated with bevacizumab p

165 ) family of RNA-binding proteins, as a novel glioblastoma multiforme (GBM) tumor suppressor.

166 s 4 and 6 (cdk4/6) occurs in the majority of glioblastoma multiforme (GBM) tumors, and represents a p

167 alovirus (HCMV) infections are seen often in glioblastoma multiforme (GBM) tumors, but whether the vi

168 ence and expression data for a collection of glioblastoma multiforme (GBM) tumors.

169 We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib

170 nts with cerebral stroke and 4 patients with glioblastoma multiforme (GBM) underwent 150-min dynamic

171 l resection, radiotherapy, and chemotherapy, glioblastoma multiforme (GBM) virtually always recurs.

172 althy control subjects and six patients with glioblastoma multiforme (GBM) with an acquisition time o

173 To compare contrast material enhancement of glioblastoma multiforme (GBM) with intraoperative contra

174 , we investigated here whether NF1-deficient glioblastoma multiforme (GBM) would respond to MEK inhib

175 Age is a powerful predictor of survival in glioblastoma multiforme (GBM) yet the biological basis f

176 The cancer stem cells (CSCs) of glioblastoma multiforme (GBM), a grade IV astrocytoma, h

177 is a potential oncolytic virus for treating glioblastoma multiforme (GBM), an aggressive brain tumor

178 is a major cause for the dismal prognosis of glioblastoma multiforme (GBM), but the underlying mechan

179 In glioblastoma multiforme (GBM), epidermal growth factor r

180 Glioblastoma multiforme (GBM), like most cancers, posses

181 Glioblastoma multiforme (GBM), the grade IV astrocytoma,

182 is of particular importance in patients with glioblastoma multiforme (GBM), the highest grade and mos

183 RT-qPCR) based molecular-subtyping assay for glioblastoma multiforme (GBM), the most aggressive prima

184 Glioblastoma multiforme (GBM), the most common and aggre

185 are currently available for the treatment of glioblastoma multiforme (GBM), the most common and letha

186 , chemotherapy, and radiation, patients with glioblastoma multiforme (GBM), the most common histologi

187 Glioblastoma multiforme (GBM), the most common intracran

188 delivered in the treatment of patients with glioblastoma multiforme (GBM), the tumors invariably rec

189 In glioblastoma multiforme (GBM), translocator protein (TSP

190 olecular basis for prognostic differences in glioblastoma multiforme (GBM), we employed a combinatori

191 nalysis of The Cancer Genome Atlas's data on glioblastoma multiforme (GBM), we found that the genomic

192 Glioblastoma multiforme (GBM), which account for more th

193 H3K4me3 in the MRI-classified SVZ-associated Glioblastoma Multiforme (GBM), which has a transcription

194 These include glioblastoma multiforme (GBM), which is characterized by

195 vity is elevated in astrocytes isolated from glioblastoma multiforme (GBM)-prone H-Ras(12V) knock-in

196 ial oncogenic/tumor suppressive functions in glioblastoma multiforme (GBM).

197 ivated genes across human cancers, including glioblastoma multiforme (GBM).

198 a cell line sharing characteristics of human glioblastoma multiforme (GBM).

199 hobiology of myriad cancers, one of which is glioblastoma multiforme (GBM).

200 n applied to high-grade brain tumors such as glioblastoma multiforme (GBM).

201 e effectiveness of single-agent therapies in glioblastoma multiforme (GBM).

202 receptor (EGFR) gene are frequently found in glioblastoma multiforme (GBM).

203 r-associated receptor overexpressed in human glioblastoma multiforme (GBM).

204 We applied our approach to Glioblastoma Multiforme (GBM).

205 receptor (EGFRvIII) in a cell line model of glioblastoma multiforme (GBM).

206 ignaling of the highly malignant brain tumor glioblastoma multiforme (GBM).

207 lioma in a young man with a history of brain glioblastoma multiforme (GBM).

208 ) are considered to be the cell of origin of glioblastoma multiforme (GBM).

209 , SLFN5, promotes the malignant phenotype in glioblastoma multiforme (GBM).

210 types, particularly in the highly malignant glioblastoma multiforme (GBM).

211 gene play a crucial role in pathogenesis of glioblastoma multiforme (GBM).

212 terminant of tumor growth and progression in glioblastoma multiforme (GBM).

213 of differentiation-4 is highly expressed in glioblastoma multiforme (GBM).

214 n treating infiltrative brain tumors such as glioblastoma multiforme (GBM).

215 en linked to poor prognosis in patients with glioblastoma multiforme (GBM).

216 rrant vascularization and chemoresistance in glioblastoma multiforme (GBM).

217 ous diseases, among which the most deadly is glioblastoma multiforme (GBM).

218 th and increased invasive characteristics in glioblastoma multiforme (GBM).

219 hich are key factors for the incurability of glioblastoma multiforme (GBM).

220 to develop nanocarriers for the treatment of glioblastoma multiforme (GBM).

221 apeutic resistance of solid tumors, foremost glioblastoma multiforme (GBM).

222 ve therapeutic paradigm for the treatment of glioblastoma multiforme (GBM).

223 its adjacent CDKN2A on chromosome 9p21.3 in glioblastoma multiforme (GBM).

224 ircumvent inherent therapeutic resistance of glioblastoma multiforme (GBM).

225 e nucleotide polymorphism (SNP) genotypes in glioblastoma multiforme (GBM).

226 Glioblastoma multiforme (GBM)/astrocytoma grade IV is a

227 he understanding of the molecular biology of glioblastoma multiforme (GBM); thus, complex genetic alt

228 letion mutant (EGFRvIII), occurs commonly in glioblastoma multiformes (GBM).

229 AIL resistance in aggressive tumors, such as glioblastoma-multiforme (GBM), and understanding the mol

230 I gliomas as well as grade IV glioblastomas (glioblastoma multiforme [GBM]).

231 radiotherapy improves survival in patients, glioblastoma multiformes (GBMs) tend to relapse with aug

232 tant was common, being present in 40% of the glioblastoma multiformes (GBMs) with PDGFRA amplificatio

233 ways are drivers of malignant progression in glioblastoma multiforme, glioma cells exhibit intrinsic

234 e Warburg phenotype to OXPHOS and inhibiting glioblastoma multiforme growth and proliferation.

235 he tumor and inhibits tumor angiogenesis and glioblastoma multiforme growth in a mouse orthotopic bra

236 mor samples (including renal cell carcinoma, glioblastoma multiforme, head and neck squamous cell car

237 ) localizes to genetically diverse models of glioblastoma multiforme in vivo.

238 Glioblastoma multiforme is a very aggressive and common

239 Glioblastoma multiforme is an aggressive, invasive brain

240 Glioblastoma multiforme is an aggressive, treatment-refr

241 Glioblastoma multiforme is generally recalcitrant to cur

242 Current therapy for glioblastoma multiforme is insufficient, with nearly uni

243 Glioblastoma multiforme is the most aggressive primary b

244 Glioblastoma multiforme is the most aggressive type of p

245 Glioblastoma multiforme is the most common and lethal pr

246 Glioblastoma multiforme is the most common glioma varian

247 Glioblastoma multiforme is the most common primary malig

248 Glioblastoma multiforme is the most common type of prima

249 lthough YKL-40 expression is up-regulated in glioblastoma multiforme, its regulation and functions in

250 from patients with colorectal carcinoma and glioblastoma multiforme, known to be highly tumorigenic,

251 Glioblastoma multiforme lacks effective therapy options.

252 In human glioblastoma multiforme, mitochondrial serine hydroxymet

253 l vectors is a novel way to generate a mouse glioblastoma multiforme model in a region- and cell type

254 d brain invasion and prolonged survival in a glioblastoma multiforme model, prevented metastatic dise

255 Based on a model that assumed the glioblastoma multiforme mutations are a mixture of drive

256 ned carriers also had neuroblastoma (n = 1), glioblastoma multiforme (n = 1), choroid plexus carcinom

257 oma/primitive neuroectodermal tumor (n = 4), glioblastoma multiforme (n = 2), atypical teratoid/rhabd

258 ioma cells, including freshly isolated human glioblastoma multiforme neurosphere cultures (containing

259 association with rs55705857 confined to non-glioblastoma multiforme (non-GBM) tumours (P = 1.07 x 10

260 tion into the role of EC-CSC interactions in glioblastoma multiforme pathobiology.

261 ets as well as large-scale Breast Cancer and Glioblastoma Multiforme patient samples from The Cancer

262 s and freshly resected surgical tissues from glioblastoma multiforme patients strongly expressed gBK

263 elevance, we found that T cells derived from glioblastoma multiforme patients that were sensitized to

264 egy may provide a path to DON utilization in glioblastoma multiforme patients.

265 g macrophages were a major source of CCL2 in glioblastoma multiforme patients.

266 the gamma-secretase enzyme were elevated in glioblastoma multiformes patients.

267 ted this algorithm on synthetic data and 100 Glioblastoma Multiforme primary tumor samples.

268 We show that, in the case of glioblastoma multiforme, primary tumors and xenografts a

269 In many aggressive cancers, such as glioblastoma multiforme, progression is enabled by local

270 in liver tumors, esophageal adenocarcinoma, glioblastoma multiforme, prostate tumors, non-small cell

271 babilities on the basis of 498 patients with glioblastoma multiforme receiving radiation and chemothe

272 vels of metabolites predominant in recurrent glioblastoma multiforme (rGBM) to characterize the respo

273 arrays to screen for copy-number changes in glioblastoma multiforme samples and found that the most

274 ray expression profiles available for common glioblastoma multiforme samples from The Cancer Genome A

275 east cancer and performed SP analyses on 118 glioblastoma multiforme samples obtained from TCGA.

276 ighly amplified tumor regions in a subset of glioblastoma multiforme samples sequenced by The Cancer

277 CSF samples from patients with glioblastoma multiforme show elevated Igf2 and stimulate

278 PDK1, EGFR, and HIF-1alpha were elevated in glioblastoma multiforme specimens when compared with nor

279 orme data resulted in informative cancer and glioblastoma multiforme subtype-related findings.

280 Three patients with MGMT unmethylated glioblastoma multiforme survived 6.5, 8.7, and 46.4 mont

281 enomes include the sequencing of 22 cases of glioblastoma multiforme that identified IDH1, the gene e

282 ng those estimated for colorectal cancer and glioblastoma multiforme, the distribution of sizes of su

283 Two hallmarks of glioblastoma multiforme, the most common malignant brain

284 tive and immediately targetable molecule for glioblastoma multiforme therapy.

285 zolomide poses a major clinical challenge in glioblastoma multiforme treatment, and the mechanisms un

286 ow that data derived from non-microdissected glioblastoma multiforme tumor tissue is either masked or

287 Cancer stem cells from Glioblastoma Multiforme tumors express markers that are

288 also useful for analysis of a larger set of glioblastoma multiforme tumors for which exome sequencin

289 Human glioblastoma multiforme tumors often contain rapidly pro

290 igned to target an overexpressed receptor in glioblastoma multiforme tumors.

291 7EGFRvIII cells relative to U87PTEN cells in glioblastoma multiforme tumors.

292 B may thus contribute to the poor outcome of glioblastoma multiforme tumors.

293 Two patients with histologically confirmed glioblastoma multiforme underwent brain imaging.

294 f glioma serum samples and sub-categories of glioblastoma multiforme using Human Proteome chips conta

295 In clinical specimens of glioblastoma multiforme, we found that immunohistochemic

296 s properties with respect to human models of glioblastoma multiforme were studied in vivo.

297 lopment of the highest grade of astrocytoma, Glioblastoma multiforme were: COL4A1, EGFR, BTF3, MPP2,

298 that Hes3 is also expressed in cultures from glioblastoma multiforme which express neural stem cell m

299 ars]; 12 female [median age, 59 years]) with glioblastoma multiforme who were treated with RT-TMZ wer

300 ples-leading to the discovery of clusters of glioblastoma multiforme with differential survival.