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 rectly correlates with that of CBX7 in human glioblastoma multiforme.

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

4 the recently described proneural subtype of glioblastoma multiforme.

5 y driver and candidate therapeutic target in glioblastoma multiforme.

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

7 amyotrophic lateral sclerosis, dementia and glioblastoma multiforme.

8 on regarding life expectancy to survivors of glioblastoma multiforme.

9 al trials with selected kinase inhibitors in glioblastoma multiforme.

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

11 ne responses to immune checkpoint therapy in glioblastoma multiforme and demonstrate that comprehensi

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

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

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

15 On average, glioblastoma multiforme and medulloblastoma had uniform,

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

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

18 tes DICER in multiple cancer cells including glioblastoma multiforme and prostate, breast, lung, and

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

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

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

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

23 Using a xenograft nude mouse model of human glioblastoma multiforme, blocking the efflux function of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 Glioblastoma multiforme contains a subpopulation of canc

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

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

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

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

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

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

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

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

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

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

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

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

56 In human glioblastoma multiforme, expression of CD44 correlated w

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

58 26% (95% CI: 17-35%, P = 1.05 x 10(-8)) for glioblastoma multiforme (GBM) and 25% (95% CI: 17-32%, P

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

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

61 Glioblastoma multiforme (GBM) and other solid malignanci

62 Glioblastoma multiforme (GBM) and the mesenchymal GBM su

63 To date current therapies of glioblastoma multiforme (GBM) are largely ineffective.

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

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

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

67 cose uptake and lactate production, inhibits glioblastoma multiforme (GBM) autophagy, and induces apo

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

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

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

71 lopment of new drugs and active targeting in glioblastoma multiforme (GBM) cancer therapy.

72 Glioblastoma multiforme (GBM) cell line, highly malignan

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

74 Glioblastoma Multiforme (GBM) cells are highly invasive,

75 ndent mechanism of cell death in p53-mutated glioblastoma multiforme (GBM) cells exposed to plasma.

76 the uptake of gold nanoparticle into U373MG Glioblastoma multiforme (GBM) cells predicts that CAP ma

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

78 Temozolomide (TMZ)-resistant glioblastoma multiforme (GBM) cells would have abnormal

79 on a murine tumor model comprised of U-87 MG glioblastoma multiforme (GBM) cells, known to form highl

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

81 ds (TTFields)," had an antimitotic effect on glioblastoma multiforme (GBM) cells.

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

83 Glioblastoma multiforme (GBM) comprises several molecula

84 Glioblastoma multiforme (GBM) contains a subpopulation o

85 Glioblastoma multiforme (GBM) continues to have a dismal

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

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

88 Glioblastoma multiforme (GBM) displays cellular hierarch

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

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

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

92 Glioblastoma multiforme (GBM) has few clinically approve

93 Mortality of glioblastoma multiforme (GBM) has not improved over the

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

95 failure of checkpoint-blockade therapies for glioblastoma multiforme (GBM) in late-phase clinical tri

96 Glioblastoma multiforme (GBM) is a devastating brain tum

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

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

99 Glioblastoma multiforme (GBM) is a highly aggressive mal

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 highly proliferative

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 brain tumor

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

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

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

112 Glioblastoma multiforme (GBM) is an aggressive and diffi

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 cancer wi

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

118 Glioblastoma multiforme (GBM) is an intractable tumor de

119 Glioblastoma multiforme (GBM) is characterized by a path

120 Glioblastoma multiforme (GBM) is characterized by overex

121 ferent tumors, its effectiveness in treating glioblastoma multiforme (GBM) is constrained by insuffic

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

123 Glioblastoma multiforme (GBM) is highly invasive and uni

124 Glioblastoma multiforme (GBM) is impossible to fully rem

125 Recurrent glioblastoma multiforme (GBM) is incurable with current

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

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

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

129 Glioblastoma multiforme (GBM) is one of the most common

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

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

132 Glioblastoma multiforme (GBM) is the deadliest form of b

133 Glioblastoma multiforme (GBM) is the most aggressive and

134 Glioblastoma multiforme (GBM) is the most aggressive and

135 Glioblastoma multiforme (GBM) is the most aggressive for

136 Glioblastoma multiforme (GBM) is the most aggressive of

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

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

139 Glioblastoma multiforme (GBM) is the most common and dea

140 Glioblastoma multiforme (GBM) is the most common and dev

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

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

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

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

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

146 Glioblastoma multiforme (GBM) is the most common primary

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

148 Glioblastoma multiforme (GBM) is the most deadly brain t

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

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

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

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

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

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

155 ng and functional studies of glioma cells in glioblastoma multiforme (GBM) models establish that PTEN

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

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

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

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

160 Glioblastoma multiforme (GBM) remains a mainly incurable

161 Importance: Glioblastoma multiforme (GBM) remains almost invariably

162 Glioblastoma multiforme (GBM) remains the deadliest brai

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

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

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

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

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

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

169 Patients with glioblastoma multiforme (GBM) survive on average 12 to 1

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

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

172 Glioblastoma multiforme (GBM) tumors are highly metaboli

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

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

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

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

177 ntal roles in tumour malignancies, including glioblastoma multiforme (GBM) which presents largely der

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

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

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

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

182 Glioblastoma multiforme (GBM), a deadly cancer, is the m

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

184 apy plays a pivotal role in the treatment of glioblastoma multiforme (GBM), an aggressive form of pri

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

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

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

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

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

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

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

192 opulations in the tumour microenvironment in glioblastoma multiforme (GBM), the most common malignant

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

194 These pathologies are glioblastoma multiforme (GBM), traumatic brain injuries

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

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

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

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

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

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

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

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

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

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

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

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

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

208 py is the major treatment modality for human glioblastoma multiforme (GBM).

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

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

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

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

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

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

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

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

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

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

219 There is an unmet need for the treatment of glioblastoma multiforme (GBM).

220 ible mechanisms in controlling the growth of glioblastoma multiforme (GBM).

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

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

223 d macrophages (TAMs) promotes progression of glioblastoma multiforme (GBM).

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

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

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

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

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

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

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

231 role in the progression and invasiveness of glioblastoma multiforme (GBM); however, the exact crosst

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

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

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

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

236 east cancers (BRCAs) into five subgroups and glioblastoma multiformes (GBMs) into six subgroups with

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

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

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

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

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

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

243 Glioblastoma multiforme is a very aggressive and common

244 Glioblastoma multiforme is an aggressive, invasive brain

245 Glioblastoma multiforme is an aggressive, treatment-refr

246 Glioblastoma multiforme is generally recalcitrant to cur

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

248 Glioblastoma multiforme is the most aggressive primary b

249 Glioblastoma multiforme is the most aggressive type of p

250 Glioblastoma multiforme is the most common glioma varian

251 Glioblastoma multiforme is the most common primary malig

252 Glioblastoma multiforme is the most common type of prima

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

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

255 Glioblastoma multiforme lacks effective therapy options.

256 In human glioblastoma multiforme, mitochondrial serine hydroxymet

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

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

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

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

261 cell lung cancer, esophageal adenocarcinoma, glioblastoma multiforme, ovarian cancer and liver cancer

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

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

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

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

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

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

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

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

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

271 point therapy and those that do not, such as glioblastoma multiforme, prostate cancer and colorectal

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

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

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

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

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

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

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

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

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

281 unique population of CD73(hi) macrophages in glioblastoma multiforme that persists after anti-PD-1 tr

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 CD73 improved survival in a murine model of glioblastoma multiforme treated with anti-CTLA-4 and ant

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

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

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

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

290 Human glioblastoma multiforme tumors often contain rapidly pro

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 ant for a successful combination strategy in glioblastoma multiforme, we performed reverse translatio

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

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

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

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