ライフサイエンスコーパス: multiforme

1 lioblastoma (GB; formerly referred to as 'GB multiforme').

2 s, 5 gliomatosis cerebri, and 1 glioblastoma multiforme).

3 ates with that of CBX7 in human glioblastoma multiforme.

4 on, or certain cancers, such as glioblastoma multiforme.

5 described proneural subtype of glioblastoma multiforme.

6 candidate therapeutic target in glioblastoma multiforme.

7 cancer in children and adults: glioblastoma multiforme.

8 lateral sclerosis, dementia and glioblastoma multiforme.

9 life expectancy to survivors of glioblastoma multiforme.

10 h selected kinase inhibitors in glioblastoma multiforme.

11 Twenty-two patients had glioblastoma multiforme, 2 had anaplastic oligodendroglioma, 1 had an

12 to immune checkpoint therapy in glioblastoma multiforme and demonstrate that comprehensive human and

13 ssed in lung adenocarcinoma and glioblastoma multiforme and documented in several other cancer types

14 A2 receptor is overexpressed in glioblastoma multiforme and has been to shown to contribute to cell t

15 lure, and patients with primary glioblastoma multiforme and high tumor CcO activity have worse clinic

16 On average, glioblastoma multiforme and medulloblastoma had uniform, intense upta

17 er cell lines: primary cancers (glioblastoma multiforme and neuroblastoma), human brain cancer cell l

18 he Cancer Genome Atlas project: glioblastoma multiforme and ovarian serous cystadenocarcinoma.

19 multiple cancer cells including glioblastoma multiforme and prostate, breast, lung, and liver carcino

20 nificant impact on treatment of glioblastoma multiforme and suggests previously undescribed routes fo

21 ism; grade 3 iridocyclitis, grade 1 erythema multiforme, and grade 3 erythema; and grade 2 infusion-r

22 entities like neuroblastoma and glioblastoma multiforme are still difficult to treat and have discour

23 s detected in highly aggressive glioblastoma multiforme as compared with Grade II/III glioblastomas,

24 l lines representing the cancer glioblastoma multiforme, at the basal level, under EGF stimulation, a

25 graft nude mouse model of human glioblastoma multiforme, blocking the efflux function of P-gp with ve

26 pes of cancer including mesothelioma, glioma multiforme, breast, colorectal, skin, clear cell renal c

27 despread oncogenic signature in glioblastoma multiforme, but the complexity of its contributions is n

28 exploit this characteristic of glioblastoma multiforme by engineering aligned polycaprolactone (PCL)

29 ive the aggressive character of glioblastoma multiforme by promoting aerobic glycolysis rather than p

30 ted on colorectal carcinoma and glioblastoma multiforme cancer stem cells (CSCs) from patients, 2b wa

31 , H23 (lung cancer), and A-172 (glioblastoma multiforme) cell lines and knocked out in HUH7 (liver ca

32 dulates DR5 expression in human glioblastoma multiforme cells and can enhance TRAIL efficacy.

33 e cells inhibited growth of the glioblastoma multiforme cells in mouse brain in vivo.

34 iferation and survival in human glioblastoma multiforme cells in vitro and in vivo.

35 tein responses in CypB-depleted glioblastoma multiforme cells indicated that CypB alleviates oxidativ

36 f transfected miR-25 and -32 in glioblastoma multiforme cells inhibited growth of the glioblastoma mu

37 e obtained in U87MG and primary glioblastoma multiforme cells maintained in primary culture and follo

38 tool is reported to encapsulate glioblastoma multiforme cells within miniaturized gelatin hydrogels c

39 were transfected into U-251 MG glioblastoma multiforme cells, and functional activity of each mutant

40 reatly reduced the viability of glioblastoma multiforme cells.

41 an essential survival signal in glioblastoma multiforme cells.

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

43 red with bevacizumab-responsive glioblastoma multiforme cells.

44 yeloid leukemia, breast cancer, glioblastoma multiforme, colon, skin and lung cancer.

45 ar analyses (SSU & ITS) of D. minimum and D. multiforme confirm that they are Goup 4 new species.

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

47 Glioblastoma multiforme contains a subpopulation of cancer stem-like

48 owed the highest effect against glioblastoma multiforme CSCs.

49 rain tumors, such as aggressive glioblastoma multiforme, CTC assays are needed that do not rely on ex

50 sed method on breast cancer and glioblastoma multiforme data obtained from TCGA.

51 ion studies, and application to glioblastoma multiforme data resulted in informative cancer and gliob

52 ta from the Cancer Genome Atlas Glioblastoma multiforme dataset and show that survival is related to

53 orectal cancer datasets and two glioblastoma multiforme datasets and show that our multipathway-based

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

55 bal DNA methylation patterns in glioblastoma multiforme divide adult and pediatric tumors into subgro

56 ng, we then found that the anti-glioblastoma multiforme drug lead vacquinol is an inhibitor of Mycoba

57 in lower grade glioma) and GBM (Glioblastoma multiforme), due to the possible progression from LGG to

58 In clinical specimens of glioblastoma multiforme, elevated levels of CCL2 expression correlate

59 onary arterial hypertension and glioblastoma multiforme exhibited a markedly increased abundance of I

60 In human glioblastoma multiforme, expression of CD44 correlated with hypoxia-i

61 The patients had glioblastoma multiforme (GBM) (n = 20), metastasis (n = 21), or menin

62 17-35%, P = 1.05 x 10(-8)) for glioblastoma multiforme (GBM) and 25% (95% CI: 17-32%, P = 1.26 x 10(

63 ve phenotype in mouse models of glioblastoma multiforme (GBM) and in a subset of GBM patients treated

64 1; MTDH) is highly expressed in glioblastoma multiforme (GBM) and many other types of cancer, where i

65 Glioblastoma multiforme (GBM) and other solid malignancies are hetero

66 Glioblastoma multiforme (GBM) and the mesenchymal GBM subtype in part

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

68 Using glioblastoma multiforme (GBM) as a model system, we sought to determi

69 xpressed at a high frequency by glioblastoma multiforme (GBM) as well as several other tumor types.

70 ET in predicting progression of glioblastoma multiforme (GBM) at follow-up.

71 nd lactate production, inhibits glioblastoma multiforme (GBM) autophagy, and induces apoptosis in GBM

72 RNAi viability screen in human glioblastoma multiforme (GBM) brain tumor stem cells.

73 In a glioblastoma multiforme (GBM) cancer cell model, we examined the resp

74 lipid metabolism genes in human glioblastoma multiforme (GBM) cancer cells.

75 w drugs and active targeting in glioblastoma multiforme (GBM) cancer therapy.

76 Glioblastoma multiforme (GBM) cell line, highly malignant glioma cell

77 bolic and functional studies in glioblastoma multiforme (GBM) cell lines, preclinical models, and cli

78 Glioblastoma Multiforme (GBM) cells are highly invasive, infiltrating

79 sm of cell death in p53-mutated glioblastoma multiforme (GBM) cells exposed to plasma.

80 f gold nanoparticle into U373MG Glioblastoma multiforme (GBM) cells predicts that CAP may introduce a

81 e the susceptibility of U-87 MG glioblastoma multiforme (GBM) cells to subsequent treatment with the

82 Temozolomide (TMZ)-resistant glioblastoma multiforme (GBM) cells would have abnormal redox status

83 umor model comprised of U-87 MG glioblastoma multiforme (GBM) cells, known to form highly vascularize

84 -13 (IL-13) effectively targets glioblastoma multiforme (GBM) cells, which are known to overexpress I

85 ," had an antimitotic effect on glioblastoma multiforme (GBM) cells.

86 L-24) in invasive primary human glioblastoma multiforme (GBM) cells.

87 Glioblastoma multiforme (GBM) comprises several molecular subtypes, i

88 Glioblastoma multiforme (GBM) contains a subpopulation of cells, GBM

89 Glioblastoma multiforme (GBM) continues to have a dismal prognosis an

90 rk (WGCN) analysis algorithm on glioblastoma multiforme (GBM) data obtained from the TCGA project and

91 of RCytoscape, a portion of the Glioblastoma multiforme (GBM) data set from the Cancer Genome Atlas (

92 Glioblastoma multiforme (GBM) displays cellular hierarchies harboring

93 The malignant brain cancer glioblastoma multiforme (GBM) displays invasive growth behaviors that

94 ting monocytes in patients with glioblastoma multiforme (GBM) express ligands for activating the Natu

95 202 tumors of the brain cancer glioblastoma multiforme (GBM) given at the Cancer Genome Atlas (TCGA)

96 Glioblastoma multiforme (GBM) has few clinically approved therapeutic

97 Mortality of glioblastoma multiforme (GBM) has not improved over the last two deca

98 bias for amino acid changes in glioblastoma multiforme (GBM) in comparison to the low-grade tumors.

99 eckpoint-blockade therapies for glioblastoma multiforme (GBM) in late-phase clinical trials has direc

100 Glioblastoma multiforme (GBM) is a devastating brain tumor with poor

101 malignant primary brain tumor, glioblastoma multiforme (GBM) is a devastating disease with a grim pr

102 Glioblastoma multiforme (GBM) is a fatal brain tumor characterized by

103 Glioblastoma multiforme (GBM) is a highly aggressive malignant brain

104 Glioblastoma multiforme (GBM) is a highly invasive brain tumour that

105 Glioblastoma multiforme (GBM) is a highly malignant primary brain can

106 Glioblastoma multiforme (GBM) is a highly malignant primary central n

107 Glioblastoma multiforme (GBM) is a highly proliferative and locally i

108 Glioblastoma multiforme (GBM) is a lethal cancer characterized by flo

109 Glioblastoma multiforme (GBM) is a lethal, therapy-resistant brain ca

110 monitoring of drug efficacy in glioblastoma multiforme (GBM) is a major clinical problem as serial r

111 Glioblastoma multiforme (GBM) is a malignant brain tumor with a poor

112 Glioblastoma Multiforme (GBM) is a tumor with high mortality and no k

113 The brain tumor glioblastoma multiforme (GBM) is among the most lethal forms of human

114 Glioblastoma multiforme (GBM) is among the most lethal of human malig

115 Glioblastoma multiforme (GBM) is an aggressive and difficult to treat

116 Glioblastoma multiforme (GBM) is an aggressive brain tumor driven by

117 Glioblastoma multiforme (GBM) is an aggressive brain tumor for which

118 Glioblastoma multiforme (GBM) is an aggressive brain tumor, fatal wit

119 Glioblastoma multiforme (GBM) is an aggressive cancer without current

120 Glioblastoma multiforme (GBM) is an aggressive, Grade IV astrocytoma

121 Glioblastoma multiforme (GBM) is an intractable tumor despite therape

122 Glioblastoma multiforme (GBM) is characterized by a pathogenic vascul

123 Glioblastoma multiforme (GBM) is characterized by overexpression of e

124 , its effectiveness in treating glioblastoma multiforme (GBM) is constrained by insufficient penetrat

125 The aggressiveness of glioblastoma multiforme (GBM) is defined by local invasion and resist

126 Glioblastoma multiforme (GBM) is highly invasive and uniformly fatal,

127 Glioblastoma multiforme (GBM) is impossible to fully remove surgicall

128 Recurrent glioblastoma multiforme (GBM) is incurable with current therapies.

129 Glioblastoma multiforme (GBM) is one of the most aggressive cancers,

130 Glioblastoma multiforme (GBM) is one of the most aggressive human bra

131 Glioblastoma multiforme (GBM) is one of the most aggressive human mal

132 Glioblastoma multiforme (GBM) is one of the most common malignant bra

133 Glioblastoma multiforme (GBM) is one of the most intractable of human

134 ncy of abnormal PI3K signaling, glioblastoma multiforme (GBM) is particularly relevant because the pa

135 Glioblastoma multiforme (GBM) is the deadliest form of brain tumor.

136 Glioblastoma multiforme (GBM) is the most aggressive and common form

137 Glioblastoma multiforme (GBM) is the most aggressive and common type

138 Glioblastoma multiforme (GBM) is the most aggressive form of brain tu

139 Glioblastoma multiforme (GBM) is the most aggressive of the astrocyti

140 Glioblastoma multiforme (GBM) is the most common and aggressive malig

141 Glioblastoma multiforme (GBM) is the most common and aggressive prima

142 Glioblastoma multiforme (GBM) is the most common and deadly brain tum

143 Glioblastoma multiforme (GBM) is the most common and devastating type

144 Glioblastoma multiforme (GBM) is the most common and lethal brain tum

145 Glioblastoma multiforme (GBM) is the most common and lethal of all gl

146 Glioblastoma multiforme (GBM) is the most common and lethal primary m

147 Glioblastoma multiforme (GBM) is the most common and malignant of all

148 Glioblastoma multiforme (GBM) is the most common form of malignant gl

149 Glioblastoma multiforme (GBM) is the most common primary malignant br

150 Glioblastoma multiforme (GBM) is the most common type of aggressive m

151 Glioblastoma multiforme (GBM) is the most deadly brain tumor, and cur

152 Glioblastoma multiforme (GBM) is the most frequent and aggressive pri

153 unction of endothelial cells in glioblastoma multiforme (GBM) is to create a niche that helps promote

154 of innovative drug targets for glioblastoma multiforme (GBM) limits patient survival to approximatel

155 Neoplastic cells of Glioblastoma multiforme (GBM) may or may not show sustained response

156 nsitivity and can differentiate glioblastoma multiforme (GBM) microvesicles from nontumor host cell-d

157 eatures, we developed a de novo glioblastoma multiforme (GBM) model derived from immortalized human n

158 onal studies of glioma cells in glioblastoma multiforme (GBM) models establish that PTEN deficiency a

159 Volumetric change in glioblastoma multiforme (GBM) over time is a critical factor in treat

160 he major cause of mortality for glioblastoma multiforme (GBM) patients.

161 Macrophages accumulate with glioblastoma multiforme (GBM) progression and can be targeted via inh

162 or patients diagnosed as having glioblastoma multiforme (GBM) remain poor.

163 Glioblastoma multiforme (GBM) remains a mainly incurable disease in d

164 Importance: Glioblastoma multiforme (GBM) remains almost invariably fatal despite

165 Glioblastoma multiforme (GBM) remains the deadliest brain tumor in ad

166 A central question in glioblastoma multiforme (GBM) research is the identity of the tumor-i

167 y of the aggressive brain tumor glioblastoma multiforme (GBM) results in part from its strong propens

168 t in approximately 20% of human glioblastoma multiforme (GBM) specimens, primarily of the Proneural s

169 tures, whereas remaining low in glioblastoma multiforme (GBM) stable cell lines, low-grade glioma-der

170 RNAi screens in patient-derived glioblastoma multiforme (GBM) stem cells (GSCs).

171 Patients with glioblastoma multiforme (GBM) survive on average 12 to 14 months afte

172 t patients newly diagnosed with glioblastoma multiforme (GBM) treated with bevacizumab plus radiother

173 NA-binding proteins, as a novel glioblastoma multiforme (GBM) tumor suppressor.

174 Glioblastoma multiforme (GBM) tumors are highly metabolic and vascula

175 V) infections are seen often in glioblastoma multiforme (GBM) tumors, but whether the virus contribut

176 ession data for a collection of glioblastoma multiforme (GBM) tumors.

177 We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the clos

178 bral stroke and 4 patients with glioblastoma multiforme (GBM) underwent 150-min dynamic SPECT scans w

179 tumour malignancies, including glioblastoma multiforme (GBM) which presents largely deregulated Myc

180 subjects and six patients with glioblastoma multiforme (GBM) with an acquisition time of 11 minutes.

181 ontrast material enhancement of glioblastoma multiforme (GBM) with intraoperative contrast-enhanced u

182 ated here whether NF1-deficient glioblastoma multiforme (GBM) would respond to MEK inhibition.

183 werful predictor of survival in glioblastoma multiforme (GBM) yet the biological basis for the differ

184 Glioblastoma multiforme (GBM), a deadly cancer, is the most lethal an

185 The cancer stem cells (CSCs) of glioblastoma multiforme (GBM), a grade IV astrocytoma, have been enri

186 ivotal role in the treatment of glioblastoma multiforme (GBM), an aggressive form of primary brain ca

187 e in aggressive tumors, such as glioblastoma-multiforme (GBM), and understanding the molecular dynami

188 use for the dismal prognosis of glioblastoma multiforme (GBM), but the underlying mechanisms remain i

189 Glioblastoma multiforme (GBM), like most cancers, possesses a unique

190 Glioblastoma multiforme (GBM), the grade IV astrocytoma, is the most

191 lar importance in patients with glioblastoma multiforme (GBM), the highest grade and most aggressive

192 d molecular-subtyping assay for glioblastoma multiforme (GBM), the most aggressive primary brain tumo

193 Glioblastoma multiforme (GBM), the most common and aggressive primary

194 y, and radiation, patients with glioblastoma multiforme (GBM), the most common histological subtype o

195 the tumour microenvironment in glioblastoma multiforme (GBM), the most common malignant brain tumour

196 In glioblastoma multiforme (GBM), translocator protein (TSPO) and murine

197 These pathologies are glioblastoma multiforme (GBM), traumatic brain injuries (TBIs), multi

198 s for prognostic differences in glioblastoma multiforme (GBM), we employed a combinatorial network an

199 e Cancer Genome Atlas's data on glioblastoma multiforme (GBM), we found that the genomic region conta

200 Glioblastoma multiforme (GBM), which account for more than 50% of all

201 e MRI-classified SVZ-associated Glioblastoma Multiforme (GBM), which has a transcriptional profile th

202 ted in astrocytes isolated from glioblastoma multiforme (GBM)-prone H-Ras(12V) knock-in mice as well

203 rization and chemoresistance in glioblastoma multiforme (GBM).

204 among which the most deadly is glioblastoma multiforme (GBM).

205 factors for the incurability of glioblastoma multiforme (GBM).

206 nocarriers for the treatment of glioblastoma multiforme (GBM).

207 tance of solid tumors, foremost glioblastoma multiforme (GBM).

208 c paradigm for the treatment of glioblastoma multiforme (GBM).

209 CDKN2A on chromosome 9p21.3 in glioblastoma multiforme (GBM).

210 erent therapeutic resistance of glioblastoma multiforme (GBM).

211 polymorphism (SNP) genotypes in glioblastoma multiforme (GBM).

212 or treatment modality for human glioblastoma multiforme (GBM).

213 across human cancers, including glioblastoma multiforme (GBM).

214 high-grade brain tumors such as glioblastoma multiforme (GBM).

215 ss of single-agent therapies in glioblastoma multiforme (GBM).

216 R) gene are frequently found in glioblastoma multiforme (GBM).

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

218 FRvIII) in a cell line model of glioblastoma multiforme (GBM).

219 he highly malignant brain tumor glioblastoma multiforme (GBM).

220 red to be the cell of origin of glioblastoma multiforme (GBM).

221 cularly in the highly malignant glioblastoma multiforme (GBM).

222 crucial role in pathogenesis of glioblastoma multiforme (GBM).

223 unmet need for the treatment of glioblastoma multiforme (GBM).

224 ms in controlling the growth of glioblastoma multiforme (GBM).

225 /tumor suppressive functions in glioblastoma multiforme (GBM).

226 sed invasive characteristics in glioblastoma multiforme (GBM).

227 (TAMs) promotes progression of glioblastoma multiforme (GBM).

228 haring characteristics of human glioblastoma multiforme (GBM).

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

230 receptor overexpressed in human glioblastoma multiforme (GBM).

231 ung man with a history of brain glioblastoma multiforme (GBM).

232 otes the malignant phenotype in glioblastoma multiforme (GBM).

233 Glioblastoma multiforme (GBM)/astrocytoma grade IV is a malignant and

234 progression and invasiveness of glioblastoma multiforme (GBM); however, the exact crosstalk between G

235 ing of the molecular biology of glioblastoma multiforme (GBM); thus, complex genetic alterations and

236 (EGFRvIII), occurs commonly in glioblastoma multiformes (GBM).

237 well as grade IV glioblastomas (glioblastoma multiforme [GBM]).

238 (BRCAs) into five subgroups and glioblastoma multiformes (GBMs) into six subgroups with distinct comb

239 improves survival in patients, glioblastoma multiformes (GBMs) tend to relapse with augmented tumor

240 ers of malignant progression in glioblastoma multiforme, glioma cells exhibit intrinsic resistance to

241 notype to OXPHOS and inhibiting glioblastoma multiforme growth and proliferation.

242 inhibits tumor angiogenesis and glioblastoma multiforme growth in a mouse orthotopic brain tumor mode

243 including renal cell carcinoma, glioblastoma multiforme, head and neck squamous cell carcinoma, melan

244 o genetically diverse models of glioblastoma multiforme in vivo.

245 Glioblastoma multiforme is a very aggressive and common form of brain

246 Glioblastoma multiforme is an aggressive, invasive brain tumour with

247 Glioblastoma multiforme is an aggressive, treatment-refractory type o

248 Glioblastoma multiforme is generally recalcitrant to current surgical

249 Current therapy for glioblastoma multiforme is insufficient, with nearly universal recurr

250 Glioblastoma multiforme is the most aggressive primary brain tumor in

251 Glioblastoma multiforme is the most aggressive type of primary brain

252 Glioblastoma multiforme is the most common primary malignant brain tu

253 Glioblastoma multiforme is the most common type of primary malignant

254 s with colorectal carcinoma and glioblastoma multiforme, known to be highly tumorigenic, resistant to

255 Glioblastoma multiforme lacks effective therapy options.

256 tous contact dermatitis include the erythema multiforme-like, the purpuric, the lichenoid, and the pi

257 In human glioblastoma multiforme, mitochondrial serine hydroxymethyltransferas

258 ion and prolonged survival in a glioblastoma multiforme model, prevented metastatic disease following

259 also had neuroblastoma (n = 1), glioblastoma multiforme (n = 1), choroid plexus carcinoma (n = 2), an

260 neuroectodermal tumor (n = 4), glioblastoma multiforme (n = 2), atypical teratoid/rhabdoid tumor (n

261 with rs55705857 confined to non-glioblastoma multiforme (non-GBM) tumours (P = 1.07 x 10(-67)).

262 cer, esophageal adenocarcinoma, glioblastoma multiforme, ovarian cancer and liver cancer, with freque

263 role of EC-CSC interactions in glioblastoma multiforme pathobiology.

264 s large-scale Breast Cancer and Glioblastoma Multiforme patient samples from The Cancer Genome Atlas

265 resected surgical tissues from glioblastoma multiforme patients strongly expressed gBK mRNA.

266 found that T cells derived from glioblastoma multiforme patients that were sensitized to the gBK pept

267 de a path to DON utilization in glioblastoma multiforme patients.

268 were a major source of CCL2 in glioblastoma multiforme patients.

269 cretase enzyme were elevated in glioblastoma multiformes patients.

270 rithm on synthetic data and 100 Glioblastoma Multiforme primary tumor samples.

271 any aggressive cancers, such as glioblastoma multiforme, progression is enabled by local immunosuppre

272 and those that do not, such as glioblastoma multiforme, prostate cancer and colorectal cancer.

273 ors, esophageal adenocarcinoma, glioblastoma multiforme, prostate tumors, non-small cell lung tumors,

274 n profiles available for common glioblastoma multiforme samples from The Cancer Genome Atlas using di

275 nd performed SP analyses on 118 glioblastoma multiforme samples obtained from TCGA.

276 ed tumor regions in a subset of glioblastoma multiforme samples sequenced by The Cancer Genome Atlas

277 and HIF-1alpha were elevated in glioblastoma multiforme specimens when compared with normal brain tis

278 r closely related syndromes such as erythema multiforme, Stevens-Johnson syndrome, and toxic epiderma

279 ulted in informative cancer and glioblastoma multiforme subtype-related findings.

280 tion of CD73(hi) macrophages in glioblastoma multiforme that persists after anti-PD-1 treatment.

281 mated for colorectal cancer and glioblastoma multiforme, the distribution of sizes of subclones carry

282 Two hallmarks of glioblastoma multiforme, the most common malignant brain cancer in hu

283 diately targetable molecule for glioblastoma multiforme therapy.

284 d survival in a murine model of glioblastoma multiforme treated with anti-CTLA-4 and anti-PD-1.

285 s a major clinical challenge in glioblastoma multiforme treatment, and the mechanisms underlying the

286 derived from non-microdissected glioblastoma multiforme tumor tissue is either masked or not accurate

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

288 for analysis of a larger set of glioblastoma multiforme tumors for which exome sequencing data are av

289 Human glioblastoma multiforme tumors often contain rapidly proliferating ol

290 ls relative to U87PTEN cells in glioblastoma multiforme tumors.

291 ntribute to the poor outcome of glioblastoma multiforme tumors.

292 s with histologically confirmed glioblastoma multiforme underwent brain imaging.

293 m samples and sub-categories of glioblastoma multiforme using Human Proteome chips containing ~17000

294 In clinical specimens of glioblastoma multiforme, we found that immunohistochemical expression

295 cessful combination strategy in glioblastoma multiforme, we performed reverse translational studies u

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

297 e highest grade of astrocytoma, Glioblastoma multiforme were: COL4A1, EGFR, BTF3, MPP2, RAB31, CDK4,

298 also expressed in cultures from glioblastoma multiforme which express neural stem cell markers, can d

299 f human cancer cells, including T98g (glioma multiforme), while its decomposition products in cell cu

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