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 on, or certain cancers, such as glioblastoma multiforme.

4 described proneural subtype of glioblastoma multiforme.

5 candidate therapeutic target in glioblastoma multiforme.

6 cancer in children and adults: glioblastoma multiforme.

7 lateral sclerosis, dementia and glioblastoma multiforme.

8 life expectancy to survivors of glioblastoma multiforme.

9 ut it is frequently silenced in glioblastoma multiforme.

10 val after surgery for recurrent glioblastoma multiforme.

11 soft tissue leiomyosarcoma, and glioblastoma multiforme.

12 h selected kinase inhibitors in glioblastoma multiforme.

13 ates with that of CBX7 in human glioblastoma multiforme.

14 mas, schwannomas, and pediatric glioblastoma multiformes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 mma serves significant roles in glioblastoma multiforme cell survival likely via a mechanism that is

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

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

35 Human glioblastoma multiforme cells demonstrate varying levels of sensitivi

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

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

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

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

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

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

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

43 reatly reduced the viability of glioblastoma multiforme cells.

44 an essential survival signal in glioblastoma multiforme cells.

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

46 red with bevacizumab-responsive glioblastoma multiforme cells.

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

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

49 Glioblastoma multiforme contains a subpopulation of cancer stem-like

50 owed the highest effect against glioblastoma multiforme CSCs.

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

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

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

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

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

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

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

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

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

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

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

62 High grade gliomas such as glioblastoma multiforme express multiple members of the epithelial so

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

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

65 17-35%, P = 1.05 x 10(-8)) for glioblastoma multiforme (GBM) and 25% (95% CI: 17-32%, P = 1.26 x 10(

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

67 1; MTDH) is highly expressed in glioblastoma multiforme (GBM) and many other types of cancer, where i

68 tissues but widely expressed in glioblastoma multiforme (GBM) and other neoplasms.

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

70 ) and CD133(-) cells from human glioblastoma multiforme (GBM) and, by subtractive analysis, establish

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

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

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

74 primary and recurrent pairs of glioblastoma multiforme (GBM) biopsies as well as primary and TMZ-res

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

76 uch as medulloblastoma (MB) and glioblastoma multiforme (GBM) can derive from neural precursors.

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

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

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

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

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

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

83 ant (EGFRvIII) present on human glioblastoma multiforme (GBM) cells were used for therapeutic targeti

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

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

86 AIL)-induced apoptosis in human glioblastoma multiforme (GBM) cells.

87 n the context of astrocytes and glioblastoma multiforme (GBM) cells.

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

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

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

91 Glioblastoma multiforme (GBM) displays cellular hierarchies harboring

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

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

94 202 tumors of the brain cancer glioblastoma multiforme (GBM) given at the Cancer Genome Atlas (TCGA)

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

96 Glioblastoma multiforme (GBM) is a deadly primary brain tumor.

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

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

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

100 Glioblastoma multiforme (GBM) is a fatal primary brain tumor harborin

101 Glioblastoma multiforme (GBM) is a highly invasive and vascularized a

102 Glioblastoma multiforme (GBM) is a highly invasive brain tumor that d

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

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

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

106 Glioblastoma multiforme (GBM) is a lethal brain tumor characterized b

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

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

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

110 Glioblastoma multiforme (GBM) is a severe brain malignancy with limit

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

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

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

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

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

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

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

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

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

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

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

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

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

124 The dismal prognosis of glioblastoma multiforme (GBM) is mainly due to the poor response of G

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

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

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

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

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

130 Glioblastoma multiforme (GBM) is the most aggressive brain tumor that

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

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

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

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

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

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

137 Glioblastoma multiforme (GBM) is the most common and lethal primary b

138 Glioblastoma multiforme (GBM) is the most common and lethal primary b

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

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

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

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

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

144 Glioblastoma multiforme (GBM) is the most frequent and incurable type

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

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

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

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

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

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

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

152 ing immortalized NHAs displayed glioblastoma multiforme (GBM) phenotypes, suggesting that FoxM1B over

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

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

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

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

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

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

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

160 We show that in glioblastoma multiforme (GBM) specimens, death-domain adaptor protein

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

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

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

164 em cells have shown promise for glioblastoma multiforme (GBM) therapy; however, key preclinical studi

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

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

167 k4/6) occurs in the majority of glioblastoma multiforme (GBM) tumors, and represents a promising mole

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

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

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

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

172 radiotherapy, and chemotherapy, glioblastoma multiforme (GBM) virtually always recurs.

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

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

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

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

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

178 al oncolytic virus for treating glioblastoma multiforme (GBM), an aggressive brain tumor.

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

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

181 In glioblastoma multiforme (GBM), epidermal growth factor receptor gene

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

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

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

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

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

187 available for the treatment of glioblastoma multiforme (GBM), the most common and lethal primary bra

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

189 Glioblastoma multiforme (GBM), the most common intracranial tumor in

190 the treatment of patients with glioblastoma multiforme (GBM), the tumors invariably recur within the

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

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

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

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

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

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

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

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

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

200 haring characteristics of human glioblastoma multiforme (GBM).

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

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

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

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

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

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

207 receptor overexpressed in human glioblastoma multiforme (GBM).

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

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

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

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

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

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

214 tumor growth and progression in glioblastoma multiforme (GBM).

215 iation-4 is highly expressed in glioblastoma multiforme (GBM).

216 filtrative brain tumors such as glioblastoma multiforme (GBM).

217 poor prognosis in patients with glioblastoma multiforme (GBM).

218 rization and chemoresistance in glioblastoma multiforme (GBM).

219 sed invasive characteristics in glioblastoma multiforme (GBM).

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

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

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

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

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

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

226 erent therapeutic resistance of glioblastoma multiforme (GBM).

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

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

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

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

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

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

233 on, being present in 40% of the glioblastoma multiformes (GBMs) with PDGFRA amplification.

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

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

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

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

238 o genetically diverse models of glioblastoma multiforme in vivo.

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

240 Glioblastoma multiforme is an aggressive, invasive brain tumour with

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

242 Glioblastoma multiforme is generally recalcitrant to current surgical

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

244 Glioblastoma multiforme is the most aggressive primary brain tumor in

245 Glioblastoma multiforme is the most aggressive type of primary brain

246 Glioblastoma multiforme is the most common and lethal primary brain c

247 Glioblastoma multiforme is the most common glioma variant in adults a

248 Glioblastoma multiforme is the most common primary malignant brain tu

249 Glioblastoma multiforme is the most common type of primary malignant

250 0 expression is up-regulated in glioblastoma multiforme, its regulation and functions in nontransform

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

252 Glioblastoma multiforme lacks effective therapy options.

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

254 In human glioblastoma multiforme, mitochondrial serine hydroxymethyltransferas

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

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

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

258 ncluding freshly isolated human glioblastoma multiforme neurosphere cultures (containing "stem cell-l

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

260 , localized myositis, folliculitis, erythema multiforme, or ophthalmological manifestations.

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

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

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

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

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

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

267 cretase enzyme were elevated in glioblastoma multiformes patients.

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

269 We show that, in the case of glioblastoma multiforme, primary tumors and xenografts are best for t

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

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

272 the basis of 498 patients with glioblastoma multiforme receiving radiation and chemotherapy.

273 olites predominant in recurrent glioblastoma multiforme (rGBM) to characterize the response of rGBM t

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 CSF samples from patients with glioblastoma multiforme show elevated Igf2 and stimulate stem cell pr

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

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

280 patients with MGMT unmethylated glioblastoma multiforme survived 6.5, 8.7, and 46.4 months.

281 e the sequencing of 22 cases of glioblastoma multiforme that identified IDH1, the gene encoding isoci

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

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

284 diately targetable molecule for glioblastoma multiforme therapy.

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 et an overexpressed receptor in glioblastoma multiforme tumors.

291 ls relative to U87PTEN cells in glioblastoma multiforme tumors.

292 ntribute to the poor outcome of glioblastoma multiforme tumors.

293 s with histologically confirmed glioblastoma multiforme underwent brain imaging.

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

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

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 le [median age, 59 years]) with glioblastoma multiforme who were treated with RT-TMZ were retrospecti

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