ライフサイエンスコーパス: glioblastoma

1 ould potentiate checkpoint immunotherapy for glioblastoma.

2 s to target resistant populations of GSCs in glioblastoma.

3 in part due to the genetic heterogeneity of glioblastoma.

4 uccessful development of immunotherapies for glioblastoma.

5 en MGMT methylation and expression levels in glioblastoma.

6 al connectivity patterns in 15 patients with glioblastoma.

7 s' tumor shares similarities with neuro- and glioblastoma.

8 urvival response to anti-VEGF monotherapy in glioblastoma.

9 point blockade therapy to eradicate existing glioblastoma.

10 tumor cell lines including neuroblastoma or glioblastoma.

11 at determines the immune refractory state in glioblastoma.

12 edict the clinical outcomes of patients with glioblastoma.

13 n attractive imaging target for detection of glioblastoma.

14 is elevated in tumors, including in primary glioblastoma.

15 h and extended survival in a rodent model of glioblastoma.

16 nsive view of early response to radiation in glioblastoma.

17 hat were formulated with doxorubicin against glioblastoma.

18 increased survival with anti-VEGF therapy in glioblastoma.

19 ecarenone in the highly treatment-refractory glioblastoma.

20 nes, and in vivo, using orthotopic models of glioblastoma.

21 hat may serve as a new therapeutic target in glioblastoma.

22 [1-(13)C]glycine for non-invasive imaging of glioblastoma.

23 ng the tumor are affected by the presence of glioblastoma.

24 al stem cells (NSCs) are a cell of origin of glioblastoma.

25 er models, including aggressive intracranial glioblastoma.

26 with VEGF-C to promote an immune response to glioblastoma.

27 T expression in the brain and thus to detect glioblastoma.

28 iomarkers as well as therapeutic targets for glioblastomas.

29 that include lower-grade gliomas (LGGs) and glioblastomas.

30 role in the proliferation and progression of glioblastoma(3,4).

31 ents with World Health Organization grade IV glioblastomas 40 mm or less from the IHM region, loss of

32 s in many diverse cancer types, particularly glioblastoma(5-8).

33 tomolecularly characterized glioma patients (glioblastoma, 90%; age range, 20-79 y) were subsequently

34 d proliferation can categorize patients with glioblastoma according to progression-free survival.

35 vidual, yet related, variants and reveal how glioblastoma alters the neuronal microenvironment.

36 ells into the tumour, rapid clearance of the glioblastoma and a long-lasting antitumour memory respon

37 ic biomarkers that are frequently present in glioblastoma and can alter clinical management.

38 responding transcriptional profiles in human glioblastoma and describe patient-derived xenografts wit

39 Nude rats bearing orthotopic U87 glioblastoma and healthy controls were investigated.

40 f unknown aetiology is a hallmark feature of glioblastoma and is characterized by decreased CD4 T-cel

41 l alkylating agent used for the treatment of glioblastoma and is now becoming a chemotherapeutic opti

42 ific copy number gains, such as trisomy 7 in glioblastoma and isochromosome 17q in medulloblastoma.

43 hether there is reciprocal crosstalk between glioblastoma and neurons remains poorly defined, as the

44 sels from tissue biopsies from patients with glioblastoma and ovarian cancer.

45 y enhance the antitumor activity of HDACi in glioblastoma and pancreatic cancer preclinical models.

46 show that GBOs maintain many key features of glioblastomas and can be rapidly deployed to investigate

47 ns of anticancer cardiac glycosides in human glioblastomas and glioma cancer stem-like cells via inhi

48 f IRS2 and other loci are evident in primary glioblastomas and may underlie the inefficacy of targete

49 on the cerebellar cortex from primary (e.g., glioblastoma) and metastatic (e.g., breast cancer) tumor

50 s in rat 9L gliosarcoma, human U87 DeltaEGFR glioblastoma, and human DU145 androgen-independent prost

51 protein expression was upregulated in human glioblastomas, and its expression directly correlated wi

52 unity that is mediated by CD8 T cells to the glioblastoma antigen is very limited when the tumour is

53 Glioblastomas are aggressive primary brain tumors known

54 Glioblastomas are highly aggressive primary brain tumour

55 Glioblastomas are highly malignant brain tumors.

56 Patients undergoing resection for glioblastoma as well as patients included in The Cancer

57 Glioblastoma-associated immune infiltrates are dominated

58 ed in The Cancer Genome Atlas (TCGA) and IVY Glioblastoma Atlas Project (IVY GAP) databases had pre-o

59 The IVY Glioblastoma Atlas Project Database was used to evaluate

60 The validation set was obtained from the Ivy Glioblastoma Atlas Project database, for which the perce

61 Glioblastoma brain tumor stem cells with low astrocytic

62 tumor cell types, including lymphoma, lung, glioblastoma, breast cancer, and several forms of leukem

63 gies are provided and have been validated in glioblastoma, breast cancer, melanoma and leukemia mouse

64 ly, Norrin mediates enhanced tumor growth of glioblastomas by activating the Notch pathway.

65 The analyses of glioblastoma cancer data and the breast cancer data from

66 re is an interphase pool of KIF11 present in glioblastoma cancer stem cells that drives tumor cell in

67 human glioma cells and patient-derived human glioblastoma cancer stem cells) to demonstrate how vital

68 enhance Temozolomide (TMZ) cytotoxicity on a glioblastoma cell line (U87MG).

69 and found to inhibit tumor growth in a mouse glioblastoma cell line and in a whole-animal study.

70 Strikingly, in the glioblastoma cell line data, PolyA-miner identified more

71 Human Reference (UHR) PolyA-seq data, recent glioblastoma cell line NUDT21 knockdown Poly(A)-ClickSeq

72 cs of human SH-SY5Y neuroblastoma and U-87MG glioblastoma cell lines cultured on polyacrylonitrile (P

73 an integrated analysis in the U251 and U343 glioblastoma cell lines to map early alterations in the

74 shown that the venom significantly affected glioblastoma cell lines.

75 m-like phenotypes, have replaced established glioblastoma cell lines.

76 time the effect of dilution on the EM of U87 glioblastoma cell-derived and plasma-derived sEVs and me

77 Here, we demonstrate that glioblastoma cells adhere to and invade HA-rich matrix u

78 AHR knockdown in glioblastoma cells also reduced the expression of LDHA (

79 esicle-mediated bilateral crosstalk, between glioblastoma cells and astrocytes, highlighting the prot

80 promotes tumorigenesis and survival of human glioblastoma cells by epigenetically activating the tran

81 as a result of necrosis, a new cell death in glioblastoma cells characterized by the leak of bulk wat

82 luorescent protein (iRFP) in patient-derived glioblastoma cells enables rapid, direct non-invasive mo

83 Silencing AVIL nearly eradicated glioblastoma cells in culture, and dramatically inhibite

84 iRFP transduction of primary patient-derived glioblastoma cells is a reliable, cost- and time-effecti

85 Live-cell imaging of glioblastoma cells overexpressing a ZYX-GFP construct de

86 ith a composite score the ability of primary glioblastoma cells to proliferate (via the protein bioma

87 vestigated in future studies for sensitizing glioblastoma cells to TMZ and other drugs available in t

88 he emergence of drug resistance in stem-like glioblastoma cells treated with RTK inhibitors.

89 inhibition of NCAM1 in Vero cells and human glioblastoma cells U-251 MG.

90 essed the migratory and invasive capacity of glioblastoma cells, partially restored following TLN1 or

91 alysis localized PHIP to the leading edge of glioblastoma cells, together with several focal adhesion

92 However, in cultured NIH3T3 and glioblastoma cells, we found that class I PI3K mediated

93 ony formation and tumorigenesis abilities of glioblastoma cells.

94 ed the effect of a physical CAP treatment on glioblastoma cells.

95 induced gene expression and tumorigenesis of glioblastoma cells.

96 hyper-phosphorylated tau (p-tau) in Vero and glioblastoma cells.

97 ue triggers the unfolded protein response in glioblastoma cells.

98 ons and provide a methodology for functional glioblastoma classification for future clinical investig

99 Translation of survival benefits observed in glioblastoma clinical trials to populations and to longe

100 rts of human high-grade astrocytomas, mostly glioblastomas, compared to healthy brain control samples

101 invasive tumor rim (intact BBB) compared to glioblastoma core (disrupted BBB).

102 Based on untreated human glioblastoma data collected in Trondheim, Norway, we fir

103 Newly collected untreated human glioblastoma data in Seattle, US, re-verify our model.

104 lastic and non-neoplastic cells from a human glioblastoma dataset, the ranking of biologically releva

105 confirmed on The Cancer Genome Atlas (TCGA) glioblastoma dataset.

106 In an orthotopic model of glioblastoma, dendrimer-triptolide achieved significantl

107 emarkably, SRSF3 is directly associated with glioblastoma development, progression, aggressiveness an

108 rotumor and antitumor roles of astrocytes in glioblastoma development.

109 2 reporting survival at >= 2 years following glioblastoma diagnosis.

110 Glioblastomas exhibit vast inter- and intra-tumoral hete

111 Our results demonstrate that glioblastomas exploit cell surface O-linked glycans for

112 temozolomide, TMZ, the standard of care for glioblastoma) for use as synthetic precursors of alkyl d

113 e, 59 years; IQR, 49-69 years; 382 men) with glioblastoma from six hospitals were used.

114 rgets tumor-associated macrophages (TAMs) in glioblastoma from systemic administration and exhibits t

115 f antineoplastic components with activity in glioblastoma (GB) cell lines.

116 Glioblastoma (GB) is a highly aggressive, difficult to t

117 ed tropism of systemic nanoparticles towards glioblastoma (GBM) and prostate carcinoma xenograft lesi

118 Precision medicine trials in glioblastoma (GBM) are often conducted at tumor recurren

119 glutamine metabolism has on the survival of glioblastoma (GBM) brain tumor stem cells (BTSC) has not

120 CRISPRi) to screen 5689 lncRNA loci in human glioblastoma (GBM) cells, identifying 467 hits that modi

121 acellular matrix (ECM) on drug resistance in glioblastoma (GBM) cells.

122 Here, we showed that glioblastoma (GBM) cultures and patients' tumors harbore

123 nding protein SERBP1 as a novel regulator of glioblastoma (GBM) development.

124 Glioblastoma (GBM) has one of the worst 5-year survival

125 Treatment for glioblastoma (GBM) includes surgical resection and adjuv

126 ed that physical and osmotic forces regulate glioblastoma (GBM) invasiveness.

127 Here, we show that necrosis in glioblastoma (GBM) involves neutrophil-triggered ferropt

128 Intratumoral genomic heterogeneity in glioblastoma (GBM) is a barrier to overcoming therapy re

129 Glioblastoma (GBM) is a brain tumour with high invasiven

130 Glioblastoma (GBM) is a complex disease with extensive m

131 Glioblastoma (GBM) is a highly aggressive and heterogene

132 Glioblastoma (GBM) is a malignant brain tumour with a di

133 Glioblastoma (GBM) is an aggressive malignancy with limi

134 Glioblastoma (GBM) is an astrocytic brain tumor with med

135 The aggressive primary brain tumor glioblastoma (GBM) is characterized by aberrant metaboli

136 The aggressive brain tumor glioblastoma (GBM) is characterized by rapid cellular in

137 Glioblastoma (GBM) is increasingly recognized as a disea

138 Glioblastoma (GBM) is the deadliest adult brain cancer,

139 Glioblastoma (GBM) is the most common and lethal primary

140 Glioblastoma (GBM) is the most common and most aggressiv

141 Glioblastoma (GBM) is the most common and most aggressiv

142 Glioblastoma (GBM) is the most prevalent and lethal adul

143 alterations of EGFR are observed in ~50% of glioblastoma (GBM) patients, and have been found to play

144 Glioblastoma (GBM) resistance to the standard of care is

145 Glioblastoma (GBM) responses to bevacizumab are invariab

146 ealed by The Cancer Genome Atlas project for glioblastoma (GBM) results in formation of high-grade gl

147 plays therapeutic oncolytic activity against glioblastoma (GBM) stem cells (GSCs).

148 Glioma stem-like cells (GSC) in glioblastoma (GBM) structure tumor cells into a hierarch

149 ing of individual primary cells from a human glioblastoma (GBM) surgical sample, revealing relationsh

150 In managing a patient with glioblastoma (GBM), a surgeon must carefully consider wh

151 usly shown that the aggressive brain cancer, glioblastoma (GBM), maintains stem-like features (glioma

152 Glioblastoma (GBM), or grade IV astrocytoma, is a malign

153 Glioblastoma (GBM), the most aggressive form of brain ca

154 ucial roles in promoting malignant growth of glioblastoma (GBM), the most lethal brain tumor.

155 dy both of these effects in a mouse model of glioblastoma (GBM), we employed murine GBM cells enginee

156 h significant cytotoxicity in the context of glioblastoma (GBM), we performed a high-throughput scree

157 eneity facilitates therapeutic resistance in glioblastoma (GBM).

158 has been associated with worse prognosis in glioblastoma (GBM).

159 ng contributes to malignant cell behavior in glioblastoma (GBM).

160 pplied this methodology in two rat models of glioblastoma (GBM; U87 human glioma cells and patient-de

161 ated tumor cells freshly isolated from human glioblastomas (GBM) and that have never known any serum

162 nt III (EGFRvIII) is frequently expressed in glioblastomas (GBM) but its impact on therapy response i

163 s efficacy in highly malignant brain-tumors, glioblastomas (GBM), is limited.

164 f soft brain tumors, showing that aggressive glioblastomas (GBMs) have higher water content while beh

165 carcinoma, lung squamous cell carcinoma, and glioblastoma, genes highly associated with cancer progre

166 for predicting the status of several common glioblastoma genetic biomarkers on preoperative MRI.

167 gmentations were used to predict nine common glioblastoma genetic biomarkers with random forest regre

168 murine metastatic breast cancer 4T1, murine glioblastoma GL261, human triple negative breast cancer

169 We investigated the glioblastoma glycocalyx as a tumor-intrinsic immune supp

170 TP1 cases include IDHwt, glioblastoma high immune infiltration and cellular proli

171 cell-lineage-based stratification model for glioblastoma, highlighting how the cell of origin genera

172 The glioblastoma immune microenvironment is recognized as hi

173 d had no impact on survival in patients with glioblastoma in a well-defined cohort.

174 eutic target as expressed in the majority of glioblastomas in our cohort.

175 t4 and Sox2 drive the stem-like phenotype in glioblastoma, in part, by differentially regulating subs

176 highlight the importance of cell lineage in glioblastoma independent of driver mutations and provide

177 ins LIMK1 and LIMK2 significantly diminishes glioblastoma invasion and spread, suggesting the potenti

178 Glioblastoma is a deadly cancer, with no effective thera

179 Glioblastoma is a devastating form of brain cancer.

180 Glioblastoma is a universally lethal form of brain cance

181 Glioblastoma is an aggressive and heterogeneous tumor in

182 Glioblastoma is an incurable brain tumor notorious for i

183 Glioblastoma is associated with high morbidity and morta

184 treatment with bevacizumab in patients with glioblastoma is controversial because progression-free s

185 The invasive behavior of glioblastoma is essential to its aggressive potential.

186 Glioblastoma is heterogeneous in the molecular subtypes

187 The challenge in the treatment of glioblastoma is the failure to identify the cancer invas

188 Glioblastoma is the most aggressive brain malignancy, fo

189 Glioblastoma is the most common human brain cancer entit

190 Glioblastoma is the most common malignant brain parenchy

191 Glioblastoma is the most common primary malignant brain

192 Glioblastoma is the most malignant brain cancer but the

193 , prognostic and therapeutic tools to tackle glioblastomas is urgently needed.

194 nostic and promising predictive biomarker in glioblastoma, its value in informing treatment decisions

195 In summary, the impact of focal glioblastoma lesions on the functional connectome is glo

196 mic architecture of IDH-wild-type multifocal glioblastomas (M-GBMs) suggests a clinically unobserved

197 We tested northstar on data from glioblastoma, melanoma, and seven different healthy tiss

198 ion cytokine IL-33 as an orchestrator of the glioblastoma microenvironment that contributes to tumori

199 Glioblastoma might have widespread effects on the neural

200 s FUS to increase BBB permeability in murine glioblastoma models and thus enhance the release of tumo

201 layer of the focal adhesion complex, drives glioblastoma motility and invasion.

202 Tumors from genetically engineered glioblastoma mouse models initiated by identical driver

203 Deep learning models were pretrained on glioblastoma MRI, instead of natural images, to determin

204 ng model was based on transfer learning from glioblastoma MRI.

205 Glioblastoma multiforme (GBM) and other solid malignanci

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

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

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

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

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

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

212 Glioblastoma multiforme (GBM) contains a subpopulation o

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

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

215 Glioblastoma multiforme (GBM) is a malignant brain tumor

216 Glioblastoma multiforme (GBM) is an aggressive and diffi

217 Glioblastoma multiforme (GBM) is an aggressive cancer wi

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

219 Glioblastoma multiforme (GBM) is impossible to fully rem

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

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

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

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

224 Glioblastoma multiforme (GBM) tumors are highly metaboli

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

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

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

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

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

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

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

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

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

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

235 slices acquired from a growth-factor driven glioblastoma murine model.

236 Accurate and automatic segmentation of glioblastoma on clinical scans is feasible using a model

237 ozolomide is the first line of treatment for glioblastoma, one of the most aggressive brain tumors th

238 m Cell (Bhaduri et al., 2020) leverage novel glioblastoma organoid models and single-cell RNA-sequenc

239 describe detailed procedures for generating glioblastoma organoids (GBOs) from surgically resected p

240 or generating and biobanking patient-derived glioblastoma organoids (GBOs) that recapitulate the hist

241 ctose-type lectin (MGL), on CD163(+) TAMs in glioblastoma patient-derived tumor tissues.

242 apitulated the immunosuppression observed in glioblastoma patients in the C57BL/6 mouse and investiga

243 s value in informing treatment decisions for glioblastoma patients remains debatable.

244 sted a doubling of 2- and 3-year survival in glioblastoma patients since 2005.

245 unohistochemistry, and a larger cohort of 73 glioblastoma patients to confirm the findings from the p

246 57 newly diagnosed cerebral glioblastoma patients were included.

247 VERDICT parameters in glioblastoma patients were most consistent with the GL26

248 In glioblastoma patients, our models outperformed comparabl

249 the only known biomarker for TMZ response in glioblastoma patients.

250 erified in six freshly dissected tumors from glioblastoma patients.

251 In glioblastoma, poor efficacy of receptor tyrosine kinase

252 cytometry dataset of 2 million cells from 28 glioblastomas, RAPID identified tumor cells whose abunda

253 Glioblastomas remain the deadliest brain tumour, with a

254 Furthermore, other tumor types, including glioblastoma, remain largely refractory.

255 pite a deeper molecular understanding, human glioblastoma remains one of the most treatment refractor

256 a rich resource for basic and translational glioblastoma research.

257 Re-analysis of TCGA glioblastoma RNA-seq unveils previously unreported kinas

258 e-cell RNA-sequencing technologies to tackle glioblastoma's heterogeneous nature, providing new tools

259 presence of heterogeneous GSCs may underlie glioblastoma's rapid progression and invasion.

260 was verified in single-cell RNA-seq of human glioblastoma samples.

261 Given the glioblastoma size in a patient, our model can predict th

262 n brain cancer entity and is maintained by a glioblastoma stem cell (GSC) subpopulation.

263 The interplay between glioblastoma stem cells (GSCs) and tumor-associated macr

264 aggressive and heterogeneous tumor in which glioblastoma stem cells (GSCs) are at the apex of an ent

265 or that increases susceptibility in NSCs and glioblastoma stem cells.

266 in all the glioblastomas we tested including glioblastoma stem/initiating cells, but hardly detectabl

267 IP copy number was elevated in the classical glioblastoma subtype and correlated with elevated EGFR l

268 The oligodendrocyte lineage-associated glioblastoma subtype requires functional ERBB3 and harbo

269 eutics in cancer cells, high MGMT expressing glioblastoma (T98G) and a high ABCB1 expressing triple-n

270 Glioblastoma the most aggressive form of brain cancer, c

271 Glioblastoma, the most lethal primary brain cancer, is e

272 Glioblastoma, the predominant adult malignant brain tumo

273 015 in 596 patients with first recurrence of glioblastoma, the subset of patients with availability o

274 ue to heterogenous tumour growth inherent in glioblastoma, the use of primary cells for orthotopic in

275 We and others had shown that a subset of glioblastomas, the most malignant of all primary brain t

276 to the brain limits the development of novel glioblastoma therapies.

277 e research, little progress has been made in glioblastoma therapy, owing in part to a lack of adequat

278 High-dose radiation is the main component of glioblastoma therapy.

279 tor kinase c-MET has emerged as a target for glioblastoma therapy.

280 1) gene and are less aggressive than primary glioblastoma, they nonetheless generally recur.

281 geted delivery platform to achieve effective glioblastoma treatment by improving efficacy while reduc

282 An ideal glioblastoma treatment needs to engage targets that driv

283 d provides potential therapeutic targets for glioblastoma treatment.

284 nate drivers of tumor invasion, we created a glioblastoma tumor cell atlas with single-cell transcrip

285 clarifies the opposing effects of Norrin on glioblastoma tumor growth and provides potential therape

286 ediates both mitotic somal translocation and glioblastoma tumor invasion.

287 mechanisms of resistance in a heterogeneous glioblastoma tumor model.

288 Glioblastoma tumors exhibit extensive inter- and intratu

289 ppressive or immunostimulatory cell types in glioblastoma tumors, including tumor-associated macropha

290 and the effects of hyperthermia in vitro on glioblastoma U251-MG cells and in vivo on zebrafish embr

291 s undergoing resection of contrast enhancing glioblastoma under general anaesthesia followed by stand

292 advillin (AVIL) is overexpressed in all the glioblastomas we tested including glioblastoma stem/init

293 Here, using a native mouse model of glioblastoma, we develop a high-throughput in vivo scree

294 Here, using a mouse model of glioblastoma, we show that the meningeal lymphatic vascu

295 6 years [range, 22-77 years]) diagnosed with glioblastoma were included from two prospective studies.

296 LX and ASCL1 should be mutually exclusive in glioblastoma, which was verified in single-cell RNA-seq

297 hinery-associated molecular dysregulation in glioblastomas, which could potentially be considered as

298 ative brain MRI from 199 adult patients with glioblastoma who subsequently underwent tumor resection

299 ategies are necessary to effectively address glioblastoma without systemic toxicities.

300 lipid heterogeneity has been visualised in a glioblastoma xenograft tumour using 3D DESI-MS imaging.