ライフサイエンスコーパス: glioblastoma

1 d by FA metrics at baseline in patients with glioblastoma.

2 t cancer, colorectal carcinoma, melanoma and glioblastoma.

3 lomustine alone in patients with progressive glioblastoma.

4 equired to show efficacy of immunotherapy in glioblastoma.

5 se survival in patients with newly diagnosed glioblastoma.

6 a from poorly motile proneural and classical glioblastoma.

7 suppression of antitumor immune responses in glioblastoma.

8 is associated with later tumor recurrence in glioblastoma.

9 derived orthotopic xenografts (PDX) of human glioblastoma.

10 characteristics of human proneural/classical glioblastoma.

11 reatment with radiotherapy for patients with glioblastoma.

12 ggested in the literature to be related with glioblastoma.

13 utic rationale to target it in patients with glioblastoma.

14 n with other immunomodulatory approaches for glioblastoma.

15 a potential target in the GSC population in glioblastoma.

16 rs a viable alternative for the treatment of glioblastoma.

17 patient survival and is a characteristic of glioblastoma.

18 A biopsy of the right optic nerve revealed glioblastoma.

19 apeutic efficacy of oncolytic virotherapy in glioblastoma.

20 ated, autochthonous genetic CRISPR screen in glioblastoma.

21 into critical roles of m(6)A methylation in glioblastoma.

22 upporting the development and progression of glioblastoma.

23 fic miRNA that enhance the aggressiveness of glioblastoma.

24 cable to patient-derived xenograft models of glioblastoma.

25 iting in tumors from patients suffering from glioblastoma.

26 may be an effective therapeutic strategy for glioblastoma.

27 survival in patients with EGFRvIII-positive glioblastoma.

28 has been observed in patients suffering from glioblastoma.

29 bo plus bevacizumab (Pla + Bev) in recurrent glioblastoma.

30 hich, until now, has been largely limited to glioblastoma.

31 e, G4s are promising therapeutic targets for glioblastoma.

32 inical benefit for patients with progressive glioblastoma.

33 as an adjuvant therapy for the treatment of glioblastoma.

34 e treatment of neurological diseases such as glioblastoma.

35 lly relevant approach to target discovery in glioblastoma.

36 hat 6OTD exhibits antitumor activity against glioblastoma.

37 h other mesenchymal transition regulators in glioblastoma.

38 e resulted in tumors that recapitulate human glioblastoma.

39 nce-based guideline on radiation therapy for glioblastoma.

40 gesting that apelin is a druggable factor in glioblastoma.

41 alone among patients at first progression of glioblastoma.

42 s one hallmark of diffuse gliomas, including glioblastomas.

43 ytic and oligodendroglial gliomas, including glioblastomas.

44 letion in 15% (grade II and III) and 50% of glioblastomas.

45 rogenase (IDH-1)-mutated and IDH-1 wild-type glioblastomas.

46 d receptors feasible therapeutic targets for glioblastoma?

47 rs, 42 of 61 (69%) were diffusively invasive glioblastomas, 14 of 61 (23%) were locally invasive, and

48 from cell membranes to the cytosol in U251 (glioblastoma), A549 (lung adenocarcinoma) and MDA-MB-231

49 in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular can

50 ) in subsets of cancers, including secondary glioblastoma, acute myeloid leukemia, intrahepatic chola

51 an option for select patients with recurrent glioblastoma, although this is not supported by prospect

52 the ASTRO guideline on radiation therapy for glioblastoma and added qualifying statements.

53 NYGGF4) inhibits growth of medulloblastoma, glioblastoma and atypical teratoid rhabdoid tumor cell l

54 Notably, in the PDX glioblastoma and BRAFi-resistant melanoma models, this d

55 levant orthotopic resection model of primary glioblastoma and engineered stem cells (SC) expressing E

56 Nine patients with newly diagnosed glioblastoma and four healthy volunteers were included i

57 that PFK1 platelet isoform is upregulated in Glioblastoma and is required for tumor growth mechanisti

58 factor (MET) expression has been reported in glioblastoma and may contribute to bevacizumab resistanc

59 Xenograft mouse models of glioblastoma and metastatic brain tumors (from lung and

60 led the complexity of tumor heterogeneity in glioblastoma and provide new insights into the genomic l

61 mography (PET) and survival in patients with glioblastoma and suspected progression at posttherapy ma

62 revalence of H3(K27M) mutations in pediatric glioblastoma and their well-established impact on global

63 Bevacizumab-resistant patient glioblastomas and both novel xenograft models of resista

64 erozygously deleted in 74.5% of the analyzed glioblastomas and predicts unfavorable patient prognosis

65 in >80% of lower grade gliomas and secondary glioblastomas and primarily affect residue 132, which he

66 owth and reduces survival in mouse models of glioblastoma, and its expression correlates with increas

67 nical outcome in breast cancer, lung cancer, glioblastoma, and pancreatic cancer.

68 e cancer types including breast, uterine and glioblastoma, and TET1 activation is associated with a w

69 n array of tumor types, including leukemias, glioblastomas, and pancreatic, breast, lung, and colorec

70 3 or Jab1 in colon cancer, breast cancer and glioblastoma are associated with significantly shorter s

71 Glioblastoma are highly aggressive brain tumours that ar

72 Glioblastomas are lethal cancers defined by angiogenesis

73 Among the challenges in treating glioblastomas are primary resistance and the rapid emerg

74 e range of human tumor cell lines, including glioblastoma, astrocytoma, neuroblastoma, lung adenocarc

75 emethylase expression are present in primary glioblastomas before treatment, potentially contributing

76 xplains why antibodies are effective against glioblastoma but generally fail in brain metastases of b

77 ene defects are found in virtually all human glioblastomas, but the genetic evidence for a direct rol

78 dicarbonyl stress status in four breast and glioblastoma cancer cell lines in relation with their gl

79 echanisms underlying the role of mcroRNAs in glioblastoma cell growth and apoptosis are not fully und

80 tin-induced apoptosis in medulloblastoma and glioblastoma cell lines is mediated in part by PID1, inv

81 splatin and etoposide in medulloblastoma and glioblastoma cell lines.

82 o differentiation conditions in conventional glioblastoma cell lines.

83 hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resi

84 character of highly infiltrating mesenchymal glioblastoma cells (Wnt5a(High)).

85 KP) is the predominant PFK1 isoform in human glioblastoma cells and its expression correlates with to

86 ng high levels of SOX5/6/21 in human primary glioblastoma cells enabled expression of CDK inhibitors

87 -1227) demonstrate that one subpopulation of glioblastoma cells expressing a mutant epidermal growth

88 Suppression of Ape1/Chk2 signaling in glioblastoma cells facilitates alternative means of dama

89 re we study the clonal evolution of barcoded glioblastoma cells in an unbiased way following serial x

90 Rats were implanted with F98 glioblastoma cells in the right hemisphere and scanned 9

91 Podoplanin-positive primary glioblastoma cells induced aggregation of human platelet

92 ibited NHEJ-mediated DSB repair and rendered glioblastoma cells more sensitive to chemotherapy.

93 tratumoural functional heterogeneity between glioblastoma cells remains poorly understood.

94 ecific knockdown of Mcl-1 broadly sensitizes glioblastoma cells to Bcl-xL inhibition-mediated apoptos

95 rgeting "HR-addicted" temozolomide-resistant glioblastoma cells via a chemical inhibitor of Rad51, we

96 let aggregation in response to primary human glioblastoma cells was investigated in vitro.

97 Human U87 glioblastoma cells were implanted into the striatum of i

98 emonstrated that pancreatic cancer cells and glioblastoma cells were specifically vulnerable to PSM a

99 re that an extracellular protein released by glioblastoma cells, fibulin-3, drives oncogenic NF-kappa

100 ACF binding to basigin in vitro and in live glioblastoma cells, respectively.

101 y expressed on tumor endothelium but also on glioblastoma cells.

102 ve phosphorylation and reduces ATP levels in glioblastoma cells.

103 oint kinase Chk2, regulates drug response of glioblastoma cells.

104 nogenic survival, migration, and invasion of glioblastoma cells.

105 g of DNA repair-supported chemoresistance in glioblastoma cells.

106 PSB over pancreatic adenocarcinoma cells and glioblastoma cells.

107 growth inhibitory effect of temozolomide in glioblastoma cells.

108 of mCpG-dependent gene regulation by KLF4 in glioblastoma cells.

109 phenotypes such as migration and invasion in glioblastoma cells.

110 with their specific uptake in brain cancer (glioblastoma) cells, while maintaining their catalytic a

111 tional signature, we show that the growth of glioblastoma clones in vivo is consistent with a remarka

112 Eligible patients had newly diagnosed glioblastoma confirmed to express EGFRvIII by central an

113 Given that glioblastomas contain both proneural and mesenchymal GSC

114 With use of fusion imaging, glioblastoma contrast enhancement at contrast-enhanced U

115 Conclusion Glioblastoma contrast enhancement with contrast-enhanced

116 Addition of 2-HG to glioblastoma cultures recapitulates the effects of the I

117 ms, including patient-derived stem cell-like glioblastoma cultures, inhibition of Bcl-xL induces sign

118 We leveraged IDH wild-type glioblastomas, derivative neurospheres, and single-cell

119 Brain invasion by glioblastoma determines prognosis, recurrence, and letha

120 inflammation within the brain contribute to glioblastoma development.

121 tential role and regulation of PFKP in human glioblastoma development.Phosphofructokinase 1 (PFK1) pl

122 enrichment was lost in bevacizumab-resistant glioblastomas, driving a tumor edge M1-to-M2 transition.

123 and patients with newly diagnosed, untreated glioblastoma enabled visualization of brain glucose phys

124 promised mice bearing subcutaneous human U87 glioblastomas expressing EGFRvIII and luciferase.

125 ruited patients aged 18 years and older with glioblastoma from 165 hospitals in 22 countries.

126 also discriminated infiltrating mesenchymal glioblastoma from poorly motile proneural and classical

127 tem showed promising therapeutic efficacy in glioblastoma (GBM) and breast cancer models.

128 and PDGFRA have been reported in up to 5% of glioblastoma (GBM) and it remains unclear why such indep

129 d in lower grade gliomas (LGG) compared with glioblastoma (GBM) and normal brain specimens in TCGA da

130 s on chromosome 9p were found in a subset of glioblastoma (GBM) and silencing of RanBP6 promoted glio

131 While molecular subtypes of glioblastoma (GBM) are defined using gene expression and

132 njugated PNPs able of high uptake into U87MG glioblastoma (GBM) cells and with astonishing EC50 value

133 izing non-small-cell lung cancer (NSCLC) and glioblastoma (GBM) cells to ascorbate through pro-oxidan

134 tic threshold in a subset of patient-derived glioblastoma (GBM) cells.

135 Glioblastoma (GBM) contains diverse microenvironments wi

136 oma stem cells (GSCs) have a central role in glioblastoma (GBM) development and chemo/radiation resis

137 , molecularly based classification model for glioblastoma (GBM) in the temozolomide era.

138 Glioblastoma (GBM) is a deadly and therapy resistant mal

139 Glioblastoma (GBM) is a devastating malignancy with few

140 Glioblastoma (GBM) is a hypervascular primary brain tumo

141 Glioblastoma (GBM) is a primary brain cancer that contai

142 Glioblastoma (GBM) is a rare tumor and one of the most c

143 Glioblastoma (GBM) is the most common primary brain tumo

144 Glioblastoma (GBM) is the most lethal form of brain tumo

145 Glioblastoma (GBM) is the most lethal type of human brai

146 Tumor recurrence in glioblastoma (GBM) is, in part, attributed to increased

147 Resistance to antiangiogenic therapy in glioblastoma (GBM) patients may involve hypoxia-induced

148 However, their roles in glioblastoma (GBM) remain unexplored.

149 Median survival for glioblastoma (GBM) remains <15 months.

150 Glioblastoma (GBM) remains one of the most fatal human m

151 Glioblastoma (GBM) stem-like cells (GSC) promote tumor i

152 g (p65) in myeloid cells inhibited syngeneic glioblastoma (GBM) through decreased CD45 infiltration i

153 id (5-ALA) is now a widely-used modality for glioblastoma (GBM) treatment.

154 ring (si) and micro (mi)RNAs to intracranial glioblastoma (GBM) tumor sites.

155 Glioblastoma (GBM) tumors exhibit potentially actionable

156 ct HGG types, including adult and paediatric glioblastoma (GBM), anaplastic oligodendroglioma, and di

157 observed in several tumor tissues, including glioblastoma (GBM), and is considered as a well-establis

158 hages (TAMs) facilitates malignant growth of glioblastoma (GBM), but the underlying mechanisms remain

159 In glioblastoma (GBM), heterogeneous expression of amplifie

160 ession is retained in some tumors, including glioblastoma (GBM), suggesting that it may support cance

161 Glioblastoma (GBM), the most aggressive brain tumor in h

162 In glioblastoma (GBM), tumor-associated macrophages (TAM) r

163 survival remains low for most patients with glioblastoma (GBM), which reveals the need for markers o

164 mplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM).

165 adaptation and mesenchymal transformation in glioblastoma (GBM).

166 g delivery to malignant brain tumors such as glioblastoma (GBM).

167 ) and overall survival (OS) in patients with glioblastoma (GBM).

168 gitudinal specimens from 52 individuals with glioblastoma (GBM).

169 rongly upregulated NADPH-producing enzyme in glioblastoma (GBM).

170 progression of diffuse gliomas, particularly glioblastoma (GBM).

171 nt response and progression in patients with glioblastoma (GBM).

172 on (MP) to an anaplastic glioma or secondary glioblastoma (GBM).

173 resection are prognostically beneficial for glioblastomas (GBM), potential negative effects have als

174 icate challenging refractory tumors, such as glioblastomas (GBM).

175 Glioblastomas (GBMs) are malignant brain tumors with a m

176 Glioblastomas (GBMs) are malignant tumors characterized

177 Application to a glioblastoma gene expression dataset identified pathways

178 ive (6OTD), limits the growth of intractable glioblastoma (grade IV glioma) and glioma stem cells (GS

179 ation drives tumor initiation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) m

180 Human glioblastomas harbour a subpopulation of glioblastoma st

181 ctor coordinating the invasive properties of glioblastoma has been identified.

182 Molecular profiling of glioblastomas has revealed the presence of key signaling

183 Conclusion IDH-mutated glioblastomas have a less invasive phenotype compared wi

184 erapeutic efficacy in an orthotopic model of glioblastoma highlights the need to balance significant

185 FA was measured in 70 patients with glioblastoma in five regions of interest (ROIs) per pati

186 are approved for the treatment of recurrent glioblastoma in many countries.

187 after biopsy or resection of newly diagnosed glioblastoma in patients up to 70 years of age.

188 In glioblastoma, incorporation of unedited GRIA2 subunits l

189 In intracranial mouse xenograft models of glioblastoma, inhibiting Wnt5a activity blocked brain in

190 Accordingly, fibulin-3 promotes glioblastoma invasion in a manner that requires NF-kappa

191 Glioblastoma is a highly aggressive brain tumor.

192 Glioblastoma is a highly lethal brain cancer that freque

193 Glioblastoma is a universally lethal cancer with a media

194 Glioblastoma is an immunosuppressive, fatal brain cancer

195 Glioblastoma is an incurable tumor, and the therapeutic

196 Glioblastoma is the most common and aggressive intrinsic

197 Glioblastoma is the most common and lethal primary malig

198 further molecular testing because some have glioblastoma-like molecular features with poor clinical

199 portant mechanistic role for this pathway in glioblastoma malignancy.

200 target multiple epigenetic regulators within glioblastomas may be effective in overcoming therapy res

201 00 Da to 70 kDa permeated into a preclinical glioblastoma model at rates proportional to their diffus

202 tyrosine kinase inhibition in a preclinical glioblastoma model, which may have important translation

203 chNKG2D) in fully immunocompetent orthotopic glioblastoma mouse models.

204 ors, 61 ovarian tumors, 70 liver tumors, 156 glioblastoma multiform samples, 27 esophageal adenocarci

205 Glioblastoma multiforme (GBM) is a highly malignant prim

206 Glioblastoma multiforme (GBM) is an aggressive brain tum

207 Glioblastoma multiforme (GBM) is an intractable tumor de

208 Glioblastoma multiforme (GBM) is highly invasive and uni

209 Glioblastoma multiforme (GBM) is the most common primary

210 Glioblastoma multiforme (GBM) remains a mainly incurable

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

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

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

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

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

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

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

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

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

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

221 growth and self-renewal potential of several glioblastoma neurosphere lines in vitro, and this activi

222 r the treatment of patients with progressive glioblastoma on the basis of uncontrolled data.

223 derstanding of genetic factors that regulate glioblastoma pathogenesis is of central importance.

224 r Cohort (n=40); and The Cancer Genome Atlas Glioblastoma Patient Cohort (n=98).

225 ociated macrophages in bevacizumab-resistant glioblastoma patient specimens and two novel glioblastom

226 pelin- and endothelial-mediated expansion of glioblastoma patient-derived cells with stem-like proper

227 irin represents a new therapeutic option for glioblastoma patients as an enhancer of the cytotoxic ef

228 The median survival for glioblastoma patients is 15 months despite aggressive s

229 ic enzymes correlated with poor prognosis in glioblastoma patients.

230 and in endothelial cells isolated from human glioblastoma patients.

231 phosphorylation levels and poor prognosis in glioblastoma patients.

232 ty could have therapeutic efficacy for adult glioblastoma patients.

233 0.0007) and THGr(Cb) values (P = 0.02) than glioblastoma patients.

234 onfirmed cerebrocerebellar diaschisis in all glioblastoma PET studies performed within 1 y of death.

235 By analysing PTEN in malignant glioblastoma primary cells derived from 16 of our patien

236 ance: Three-dimensional culture scaffolds of glioblastoma provide a better physiological representati

237 10-17 years]) with progressive HER2-positive glioblastoma received 1 or more infusions of autologous

238 lls, and both need to be targeted to prevent glioblastoma recurrence.

239 SC), a newly identified stromal component of glioblastoma, release exosomes that increase the prolife

240 cture-activity relationship, and efficacy in glioblastoma-relevant models for a library of novel 7-az

241 Its impact on glioblastoma remains largely unknown.

242 Glioblastoma remains the most common and deadliest type

243 nderlying cause of recurrences of aggressive glioblastomas, replenishing the tumor population and und

244 raft (PDX) models of glioblastoma to predict glioblastoma response to treatment with the chemotherape

245 One of these clusters contained all of the glioblastoma samples with G-CIMP, a known methylation ph

246 Conclusion:(8)F-FET uptake in glioblastomas seems to be largely independent of BBB per

247 oximal localization of TNC and BTIC in human glioblastoma specimens and in orthotopic murine xenograf

248 In addition, S386 phosphorylation in human glioblastoma specimens positively correlates with PFKP e

249 anding the molecular mechanisms that control glioblastoma stem cell (GSC) proliferation and drug resi

250 We have previously shown that glioblastoma stem cells (GSCs) are enriched in the hypox

251 ZIKV preferentially infected and killed glioblastoma stem cells (GSCs) relative to differentiate

252 Finally, we show that functionally distinct glioblastoma stem cells can be separately targeted using

253 man glioblastomas harbour a subpopulation of glioblastoma stem cells that drive tumorigenesis.

254 small population of tumor initiating cells (glioblastoma stem cells) that have many properties simil

255 ommon regulatory networks in both neural and glioblastoma stem cells, we subjected both cell types to

256 the expansion of pre-existing drug-resistant glioblastoma stem cells.

257 conserved proliferative hierarchy rooted in glioblastoma stem cells.

258 Glioblastoma stem-like cells (GSC) are hypothesized to e

259 uppressive, fatal brain cancer that contains glioblastoma stem-like cells (GSCs).

260 )A demethylase ALKBH5 is highly expressed in glioblastoma stem-like cells (GSCs).

261 regulates proliferation and self-renewal of glioblastoma stem-like cells by modulating pre-mRNA stab

262 Differentiation of glioblastoma stem-like cells drives the nuclear transloc

263 d murine glioma cell lines, as well as human glioblastoma stem-like cells, in vitro.

264 methyltransferase promoter methylation, and glioblastoma subtype.

265 ar network that controls stemness and EMT in glioblastoma, suggesting S100A4 as a candidate therapeut

266 strate that NHEJ contributes to p53-mediated glioblastoma suppression, and reveal a crucial role for

267 enetic compounds, suggesting new avenues for glioblastoma-targeted therapy.

268 yze the case for checkpoint immunotherapy in glioblastoma, the most common adult brain tumor.

269 Glioblastoma, the most common and aggressive malignant b

270 erapy against several malignancies including glioblastoma, the most common and most aggressive malign

271 Glioblastoma, the most common primary malignant brain tu

272 miR-503 as a promising molecular target for glioblastoma therapy.

273 hat targeting HR is a promising strategy for glioblastoma therapy.

274 t a new mechanism of NF-kappaB activation in glioblastoma through depletion of the KLF6 tumor suppres

275 g, and how this mechanism is circumvented in glioblastoma through KLF6 loss.

276 , we report that miR-503 is overexpressed in glioblastoma tissue compared with normal human brain tis

277 12 patient-derived xenograft (PDX) models of glioblastoma to predict glioblastoma response to treatme

278 ative, mesenchymal-like program in classical glioblastoma TPC and Wnt5a(Low) mesenchymal TPC.

279 Inhibiting Wnt5a in mesenchymal glioblastoma TPC suppressed their infiltrating capabilit

280 ed DAG homes to the brain in mouse models of glioblastoma, traumatic brain injury, and Parkinson's di

281 However, medical use of COX inhibitors in glioblastoma treatment has been limited due to their wel

282 TA loaded HNPs as a non-invasive approach in glioblastoma treatment.

283 ion, and detect elevated ADAR3 expression in glioblastoma tumors compared with adjacent brain tissue.

284 rticular, tumor spheroids of two cell lines, glioblastoma (U-87MG) and colorectal carcinoma (HCT116),

285 er cells, breast cancer MDA-MB-231 and human glioblastoma U87 cancer lines, was demonstrated in vitro

286 ter 24 h in vitro cytotoxicity against human glioblastoma U87 cell line.

287 ncer effect on intracranial human and murine glioblastoma via induction of Fas and Fas-L, with no sid

288 The ASTRO guideline on radiation therapy for glioblastoma was reviewed for developmental rigor by met

289 tal, patients with progressive HER2-positive glioblastoma were enrolled between July 25, 2011, and Ap

290 Materials and Methods Seventy patients with glioblastoma were prospectively recruited and imaged pre

291 moradiation, bevacizumab-naive patients with glioblastoma were randomly assigned 1:1 to receive Ona (

292 In a murine xenograft model of glioblastoma, whereas temozolomide only delayed tumor gr

293 maging and survival time in 56 patients with glioblastoma who were treated with postoperative concurr

294 hereas anaplastic glioma (WHO grade III) and glioblastoma (WHO grade IV) showed decreased OEF when co

295 Conclusion Patients with glioblastoma whose posttherapy MR images showed a residu

296 ); Pten(L/L); Trp53(L/L) mice, which develop glioblastoma with a penetrance of 92% and a median survi

297 ors.Significance: Combinatorial treatment of glioblastoma with temozolomide and a novel artificial nu

298 d the use of oncolytic virus therapy against glioblastoma with Zika virus (ZIKV), a flavivirus that i

299 IDH) mutations, but metabolic alterations in glioblastomas with wild-type IDH are poorly understood.

300 glioblastoma patient specimens and two novel glioblastoma xenograft models of bevacizumab resistance.