ライフサイエンスコーパス: GBM

1 GBM is among the most neovascularised neoplasms and its

2 GBM stem cells frequently express high levels of the tra

3 GBM, the most aggressive of the gliomas, is characterize

4 Consistently, analysis of 122 GBM tumour samples revealed that the number of ODZ1-posi

5 vivo BBB passage and tumor accumulation in a GBM orthotopic model.

6 acrophages comprising approximately 40% of a GBM tumor may limit virotherapeutic efficacy.

7 xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout mice.

8 hould be recommended for several years after GBM.

9 ys a potent antiproliferative effect against GBM cells.

10 t the remaining podocytes did not walk along GBM during 24 h.

11 The analysis of human datasets and GBM tumors revealed higher expression of p65 in GBM-asso

12 ly exclusive in migratory tumor lesions, and GBM patients with MSI1(high)/TNS3(low) pattern tend to h

13 ntral roles in promoting niche co-option and GBM initiation.

14 ferentiated cells (GBMDC) grown in serum and GBM neurospheres (GBMNS) grown as neurospheres in vitro.

15 ophage polarization, immune suppression, and GBM growth.

16 of Alport phenotypes by variation in another GBM component.

17 enal injury in experimental, crescentic anti-GBM nephritis.

18 apillaries, abruptly arrested following anti-GBM antibody deposition via neutrophil FcgammaRIIA and A

19 i-glomerular basement membrane-induced (anti-GBM-induced) glomerulonephritis when expressed on murine

20 et for therapy of aggressive cancers such as GBM, and defined small-molecule inhibitors such as PDZ1i

21 cing, depletion of AXL profoundly attenuates GBM proliferation both in vitro and in vivo.

22 ntiangiogenic therapy resistance, benefiting GBM patients.

23 dings show how specific interactions between GBM cell receptors and scaffold components contribute si

24 by Spon2) in the diseased FVB/N Cd151 (-/-) GBM that did not occur in the C57BL/6 diseased-resistant

25 at these tumors are similar to the classical GBM subtype observed in patients.

26 ining 24 (TRIM24) is upregulated in clinical GBM specimens and required for EGFR-driven tumorigenesis

27 PDZ1i inhibited crucial GBM signaling involving FAK and mutant EGFR, EGFRvIII, a

28 tely act with the MTKI sunitinib to decrease GBM cell viability.

29 ative role as an adjuvant therapy in defined GBM patient populations.

30 f mibefradil inhibited growth of GSC-derived GBM murine xenografts, prolonged host survival, and sens

31 tein, is robustly expressed in human-derived GBM cell lines and patient samples, with expression incr

32 platform for 3D culturing of patient-derived GBM cells, with improved pathophysiologic properties as

33 ing the promoter of Foxo3 In patient-derived GBM stem cells, CRISPR/Cas9 deletion of FOXG1 does not i

34 solated from established and patient-derived GBMs using both in vitro assays and in vivo orthotopic p

35 al in which 22 patients with newly diagnosed GBM were initially enrolled, of which 17 patients were r

36 encing of PRMT5 expression in differentiated GBM cell lines results in apoptosis and reduced tumour g

37 Tivozanib diminished GBM cell invasion through impairing the proteolytic casc

38 mindin, its early expression in the diseased GBM could represent a trigger of both further podocyte c

39 ression coordinately acts with CDK4 to drive GBM tumorigenesis.

40 tes were recruited to the tumor early during GBM initiation, where they localized preferentially to p

41 t's immune system to recognize and eliminate GBM.

42 gh expression ratio of MSI1 to TNS3 enhanced GBM tumor migration.

43 Using established GBM lines and patient-derived stem cells, we identify a

44 approach to the treatment of EGFR-expressing GBM using a combination of EGFR and TNF inhibition.

45 n with temozolomide, the first-line drug for GBM therapy.

46 mes from an H-RasV12 myr-Akt mouse model for GBM are enriched for intracellular signaling cascade pro

47 genes, we identify that BCL6 is required for GBM cell viability and that BCL6 overexpression is assoc

48 opment of novel immunotherapy strategies for GBM patients.

49 as a mechanism-based treatment strategy for GBM.

50 rapeutically targeting the immune system for GBM treatment.

51 TRIM24 as a potential therapeutic target for GBM that are associated with EGFR activation.

52 ecord for developing effective therapies for GBM has been dismal, we also review the challenges to su

53 Using gene expression data from GBM stem-like cells, astrocytes, and neural progenitor c

54 overall survival in patients suffering from GBM.

55 h inhibition was observed in syngeneic GL261 GBM (p < 0.05).

56 Glioblastoma (GBM) contains diverse microenvironments with uneven dist

57 Glioblastoma (GBM) is a deadly and therapy resistant malignant brain t

58 Glioblastoma (GBM) is a devastating malignancy with few therapeutic op

59 Glioblastoma (GBM) is a hypervascular primary brain tumor with poor pr

60 Glioblastoma (GBM) is a primary brain cancer that contains populations

61 Glioblastoma (GBM) is a rare tumor and one of the most challenging mal

62 Glioblastoma (GBM) is the most common primary brain tumor and has a di

63 Glioblastoma (GBM) is the most lethal form of brain tumor and remains

64 Glioblastoma (GBM) is the most lethal type of human brain cancer, wher

65 Glioblastoma (GBM) remains one of the most fatal human malignancies du

66 Glioblastoma (GBM) represents the most common and aggressive histologi

67 Glioblastoma (GBM) stem-like cells (GSC) promote tumor initiation, pro

68 Glioblastoma (GBM) tumors exhibit potentially actionable genetic alter

69 Glioblastoma (GBM), the most aggressive brain tumor in human patients,

70 l-cell lung cancer (NSCLC) and glioblastoma (GBM) cells to ascorbate through pro-oxidant chemistry in

71 malignant brain tumors such as glioblastoma (GBM).

72 form of primary brain cancer, glioblastoma (GBM), is characterized by significant intratumoral heter

73 in a subset of patient-derived glioblastoma (GBM) cells.

74 based classification model for glioblastoma (GBM) in the temozolomide era.

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

76 now a widely-used modality for glioblastoma (GBM) treatment.

77 mising therapeutic efficacy in glioblastoma (GBM) and breast cancer models.

78 (GSCs) have a central role in glioblastoma (GBM) development and chemo/radiation resistance, and the

79 Tumor recurrence in glioblastoma (GBM) is, in part, attributed to increased epithelial-to-

80 e to antiangiogenic therapy in glioblastoma (GBM) patients may involve hypoxia-induced expression of

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

82 ion and mutation are common in glioblastoma (GBM), but EGFR inhibition has not been effective in trea

83 In glioblastoma (GBM), heterogeneous expression of amplified and mutated

84 In glioblastoma (GBM), tumor-associated macrophages (TAM) represent up to

85 ated NADPH-producing enzyme in glioblastoma (GBM).

86 tor tyrosine kinases (RTKs) in glioblastoma (GBM).

87 mesenchymal transformation in glioblastoma (GBM).

88 veral tumor tissues, including glioblastoma (GBM), and is considered as a well-established marker for

89 ined in some tumors, including glioblastoma (GBM), suggesting that it may support cancer growth in th

90 micro (mi)RNAs to intracranial glioblastoma (GBM) tumor sites.

91 e been reported in up to 5% of glioblastoma (GBM) and it remains unclear why such independent amplifi

92 e 9p were found in a subset of glioblastoma (GBM) and silencing of RanBP6 promoted glioma growth in v

93 While molecular subtypes of glioblastoma (GBM) are defined using gene expression and mutation prof

94 hagy and the tumorigenicity of glioblastoma (GBM) cells.

95 acilitates malignant growth of glioblastoma (GBM), but the underlying mechanisms remain undefined.

96 including adult and paediatric glioblastoma (GBM), anaplastic oligodendroglioma, and diffuse intrinsi

97 diffuse gliomas, particularly glioblastoma (GBM).

98 anaplastic glioma or secondary glioblastoma (GBM).

99 loid cells inhibited syngeneic glioblastoma (GBM) through decreased CD45 infiltration in tumors, as c

100 able of high uptake into U87MG glioblastoma (GBM) cells and with astonishing EC50 value (38 pM) when

101 de gliomas (LGG) compared with glioblastoma (GBM) and normal brain specimens in TCGA datasets and in

102 ins low for most patients with glioblastoma (GBM), which reveals the need for markers of disease outc

103 survival (OS) in patients with glioblastoma (GBM).

104 imens from 52 individuals with glioblastoma (GBM).

105 d progression in patients with glioblastoma (GBM).

106 ng refractory tumors, such as glioblastomas (GBM).

107 prognostically beneficial for glioblastomas (GBM), potential negative effects have also been suggeste

108 Glioblastomas (GBMs) are malignant brain tumors with a median survival

109 Glioblastomas (GBMs) are malignant tumors characterized by their vascul

110 ASE PRESENTATION: A 21-year-old man, who had GBM 7 years ago complained of a transient shadow in his

111 In addition to being highly heterogeneous, GBM tumour cells exhibit high adaptive capacity to targe

112 KT1, PIK3CA and SOS1) in U87 and DBTRG human GBM cells.

113 neoplastic transformation in vitro in human GBM cell lines.

114 alcium channel was highly expressed in human GBM specimens and enriched in GSCs.

115 Moreover, in human GBM xenografts robust BIRC3 expression was noted within

116 e is insufficient tumor oxygenation in human GBM, despite increased tumor vascularization.

117 3Ralpha2 alone induces invasiveness of human GBM cells without affecting their proliferation.

118 In a murine xenograft model of human GBM, we found that IDH1 silencing significantly improved

119 eta8(high) cells from freshly resected human GBM samples also reveals a requirement for this integrin

120 rast, p65KO athymic chimeric mice with human GBM, failed to inhibit tumor growth, confirming the cont

121 is vital to support both mature and immature GBM tumour cell populations.

122 comprehensive characterization of Cav3.2 in GBM tumors and GSCs and provide a preclinical proof of c

123 nd biochemical basis of resistance to AAT in GBM patients.

124 ier and enhance oHSV-1 oncolytic activity in GBM.Significance: These findings suggest a strategy to e

125 athological significance of CDK4 amplicon in GBM formation remains incompletely understood.

126 of tivozanib in combinatorial approaches in GBM.

127 ial efficacy of pharmacological ascorbate in GBM and NSCLC therapy.

128 e AXL is a transcriptional target of BCL6 in GBM and mediates partially the regulatory effects of BCL

129 f infiltrating and resident myeloid cells in GBM, establishing a rationale to target infiltrating cel

130 teinuric syndromes resulting from defects in GBM structural proteins (laminin beta2 or collagen alpha

131 sed glucocorticoid to prevent brain edema in GBM patients, suppressed the observed inflammatory respo

132 sion anti-correlates with PTEN expression in GBM patient samples.

133 ever, these therapies have largely failed in GBM patients.

134 ional heterogeneity of 5-ALA fluorescence in GBM.

135 g the heterogeneity of 5-ALA fluorescence in GBM.

136 of MDA-9/Syntenin reduced invasion gains in GBM cells following radiation.

137 ion of wild-type p53 and its target genes in GBM cells.

138 r and mediator of hypoxia-driven habitats in GBM.

139 virus (CMV) antigens have been identified in GBM but not normal brain, providing an unparalleled oppo

140 A-to-I hypoediting events were identified in GBM samples.

141 therapy could improve antitumor immunity in GBM.

142 croscopy, we show that biopsy-like injury in GBM induces migration and proliferation of tumor cells t

143 prognostic relevance of ceRNA interaction in GBM.

144 Overexpression of ODZ1 in GBM cells reduced survival of xenografted mice.

145 lysine demethylase KDM1A is overexpressed in GBM.

146 thylation activity and its overexpression in GBM is associated with more aggressive disease.

147 tumors revealed higher expression of p65 in GBM-associated CD68+ macrophages compared to neighboring

148 tein biomarkers representing key pathways in GBM by a quantitative molecular microscopy-based approac

149 ere, we report the critical role of PRMT5 in GBM differentiated cells (GBMDC) grown in serum and GBM

150 r, the pathological role of this receptor in GBM remains to be established.

151 vercome the signalling pathway redundancy in GBM and, hence, promote tumour cell death.

152 erivascular niche across multiple regions in GBM patient tissue microarrays.

153 nd survivin are coordinately up-regulated in GBM patient tumors, and functional inhibition of either

154 presence of these signaling relationships in GBM.

155 roles to fuel unconstrained self-renewal in GBM stem cells via transcriptional control of core cell

156 3 as a mediator of therapeutic resistance in GBM to standard temozolomide (TMZ) chemotherapy and radi

157 ive intratumoral hypoxia plays a key role in GBM escape from AAT.

158 ed hypoxic foci and invasiveness, as seen in GBM patients receiving anti-VEGF therapy.

159 3 expression through HIF1-alpha signaling in GBM cells.

160 reliable method revealed its significance in GBM-related functions and prognosis.

161 IDH1 silencing in GBM cells reduced levels of NADPH, deoxynucleotides, and

162 ype E3 ubiquitin ligase whose suppression in GBM also correlates with poor prognosis, reduces GBM cel

163 sms that direct hypoxia-mediated survival in GBM habitats are unclear.

164 ease progression and a therapeutic target in GBM.

165 ally be exploited for combination therapy in GBM and possibly other malignancies.

166 ion for the failures of anti-EGFR therapy in GBM and suggest a new approach to the treatment of EGFR-

167 ies by CDK4 and PIKE-A stably transfected in GBM cell lines.

168 species (ROS) and mesenchymal transition in GBM cells.

169 In this review, we examine AAT resistance in GBMs, with an emphasis on six potential hypoxia-mediated

170 observed in numerous human cancers including GBM.

171 an MST4-ATG4B signaling axis that influences GBM autophagy and malignancy, and whose therapeutic targ

172 ufficient to downregulate Rictor and inhibit GBM growth and invasive characteristics in vitro and sup

173 tudy, we demonstrate that HBEGF can initiate GBM in mice in the context of Ink4a/Arf and Pten loss, a

174 sentative examples of the incorporation into GBMs of electroactive units such as porphyrins, phthaloc

175 iotherapy in treating mice with intracranial GBM xenograft markedly slows tumor growth and provides a

176 indings establish a novel marker of invading GBM cells and consequently a potential marker of disease

177 upregulated, conserved component in invasive GBM.

178 cteristics that enable targeting of invasive GBM cells.

179 ive and sustained treatments to the invasive GBM cells intermixed with functioning neural elements is

180 nsional mathematical modeling to investigate GBM progression and response to therapy.

181 PIKE-A and CDK4 in TP53/PTEN double knockout GBM mouse model additively shortens the latency of gliom

182 Gradient Boosting Machine (GBM) approach was used to explain the non-linear relatio

183 nvestigational approaches to treat or manage GBM.

184 Graphene-based materials (GBMs), with graphene, their most known member, at the he

185 ells along the glomerular basement membrane (GBM) is under debate.

186 meate into the glomerular basement membrane (GBM), in general agreement with Ogston's 1958 equation d

187 litting of the glomerular basement membrane (GBM).

188 mponent of the glomerular basement membrane (GBM).

189 erior and selective biomarker of mesenchymal GBM versus neural, proneural and classical subtypes.

190 Active Ras isolated from human and mouse GBM extracellular nanovesicles lysates using the Ras-bin

191 Herein, we demonstrate that mouse GBM cell-derived extracellular nanovesicles resembling e

192 h upon biopsy both in mice and in multifocal GBM patients.

193 Glioblastoma multiforme (GBM) is a highly malignant primary brain cancer with a d

194 Glioblastoma multiforme (GBM) is an aggressive brain tumor driven by cells with h

195 Glioblastoma multiforme (GBM) is an intractable tumor despite therapeutic advance

196 Glioblastoma multiforme (GBM) is highly invasive and uniformly fatal, with median

197 Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tum

198 Glioblastoma multiforme (GBM) is the most common primary malignant brain cancer i

199 Glioblastoma multiforme (GBM) remains a mainly incurable disease in desperate nee

200 ressive brain tumor glioblastoma multiforme (GBM) results in part from its strong propensity to invad

201 rial enhancement of glioblastoma multiforme (GBM) with intraoperative contrast-enhanced ultrasonograp

202 cteristics of human glioblastoma multiforme (GBM).

203 rs, one of which is glioblastoma multiforme (GBM).

204 rexpressed in human glioblastoma multiforme (GBM).

205 a history of brain glioblastoma multiforme (GBM).

206 essive functions in glioblastoma multiforme (GBM).

207 characteristics in glioblastoma multiforme (GBM).

208 e that genetic susceptibility to GBM and non-GBM tumors are highly distinct, which likely reflects di

209 The new RPA model (NRG-GBM-RPA) was confirmed using traditional immunohistochem

210 This new NRG-GBM-RPA model improves outcome stratification over both

211 Of 166 patients used for the new NRG-GBM-RPA model, 97 (58.4%) were male (mean [SD] age, 55.7

212 The refined NRG-GBM-RPA consisting of MGMT protein, c-Met protein, and a

213 The prognostic significance of the NRG-GBM-RPA was subsequently confirmed in an independent dat

214 DGFRA protein co-expression occurs in 37% of GBM.

215 xpression and/or mutation of EGFR in >50% of GBM.

216 ect; induction of autophagy; augmentation of GBM stem cell self-renewal; possible implications of GBM

217 drastically reduces the invasive capacity of GBM cells.

218 s show that our BUB1B(R/S) classification of GBM tumors can predict clinical course and sensitivity t

219 hanisms highlights the overall complexity of GBM treatment resistance while also providing direction

220 ds after accounting for known confounders of GBM patient outcome.

221 GBM's tumor microenvironment, the effects of GBM standard on care therapy on tumor-associated immune

222 cell self-renewal; possible implications of GBM-endothelial cell transdifferentiation; and vasoforma

223 y replicate pathophysiologic interactions of GBM cells with unique aspects of the brain extracellular

224 ent, plays a crucial role in the invasion of GBM cells.

225 to promote the motility and invasiveness of GBM cells via phosphatidylinostitol 3-kinase activation,

226 ession promotes motility and invasiveness of GBM cells, and that high levels of SLFN5 expression corr

227 o the motility and hence the invasiveness of GBM cells, and that Nrdp1 acts as a negative regulator o

228 e intricate micro-environmental landscape of GBM will abound into the development of novel immunother

229 potential use in the surgical management of GBM.

230 In the U87 xenograft model of GBM, C16 treatment overcame the microglia/macrophage bar

231 tient-derived BTIC xenograft mouse models of GBM.

232 component VANGL1 suppresses the motility of GBM cell lines, pointing to an important mechanistic rol

233 d predict metastatic and survival outcome of GBM patients.

234 a-mediated adaptive mesenchymal phenotype of GBM.

235 view summarizes the clinical presentation of GBM, diagnostic methods, evidentiary basis for the curre

236 paired miRNA and gene expression profiles of GBM, our data showed that this alternative layer of gene

237 CD11b(+)/CD163(+) TAMs and poor prognosis of GBM patients.

238 (VEGF) receptors, inhibited proliferation of GBM cells through a G2/M cell cycle arrest via inhibitio

239 The diffusely infiltrative properties of GBM result in residual tumor at neurosurgical resection

240 Here, we discuss the unique properties of GBM's tumor microenvironment, the effects of GBM standar

241 of ADC-rCBV ROIs in nonenhancing regions of GBM can be used to identify patients with poor survival

242 of ODZ1 promotes cytoskeletal remodelling of GBM cells and invasion of the surrounding environment bo

243 of BIRC3 reversed therapeutic resistance of GBM cells to RT in hypoxic microenvironments through enh

244 etabolic strategy to improve the response of GBM to radiotherapy.

245 Further, small RNA sequencing of GBM patients identified significant miRNA hypoediting wh

246 This defined subpopulation of GBM is highly sensitive to agents that disrupt this path

247 A subset of GBM tumor isolates requires BUB1B to suppress lethal kin

248 erapeutic strategy for this unique subset of GBM tumors.

249 advances have been made in the treatment of GBM, encouraging outcomes typically are not observed; pa

250 a therapeutic approach for the treatment of GBM.

251 m for tumor tissues, we collected 3 types of GBM tissues on the basis of their fluorescence intensity

252 migration, and increases viscoelasticity of GBM cells.

253 e required to exploit the vulnerabilities of GBM and other brain tumors.

254 nt functionalization and characterization of GBMs.

255 ciated vasculature to mitigate the growth of GBMs.

256 -derived GSC lines and visualized orthotopic GBM xenografts in vivo after conjugation with a near-inf

257 -derived orthotopic xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout m

258 these components is also examined in patient GBM samples and correlative associations between the rel

259 entially expressed in GSCs and also predicts GBM poor prognosis.

260 regulator Nrdp1, act coordinately to promote GBM invasiveness and malignancy.

261 utant EGFR (EGFRvIII), IL-13Ralpha2 promotes GBM cell proliferation in vitro and in vivo.

262 ncover the mechanism by which SLFN5 promotes GBM tumorigenesis, we found that this protein is a trans

263 ) through its receptor PTPRZ1 thus promoting GBM malignant growth through PTN-PTPRZ1 paracrine signal

264 mbined with radiation, PDZ1i radiosensitized GBM cells.

265 A recent trial in recurrent GBM patients demonstrated the potential clinical benefit

266 gether with antiangiogenic therapies reduced GBM tumor size but increased invasiveness.

267 also correlates with poor prognosis, reduces GBM cell migration and invasiveness by suppressing PCP s

268 ritical role of MSI1-TNS3 axis in regulating GBM migration and highlighted that the ratio of MSI1/TNS

269 Knockdown of MDA-9/Syntenin sensitizes GBM cells to radiation, reducing postradiation invasion

270 e PTN-PTPRZ1 paracrine signalling to support GBM malignant growth, indicating that targeting this sig

271 or anti-PTPRZ1 antibody potently suppressed GBM tumour growth and prolonged animal survival.

272 sted in animal models of human and syngeneic GBM.

273 apy (AAT) is a treatment option that targets GBM-associated vasculature to mitigate the growth of GBM

274 These results indicate that GBM growth responses to targeted therapies previously te

275 tive processes by podocyte walking along the GBM very unlikely.

276 on of collagen alpha3alpha4alpha5(IV) in the GBM.

277 s (laminin beta2 or collagen alpha3 IV), the GBM is irregularly swollen, the lamina densa is absent,

278 dent permeation into the lamina densa of the GBM and the podocyte glycocalyx, together with saturable

279 that permeation into the lamina densa of the GBM is size-sensitive.

280 (Lo)CCR2(Hi) monocytes were recruited to the GBM, where they transitioned to CX3CR1(Hi)CCR2(Lo) macro

281 Twenty-three GBM patients were assessed by (18)F-fluoromisonidazole (

282 substantiate that genetic susceptibility to GBM and non-GBM tumors are highly distinct, which likely

283 0 b constitutes a promising approach towards GBM treatment.

284 chemotherapeutic agent, but its use to treat GBM is limited by severe systemic toxicity and inefficie

285 We identify PRMT5 in an in vivo GBM shRNA screen and show that PRMT5 knockdown or inhibi

286 wn or inhibition potently suppresses in vivo GBM tumors, including patient-derived xenografts.

287 vivo and in situ, in patients admitted with GBM using multimodal imaging.

288 rker for glomerular diseases associated with GBM alterations.

289 mor vasculature is inversely correlated with GBM patient survival after chemotherapy.

290 in the clinical management of patients with GBM and other brain malignancies.

291 e: A randomized pilot trial in patients with GBM implicates polyfunctional T-cell responses as a biom

292 ssment of prognostic groups in patients with GBM treated with radiation and temozolomide and to influ

293 methylation, respectively, for patients with GBM treated with radiation and temozolomide and was biol

294 Three patients with GBM undergoing treatment with tumor lysate-pulsed DC vac

295 Materials and Methods Ten patients with GBM were retrospectively identified by using routinely c

296 umor growth and progression in patients with GBM.

297 the tumor microenvironment in patients with GBM.

298 therapeutic interventions for patients with GBM.

299 ncy of signaling pathways represented within GBMs contributes to their therapeutic resistance.

300 MCF-7 breast carcinoma, B16F10 melanoma, WT-GBM glioma and MKN45-P gastric carcinoma.