ライフサイエンスコーパス: GBM

1 GBM can be subcategorized into four distinct subtypes; t

2 GBM cells and patient-derived GBM cells cultured in 3D m

3 GBM cells coexist with normal non-neoplastic cells, incl

4 GBM tumors exhibit a metabolic gradient that should be t

5 GBM tumors show nuclear factor-kappaB (NF-kappaB) activi

6 GBMs eventually relapse after treatment and the average

7 Here, we report that across a panel of 19 GBM BTSC lines, inhibition of glutaminase (GLS) showed a

8 From 2012-2019, between 2434 and 3476 GBM with HIV-infection attended our primary-care sites a

9 rtially reduced CBD-induced cell death in 3D GBM cultures.

10 ell death in CBD- or CBD/gamma-irradiated 3D GBM cultures.

11 Our results identify ABCB5 as a GBM chemoresistance marker and point to the potential ut

12 Moreover, we identify a GBM-selective cytolytic death mechanism involving plasma

13 els positively correlated with survival in a GBM subtype defined by low expression of ASCL1, a proneu

14 A prolonged survival from 27 to 70 days in a GBM xenograft mouse resection model with no sign of tumo

15 al therapy are those that are potent against GBM and work in combination with both standard-of-care t

16 Because almost all GBM tumors have dysregulated phosphoinositide signaling

17 tor domain (ED) peptides potently target all GBM molecular classes while sparing normal human astrocy

18 clines in HCV incidence and prevalence among GBM with HIV-infection provides proof-of-concept for HCV

19 ults in a positive feedback loop, amplifying GBM necrosis development to its fullest extent.

20 ufficient to distinguish between control and GBM samples.

21 s were evaluated in TCGA datasets in LGG and GBM patients.

22 -matched human mature cerebral organoids and GBM surgical specimens, which was reversed by integrin a

23 on, invasion, migration, drug resistance and GBM recurrence.

24 and prime the immune system to develop anti-GBM immunological memory.

25 f lupus nephritis, 1 was diagnosed with anti-GBM nephritis, and 4 were diagnosed with isolated acute

26 Collectively, 3D-bioprinted GBM and BBB models are promising systems and biomimetic

27 ry potential, providing additional candidate GBM genes.

28 rme (GBM) contains a subpopulation of cells, GBM stem cells (GSCs), that maintain the bulk tumor and

29 epresent a novel and promising way to combat GBM by striking its ability to divide immortally.

30 could serve as a viable basis for combating GBM infiltration.

31 1/2 suppression on GBM invasion by combining GBM culture models, engineered invasion paradigms, and m

32 tility of targeting ABCB5 to improve current GBM therapies.

33 tly altered cell proliferation by decreasing GBM viability, suppressed NF-kappaB pathway and enhanced

34 in the migration pattern of patient-derived GBM cells by modulating actin cytoskeleton pathway.

35 GBM cells and patient-derived GBM cells cultured in 3D microwells were co-treated with

36 We observed that patient-derived GBM cells expressing shRNAs of VEGF or neuropilin-1 (NRP

37 trate that NRP-1 ablation of patient-derived GBM cells improves the sensitivity of TMZ and enhances t

38 o picomolar efficacy against patient-derived GBM stem-like cells, thus proving the concept that targe

39 ckdown inhibit the growth of patient-derived GBM xenografts in both zebrafish and mouse models.

40 nterestingly, NRP-1-depleted patient-derived GBM xenografts substantially prolonged survival in mice

41 ncing data for patients with newly diagnosed GBM were obtained from The Cancer Genome Atlas.

42 In differentiated GBM cells, ERK-mediated repression of miR-199a-3p induce

43 al coactivator with PDZ-binding motif-driven GBM mouse model, neutrophils coincide with necrosis temp

44 s fluidity of neurotumors physically enables GBMs to penetrate surrounding tissue, a phenomenon simil

45 contributors to cancer recurrence and failed GBM therapy.

46 may represent a successful strategy to fight GBM.

47 a clinical standard-of-care chemotherapy for GBM, and everolimus, a mammalian target of rapamycin (mT

48 (EDT) were developed as a carrier of DOX for GBM chemotherapy.

49 tional cancer stem cell marker essential for GBM maintenance and ZIKV infection, providing potential

50 er prognosis and overall quality of life for GBM patients.

51 s a potentially novel therapeutic option for GBM patients.

52 otherapeutic polymeric drug, PEAMOtecan, for GBM therapy.

53 accelerate the drug development process for GBM.

54 inical translation as an adjunct therapy for GBM treatment.

55 Clinical trials for GBM continue to fall short of showing significant surviv

56 yTOF analysis of resected-tumor samples from GBM-patients and mouse GBM-tumors show stark similaritie

57 Glioblastoma (GBM) has one of the worst 5-year survival rates of all c

58 Glioblastoma (GBM) is a brain tumour with high invasiveness and poor p

59 Glioblastoma (GBM) is a complex disease with extensive molecular and t

60 Glioblastoma (GBM) is an aggressive malignancy with limited effectiven

61 Glioblastoma (GBM) is an astrocytic brain tumor with median survival t

62 Glioblastoma (GBM) is increasingly recognized as a disease involving d

63 Glioblastoma (GBM) is the deadliest adult brain cancer, and all patien

64 Glioblastoma (GBM) is the most common and most aggressive brain tumour

65 Glioblastoma (GBM) is the most prevalent and lethal adult primary cent

66 Glioblastoma (GBM) resistance to the standard of care is prompting sci

67 Glioblastoma (GBM) responses to bevacizumab are invariably transient w

68 Glioblastoma (GBM), or grade IV astrocytoma, is a malignant brain canc

69 Glioblastoma (GBM), the most aggressive form of brain cancer, has witn

70 tic oncolytic activity against glioblastoma (GBM) stem cells (GSCs).

71 t the aggressive brain cancer, glioblastoma (GBM), maintains stem-like features (glioma stem cell, GS

72 Treatment for glioblastoma (GBM) includes surgical resection and adjuvant radiothera

73 reen 5689 lncRNA loci in human glioblastoma (GBM) cells, identifying 467 hits that modify cell growth

74 ual primary cells from a human glioblastoma (GBM) surgical sample, revealing relationships between si

75 Precision medicine trials in glioblastoma (GBM) are often conducted at tumor recurrence.

76 ix (ECM) on drug resistance in glioblastoma (GBM) cells.

77 lioma stem-like cells (GSC) in glioblastoma (GBM) structure tumor cells into a hierarchical organizat

78 ates therapeutic resistance in glioblastoma (GBM).

79 ciated with worse prognosis in glioblastoma (GBM).

80 to malignant cell behavior in glioblastoma (GBM).

81 abolism has on the survival of glioblastoma (GBM) brain tumor stem cells (BTSC) has not yet been eluc

82 SERBP1 as a novel regulator of glioblastoma (GBM) development.

83 f EGFR are observed in ~50% of glioblastoma (GBM) patients, and have been found to play important rol

84 promoting malignant growth of glioblastoma (GBM), the most lethal brain tumor.

85 se effects in a mouse model of glioblastoma (GBM), we employed murine GBM cells engineered to constit

86 cytotoxicity in the context of glioblastoma (GBM), we performed a high-throughput screen in adult and

87 thodology in two rat models of glioblastoma (GBM; U87 human glioma cells and patient-derived human gl

88 al and osmotic forces regulate glioblastoma (GBM) invasiveness.

89 Here, we showed that glioblastoma (GBM) cultures and patients' tumors harbored super-enhanc

90 systemic nanoparticles towards glioblastoma (GBM) and prostate carcinoma xenograft lesions in nude mi

91 aggressive primary brain tumor glioblastoma (GBM) is characterized by aberrant metabolism that fuels

92 The aggressive brain tumor glioblastoma (GBM) is characterized by rapid cellular infiltration of

93 In managing a patient with glioblastoma (GBM), a surgeon must carefully consider whether sufficie

94 s freshly isolated from human glioblastomas (GBM) and that have never known any serum culture conditi

95 I) is frequently expressed in glioblastomas (GBM) but its impact on therapy response is still under c

96 ighly malignant brain-tumors, glioblastomas (GBM), is limited.

97 mors, showing that aggressive glioblastomas (GBMs) have higher water content while behaving like soli

98 Malignant gliomas/GBMs grow as a single mass (Type 1) and multifocal masse

99 -1 prolonged median survival time in 005 GSC GBM-bearing mice.

100 We analyzed GLS2 expression in HCC, GBM and neuroblastoma cells, as well as in monkey COS-7

101 apy could overcome drug resistance; however, GBM's location behind the blood-brain barrier severely l

102 ility of continuous culture models and human GBM tumor-initiating cells (TIC) in both Boyden chamber

103 e model simulations and validated from human GBM patient histology.

104 Using CellTrace-labeled human GBM and microglial (MG) cells, we established a 2D co-cu

105 P3, IGFBP5 signature genes in the U251 human GBM cell line increased responsiveness to 12ADT.

106 poptosis in vitro Likewise, in in vivo human GBM xenograft experiments with immunodeficient mice, mAb

107 Furthermore, analyses of human GBMs support that neutrophils and ferroptosis are associ

108 hlights a multidimensional immunosuppressive GBM microenvironment in patients with higher CYT and pot

109 enin-WISP1 signaling may effectively improve GBM treatment and the patient survival.

110 In GBM cells, where miR-1300 is normally not expressed, the

111 es associated with disease aggressiveness in GBM, particularly tumor infiltration (P = .0044) and hyp

112 with a comprehensive metabolite analysis in GBM models, we found that FDA-approved global (panobinos

113 eting HIF2alpha as a therapeutic approach in GBM is warranted.

114 role of GBP2/Stat3/FN1 signaling cascade in GBM invasion and suggest GBP2 may serve as a potential t

115 these peptides produce rapid cytotoxicity in GBM that overcomes caspase inhibition.

116 Defects in GBM components are associated with a range of hereditary

117 several of these genes are downregulated in GBM, potentially through epigenetic silencing as indicat

118 imultaneously induces a protective effect in GBM by upregulating autophagy.

119 dels fail to predict therapeutic efficacy in GBM, in vitro 3D models of GBM and BBB leveraging patien

120 marker expression and stem-like features in GBM cells.

121 otypic alterations are initiated by HDAC1 in GBM core cells which subsequently affect edge cells by s

122 described spatial metabolic heterogeneity in GBM biology and opportunities for MSI investigations.See

123 iating cells (BTICs) have been implicated in GBM recurrence and its resistance to therapy.

124 enes that have previously been implicated in GBM.

125 anscripts and cell surface protein levels in GBM cells.

126 etwork has been implicated in oncogenesis in GBM, making it an appealing target for advancing novel t

127 ggability of the EFNA5 signalling pathway in GBM xenografts overexpressing Bmi1.

128 downstream effectors of the AADR pathway in GBM.

129 ozolomide (TMZ) on the signaling pathways in GBM pathogenesis.

130 th and impacts cancer-relevant phenotypes in GBM and glioma stem cell lines.

131 ding mutations, with regulatory potential in GBM, under the hypothesis that regions of evolutionary c

132 rrelation between oHSV-mediated reduction in GBM volume and increased infiltration of both viral and

133 direct modulator of epigenetic regulation in GBM.

134 Bevacizumab resistance in GBM is associated with mesenchymal/glycolytic shifts inv

135 eveals that MBNL1 plays an essential role in GBM stemness and tumor progression, where hypoxic respon

136 ith radiation enhances the efficacy of RT in GBM by preventing radiation-induced phenotype conversion

137 ver, characterization of stem cell states in GBM and ability of stem cell state signature genes to se

138 hesis is associated with shorter survival in GBM patients.

139 aintaining GSCs and tumor-supportive TAMs in GBM, indicating that targeting Wnt/beta-catenin-WISP1 si

140 and invasion and are markedly upregulated in GBM and many other infiltrative cancers.

141 ll survival/proliferation, is upregulated in GBM, but little is known about the potential role of thi

142 High SERBP1 expression is prevalent in GBMs and correlates with poor patient survival and poor

143 enriched in neurological cancers, including GBM, and its levels positively correlated with survival

144 e found to be effective in apoptotic-induced GBM cell death (over 90%) within 48 h of treatment.

145 potential therapeutic target for inhibiting GBM invasion.

146 SiNP) and studied their effect on inhibiting GBM migration by means of a microfluidic-based migration

147 -supportive TAMs (M2), and potently inhibits GBM growth.

148 reduction in PD-1+ CD8+ T cells in injected GBMs and an increase in IFNgamma+ CD8+ T cells.

149 brain after venous injection, penetrate into GBM cells via endocytosis, dissociate to be cytotoxic, a

150 stable, biocompatible, and their uptake into GBM cells was enhanced by receptor-mediated internalisat

151 contact co-culture of fluorescently labeled GBM and MG demonstrated that MG cells modestly promoted

152 ow that Mlc1 is expressed in human stem-like GBM cells (GSCs) and is linked to the development of pri

153 An in vitro MDCK-MDR1-GBM co-culture model was used to assess the BBB permeabi

154 rmeability and cytotoxicity in the MDCK-MDR1-GBM co-culture model.

155 We utilized MRI-based volumetrics to measure GBM responses after injection with the oHSV and biolumin

156 ne expression are important in oHSV-mediated GBM therapy.

157 The glomerular basement membrane (GBM) is a key component of the glomerular capillary wall

158 al core of the glomerular basement membrane (GBM).

159 iptional profile of TAMs driving mesenchymal GBM pathogenesis, providing potential therapeutic target

160 The Gamma-ray Burst Monitor (GBM) on board the Fermi spacecraft provided the energeti

161 ed-tumor samples from GBM-patients and mouse GBM-tumors show stark similarities in one of the mouse G

162 show stark similarities in one of the mouse GBM-tumors tested.

163 Glioblastoma multiforme (GBM) and other solid malignancies are heterogeneous and

164 urrent therapies of glioblastoma multiforme (GBM) are largely ineffective.

165 article into U373MG Glioblastoma multiforme (GBM) cells predicts that CAP may introduce a new uptake

166 ide (TMZ)-resistant glioblastoma multiforme (GBM) cells would have abnormal redox status due to bio-t

167 omprised of U-87 MG glioblastoma multiforme (GBM) cells, known to form highly vascularized tumors.

168 timitotic effect on glioblastoma multiforme (GBM) cells.

169 Glioblastoma multiforme (GBM) contains a subpopulation of cells, GBM stem cells (

170 Mortality of glioblastoma multiforme (GBM) has not improved over the last two decades despite

171 ckade therapies for glioblastoma multiforme (GBM) in late-phase clinical trials has directed interest

172 Glioblastoma multiforme (GBM) is a malignant brain tumor with a poor prognosis re

173 Glioblastoma multiforme (GBM) is an aggressive and difficult to treat form of bra

174 Glioblastoma multiforme (GBM) is an aggressive cancer without currently effective

175 iveness in treating glioblastoma multiforme (GBM) is constrained by insufficient penetration across t

176 Glioblastoma multiforme (GBM) is impossible to fully remove surgically and almost

177 Glioblastoma multiforme (GBM) is one of the most common malignant brain tumors an

178 Glioblastoma multiforme (GBM) is the most common and deadly brain tumor in adults

179 Glioblastoma multiforme (GBM) is the most common and devastating type of primary

180 Glioblastoma multiforme (GBM) tumors are highly metabolic and vascularized, yet l

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

182 ese pathologies are glioblastoma multiforme (GBM), traumatic brain injuries (TBIs), multiple sclerosi

183 modality for human glioblastoma multiforme (GBM).

184 otes progression of glioblastoma multiforme (GBM).

185 el of glioblastoma (GBM), we employed murine GBM cells engineered to constitutively express the type

186 se substrate (MARCKS) could serve as a novel GBM therapeutic.

187 egression and long-term survival in 87.5% of GBM-bearing mice and prime the immune system to develop

188 Remarkably, >65% of GBM cases in The Cancer Genome Atlas express the non-res

189 ulates aberrant signaling present in >80% of GBM patients.

190 iary-care services providing care for 85% of GBM with HIV in our jurisdiction.

191 tant roles in the metabolic abnormalities of GBM.

192 efully in understanding the protein-basis of GBM maintenance and repair.

193 astic cells and matrix on chemoresistance of GBM cells to three agents with different mechanisms of a

194 le of ABCB5 in growth and chemoresistance of GBM.

195 verolimus for post-surgical tumor control of GBM.

196 egulates a mechanism of dedifferentiation of GBM cells into a stem-like state expressing markers of p

197 molecular mechanism of dedifferentiation of GBM cells into a stem-like state, expressing markers of

198 pathways contributing to the development of GBM and radio/TMZ-resistant GBM.

199 c targets for improving the effectiveness of GBM immunotherapy.

200 ions are expected to enhance the efficacy of GBM chemotherapy using the DOX-EDT-IONPs.

201 l physiological and pathological features of GBM and BBB.

202 ncoprotein EGFRvIII sensitizes a fraction of GBM to current standard of care treatment through the up

203 t IDH WT tumors establishes the frequency of GBM driver instability after chemoradiotherapy with temo

204 creased with glioma grade, with over half of GBM specimens HIF2alpha positive.

205 (17%-30% increase) and greater migration of GBM cells (>1.5-fold increase).

206 cid-gelatin hydrogel to culture a mixture of GBM and MG and evaluate drug resistance.

207 eutic efficacy in GBM, in vitro 3D models of GBM and BBB leveraging patient- or healthy-individual-de

208 We establish regionally derived models of GBM edge and core that retain their spatial identity in

209 two clinically relevant orthotopic models of GBM resection and recurrence.

210 oss dozens of genomically-distinct models of GBM, we find that purine metabolites, especially guanyla

211 ipids in patient-derived xenograft models of GBM.

212 thotopic patient-derived xenograft models of GBM.

213 orthotopic xenograft (PDOX) mouse models of GBM.

214 Tested against a panel of GBM cell lines in vitro, paclitaxel was found to be effe

215 icroRNAs were validated in a larger panel of GBM cells using state-of-the-art in vitro assays.

216 pment and physiology, in the pathogenesis of GBM.

217 that pSiNP uptake reduced the plasticity of GBM cells in reducing cell volume, an effect that proved

218 The osmotic pressure of GBM cell culture medium was adjusted using sodium chlori

219 death and increases the radiosensitivity of GBM by enhancing apoptosis.

220 tentially improving the therapeutic ratio of GBM.

221 ions in the non-coding regulatory regions of GBM have largely remained unexplored.

222 dose Amiodarone markedly reduced the size of GBM xenograft tumors and displayed a strong anti-angioge

223 hich drive the malignant phenotypic state of GBM, and identify macrophage receptor with collagenous s

224 In this study, stratification of GBM to core and edge demonstrates clinically relevant su

225 kade inhibited proliferation and survival of GBM cells and sensitized them to temozolomide (TMZ)-indu

226 after treatment and the average survival of GBM patients is less than two years.

227 iR-486-5p axis that enhances the survival of GBM stem cells by repressing tumor suppressor pathways.

228 s greater in the 3D model (>100% survival of GBM when challenged with cytotoxics).

229 vo, significantly increasing the survival of GBM-bearing animals.

230 as an adjunct therapy for local treatment of GBM following maximal tumor resection.

231 r therapeutic strategies in the treatment of GBM.

232 immunotherapy strategy for the treatment of GBM.

233 Nonetheless, understanding of GBM heterogeneity is largely limited to the surgically r

234 may offer an indispensable understanding of GBM that holds the potential to provide a better prognos

235 ere used to evaluate the effects of drugs on GBM cells.

236 The protective effect of MG on GBM was greater in the 3D model (>100% survival of GBM w

237 vestigated effects of LIMK1/2 suppression on GBM invasion by combining GBM culture models, engineered

238 Grade 4 glioma or GBM has poor prognosis and is the most aggressive grade

239 6-5p antagomirs to preestablished orthotopic GBM neurosphere-derived xenografts using advanced nanopa

240 of our cohort was identical to that of other GBM cohorts (IDH wild-type [WT], 95%; EGFR amplified, ap

241 We validate our GBM cohort, finding similar copy number aberrations and

242 tors or suppressors can allow us to overcome GBM regrowth in the context of tumor heterogeneity.

243 igh-throughput screen in adult and pediatric GBM cells using a synthetic oligonucleotide library repr

244 changes on HCV incidence among HIV-positive GBM up to 2025 using a HCV transmission model parameteri

245 an FDA-approved drug, represents a potential GBM therapeutic that functions through inhibition of the

246 response to osmotic and mechanical pressure, GBM cell lines U87 and U251 and patient-derived neural o

247 n this retrospective study, 156 pretreatment GBM MR images (gadolinium-enhanced T1-weighted, T2-weigh

248 lament hydrogel, effectively killing primary GBM cells derived from patients.

249 al.METHODSTwenty-eight patients with primary GBM were recruited to this prospective study, 25 of whom

250 n adjuvant setting for patients with primary GBM, with an ultimate goal to prevent or delay recurrenc

251 Consistently, GBP2 dramatically promotes GBM tumor growth and invasion in mice and significantly

252 hanisms by which increased pressure promotes GBM invasiveness may help to develop innovative therapeu

253 GBP2 overexpression significantly promotes GBM cell migration and invasion in vitro, and GBP2 silen

254 Inhibiting GTP synthesis radiosensitizes GBM cells and patient-derived neurospheres by impairing

255 to the development of primary and recurrent GBM.

256 However, second surgeries for recurrent GBM are not routinely performed, and therefore, molecula

257 h could transform the treatment of recurrent GBM patients by improving survival and reducing toxicity

258 ession in patients with primary or recurrent GBM.

259 We collected 186 pairs of primary-recurrent GBM samples from patients receiving chemoradiotherapy wi

260 litaxel and everolimus significantly reduced GBM growth and improved progression free survival in two

261 evated fatty acid oxidation (FAO), rendering GBM cells dependent on these pathways.

262 er of the GBM improves, therapies to replace GBM components or to stimulate GBM repair could translat

263 on with up-regulation in radio/TMZ-resistant GBM, transcriptionally regulating HSPB1.

264 e development of GBM and radio/TMZ-resistant GBM.

265 genous purine nucleosides protects sensitive GBM models from radiation by promoting DNA repair.

266 NP interactions to sensitize GBM to RT and TMZ were shown to involve these pathways b

267 es to replace GBM components or to stimulate GBM repair could translate into new therapies for patien

268 motherapy helping in a better stratification GBM patients.

269 1 signaling by carnosic acid (CA) suppresses GBM tumor growth.

270 design and the high efficacy in suppressing GBM growth enable the unique potential of this SAPD hydr

271 identify adult patients with supratentorial GBM that underwent craniotomy and resection.

272 ppaB or JAK2-STAT3 pathways killed surviving GBM cells in both 2D and 3D cultures, potentially improv

273 ved neurosphere-forming cells and found that GBM cells can be distinguished into "responder" and "non

274 Here, we show that GBM-initiating cells induce mTOR signalling in the micro

275 In addition, the GBM is affected by acquired autoimmune disorders and met

276 TGFs detected by the GBM with sources at farther horizontal distances are exp

277 ng about the maintenance and turnover of the GBM improves, therapies to replace GBM components or to

278 The major components of the GBM include laminins, type IV collagen, nidogens and hep

279 A prominent feature of the GBM microenvironment is compressive solid stress (CSS) c

280 (iDES) for insertion into the margin of the GBM resection cavity to provide a sustained high local d

281 essor genes PTEN and FoxO1 and regulates the GBM stem-like cells.

282 We now know that the GBM is a complex macromolecular structure that undergoes

283 iling the mechanisms by which EVs within the GBM TME are secreted and target recipient cells may offe

284 Therefore, GBM respond to osmotic or mechanical pressure by increas

285 xplore the key genes and proteins related to GBM.

286 eptide therapeutics may overcome traditional GBM resistance mechanisms, supporting further developmen

287 rapeutic potential of La(2)O(3) NPs to treat GBM cells in vitro, and encourage translational explorat

288 ntially offer a disruptive strategy to treat GBM.

289 istant protein 1 (MDCK-MDR1), and human U251 GBM cells.

290 Unfortunately, GBMs also harbor several signaling alterations that prot

291 We utilized GBM neurospheres that display GSC characteristics and fo

292 ved macrophages in both in vitro and in vivo GBM mouse models.

293 rent treatments for diseases associated with GBM involvement aim to reduce intraglomerular pressure a

294 e network regulatory modules associated with GBM.

295 /193 (MEGENA), significantly associated with GBM.

296 anslate into new therapies for patients with GBM-associated disease.

297 n of surgical resectability in patients with GBM.

298 atabase (NCDB) was queried for patients with GBM.

299 ms for the clinical benefit of patients with GBM.

300 rvations of metabolic gradients in xenograft GBM models.