ライフサイエンスコーパス: glioma

1 rs (gliomas) within the optic pathway (optic gliomas).

2 th newly diagnosed non-co-deleted anaplastic glioma.

3 y provide an effective therapy for malignant glioma.

4 loped into a potential therapy for malignant glioma.

5 at regulates TOP2A by sponging miR-411-5p in glioma.

6 inimally affects downstream mTOR activity in glioma.

7 roportion of recurrent glioma versus primary glioma.

8 tial therapeutic target for the treatment of glioma.

9 logy review for 133 patients with high-grade glioma.

10 he progression of KrasG12V-driven high-grade glioma.

11 the cerebrum and cerebellum of patients with glioma.

12 nverse association between blood glucose and glioma.

13 ter trial involving patients with high-grade glioma.

14 significantly inferior survival in low-grade glioma.

15 DM) confers resistance to the development of glioma.

16 lack of effect in diffuse intrinsic pontine glioma.

17 pression across a host of cancers, including glioma.

18 sis and investigated its prognostic value in glioma.

19 ations in IDH1 are highly prevalent in human glioma.

20 tumor regression and improve survival in rat glioma.

21 y represent a novel therapeutic strategy for gliomas.

22 etabolites, and slowed progression of murine gliomas.

23 rillary astrocytoma to high-grade anaplastic gliomas.

24 ide in adults with non-co-deleted anaplastic gliomas.

25 s great potential in the characterization of gliomas.

26 of brain-resident microglia in pre-treatment gliomas.

27 new therapeutic targets to attack aggressive gliomas.

28 activating effect on NF-kappaB in malignant gliomas.

29 argeting PAK4 to overcome radioresistance in gliomas.

30 t of murine syngeneic intracranial malignant gliomas.

31 ancer stem cells (GCSCs) in the virulence of gliomas.

32 in the majority of patients with lower grade gliomas.

33 annotated and genetically-defined high grade gliomas.

34 d in vivo testing in orthotopic experimental gliomas.

35 ignant tissue during resection of high grade gliomas.

36 agnoses were meningioma (37%) and high-grade glioma (20%).

37 ide, a clinical DNA-alkylating agent against glioma, 6OTD required lower concentrations to exert anti

38 specimens of 213 patients (mostly high-grade gliomas [89%]) included in the Vienna Cancer and Thrombo

39 Gliomas, a common type of brain tumor, are characterized

40 aloged genomic and epigenomic alterations in gliomas across ages, grades, and histologies.

41 latory gene which is aberrantly expressed in glioma and associated with patient survival would increa

42 cases show that DESI-MS allows detection of glioma and estimation of high tumor cell percentage (TCP

43 d correlative populations in mouse and human glioma and found that the emergence of specific subpopul

44 -7 breast carcinoma, B16F10 melanoma, WT-GBM glioma and MKN45-P gastric carcinoma.

45 used genetically engineered mouse models of glioma and quantitative metabolomics to investigate IDH1

46 report HuR aggregation (multimerization) in glioma and the analysis of this tumor-specific HuR prote

47 y re-establishes mTOR as a central target in glioma and traces the failure of existing drugs to incom

48 ork provides a unifying model for IDH-mutant gliomas and a general framework for dissecting the diffe

49 he IDEAL fitting to quantify CEST MRI in rat gliomas and confirmed its advantage for in vivo CEST qua

50 1-activated kinases 4 (PAK4) upregulation in gliomas and further determined its role in mesenchymal t

51 perform single-cell RNA-sequencing of human gliomas and identify phenotypic differences in TAMs of d

52 ssociated macrophages (TAMs) are abundant in gliomas and immunosuppressive TAMs are a barrier to emer

53 ns and is now open for further validation in gliomas and other cerebral diseases.

54 ydrogenase 1 and 2) drive the development of gliomas and other human malignancies.

55 us, BIRDS can be used to map the DeltapHe in gliomas and provide a physiological readout of the thera

56 Median GARD values were lowest for gliomas and sarcomas and highest for cervical cancer and

57 have been implicated in >80% of lower grade gliomas and secondary glioblastomas and primarily affect

58 f SLFN5 expression correlate with high-grade gliomas and shorter overall survival in patients sufferi

59 L1 antibody showed synergistic inhibition of gliomas and significantly increased survival in mice.

60 een physical properties of mouse optic nerve gliomas and the extracellular matrix.

61 The life-limiting nature of gliomas and the presence of specific symptoms related to

62 ad symptomatic or asymptomatic optic pathway gliomas and/or skeletal abnormalities.

63 growth of intractable glioblastoma (grade IV glioma) and glioma stem cells (GSCs).

64 ling cascades downstream of NLGN3 binding in glioma, and determine a therapeutically targetable mecha

65 ls of spatial heterogeneity in MB, malignant glioma, and renal cell carcinoma (RCC).

66 Optic gliomas are brain tumors characterized by slow growth, p

67 e initiation, progression, and recurrence of gliomas are driven, at least partly, by cancer stem-like

68 S100A4(+) cells in gliomas are enriched with cancer cells that have tumor-i

69 We found that although subtypes of optic gliomas are indistinguishable on imaging, the microvascu

70 These results demonstrate that IDH1-mutated gliomas are particularly vulnerable to Bcl-xL inhibition

71 Malignant optic gliomas are rare, but they rapidly become lethal visual

72 Gliomas are the most common CNS tumors in children and a

73 differentiation between low- and high-grade glioma (area under the receiver operating characteristic

74 lin 1 in macrophages and microglial cells in gliomas as a pivotal modifier of tumor neovascularizatio

75 y to define the oncogenic potential of novel glioma-associated genomic rearrangements and to generate

76 may allow us to gain important insights into glioma-associated inflammation (GAM, MMP).

77 Glioma-associated microglia and macrophages (GAM), which

78 Glioma-associated microglia/macrophages (GAM) were ident

79 Uncontrolled hedgehog (HH)/glioma-associated oncogene (GLI) and WNT/beta-catenin si

80 rafenib resistance, show increased levels of glioma-associated oncogene homolog 1 and 2 (GLI1/GLI2) c

81 macrophages from non-malignant human tissue, glioma atlases, and murine glioma models.

82 for IDH gene mutation detection in low-grade glioma (AUC, 0.818) and MTI in high-grade glioma (AUC, 0

83 de glioma (AUC, 0.818) and MTI in high-grade glioma (AUC, 0.854) and for all WHO grades (AUC, 0.899)

84 We demonstrate that housing glioma-bearing mice in enriched environment (EE) reverts

85 prolonged survival, and cured a fraction of glioma-bearing mice.

86 machine-learning-driven survival models for glioma built on in vivo (11)C-MET PET characteristics, e

87 n tumor-initiating cells (BTIC) in malignant glioma, but the mechanism of its activation is unknown.

88 ces in isocitrate dehydrogenase (IDH)-mutant gliomas by combining 14,226 single-cell RNA sequencing (

89 e show these cells suppress oHSV-1 growth in gliomas by internalizing the virus through phagocytosis.

90 earch and clinical area to effectively treat gliomas by reaching a high antineoplastic drug concentra

91 ld increase the understanding of the role of glioma cancer stem cells (GCSCs) in the virulence of gli

92 demonstrate that neural precursor cell (NPC):glioma cell communication underpins this propensity of g

93 ify a functional role for SOX1 in regulating glioma cell heterogeneity and plasticity, and suggest SO

94 gliosis in peritumoral area; and (4) reduces glioma cell infiltration in healthy parenchyma.

95 In multiple glioma cell lines and patient-derived glioma stem cells

96 ts target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, resulting in decreased cell prolifera

97 induces cell death and apoptosis in several glioma cell lines, targets HIF-1alpha-mediated pathways,

98 confirm, that the stiffness optimum of U251 glioma cell migration, morphology and F-actin retrograde

99 PCL nanoparticles could efficiently suppress glioma cell proliferation and induce cell apoptosis in v

100 r, these results suggested netrin-1 promotes glioma cell proliferation by activating NF-kappaB signal

101 stant tumor cell conditioned media increased glioma cell proliferation compared with media from macro

102 uction had no effect on in vitro IDH1 mutant glioma cell proliferation.

103 idence, malignancy, and the ability of mouse glioma cells (GC) to be cultured under stem cell conditi

104 it did the growth of differentiated non-stem glioma cells (NSGCs).

105 Chemical screening of patient-derived glioma cells (PDCs) shows that therapeutic response is a

106 We show that in glioma cells expressing either EGFR wild type or the mut

107 Therapies aimed at mechanisms intrinsic to glioma cells have translated to only limited success; ef

108 tion of chemoattractant signals toward which glioma cells home.

109 ells efficiently killed HLA-A2(+)H3.3K27M(+) glioma cells in an antigen- and HLA-specific manner.

110 hat primary resistance to EGFR inhibition in glioma cells results from a rapid compensatory response

111 arison to 2-dimensional bulk cultures of U87 glioma cells revealed 3 groups of genes essential for th

112 tern blot analysis, we identified that human glioma cells that were exposed to VP without light activ

113 hin (PTN)-containing complex, which attracts glioma cells through ROCK/Rho activation.

114 Ms have been associated with the capacity of glioma cells to effectively invade the brain and prolife

115 We also demonstrate that exposing glioma cells to the HuR inhibitor tanshinone group compo

116 pathway extensively sensitized IDH1-mutated glioma cells to TMZ.

117 Glioma cells were evaluated for CXCR4 expression and pol

118 Treatment of the U251 glioma cells with NA in vitro results in reduced invasio

119 Glioma cells with one or two TMs were mainly responsible

120 his adaptive axis at multiple nodes rendered glioma cells with primary resistance sensitive to EGFR i

121 in part by altering mevalonate metabolism in glioma cells, suggesting a therapeutic strategy in this

122 significant radiosensitization of malignant glioma cells, which will guide the development of combin

123 gulation of several synapse-related genes in glioma cells.

124 come together during HuR multimerization in glioma cells.

125 r DNA damage and apoptotic changes in mutant glioma cells.

126 omide or irradiation increases cell death in glioma cells.

127 developed a model of HuR multimerization in glioma cells.

128 rusions [tumor microtubes (TMs)] extended by glioma cells.

129 onal information on tumor extent of cerebral gliomas compared with anatomic imaging; however, compara

130 Glioma contact with this niche predicts worse prognosis,

131 Optic gliomas contain various amounts of myxoid matrix, which

132 ic stress, whereas their expression in human glioma decreases during malignant progression.

133 Within gliomas, despite the presence of heterogeneously leaky m

134 However, a significant fraction of gliomas develop over a short period of time and progress

135 In both systems, oleandrin impaired glioma development, reduced tumor size, and inhibited ce

136 stics in pediatric diffuse intrinsic pontine glioma (DIPG) and to correlate these metrics with baseli

137 s in children with diffuse intrinsic pontine glioma (DIPG) by measuring the tumor uptake of (89)Zr-la

138 for children with diffuse intrinsic pontine glioma (DIPG) is less than one year.

139 atric brain tumor, diffuse intrinsic pontine glioma (DIPG).

140 odendroglioma, and diffuse intrinsic pontine glioma (DIPG).

141 u antigen R (HuR) as a positive regulator of glioma disease progression.

142 strates that BCAN-NTRK1 is a bona fide human glioma driver and describes a general strategy to define

143 GFR blockade by tivozanib has potential anti-glioma effects in vitro.

144 ite multimodality treatment, most high-grade gliomas eventually recur and are ultimately incurable.

145 tor overexpression, would be adaptive during glioma evolution.

146 leagues present an elegant dissection of how gliomas exploit an enzymatic activity acquired through a

147 involved in the management of patients with glioma, for patients and caregivers, and for health-care

148 quired for NFIA expression and contribute to glioma formation.

149 g the molecular biology underlying pediatric gliomas, fueling hopes to achieve both goals.

150 gene, and MTI was significantly increased in glioma grade III with IDH mutation (P = .013) when compa

151 thelial growth factor (VEGF) therapy-induced glioma growth and dissemination.

152 S), and whether this treatment could control glioma growth and invasiveness.

153 stoma (GBM) and silencing of RanBP6 promoted glioma growth in vivo.

154 thermore, Dox-HK-MPEG-PCL micelles inhibited glioma growth more significantly than Dox-MPEG-PCL and H

155 utocrine expression of CNTF, was involved in glioma growth regulation.

156 Factors of glioma growth, inflammation, and invasion, such as the t

157 ggested that Netrin-1 has a critical role in glioma growth.

158 SUV quantification of (18)F-FLT uptake in glioma had an RC in the range of 18%-24% when imaging be

159 Gliomas harboring mutations in isocitrate dehydrogenase

160 analysis of tumor-associated macrophages in gliomas has unveiled a new aspect of the complex tumor m

161 Organization [WHO] grade II) from high-grade glioma (HGG) (WHO grade III or IV).

162 High-grade glioma (HGG) is a group of primary malignant brain tumor

163 High-grade gliomas (HGGs) include the most common and the most aggr

164 classified as WHO grade III or IV high-grade gliomas (HGGs).

165 The high prevalence of IDH1 mutations in glioma highlights the need for brain-penetrant IDH1 muta

166 now in progress for patients with malignant gliomas; however, a better understanding of how these tu

167 blood glucose was inversely associated with glioma in the AMORIS (HR = 0.78, 95% CI 0.66 to 0.93) bu

168 tures results from mutations in leucine-rich glioma-inactivated 1 (LGI1), a soluble glycoprotein secr

169 -of-function mutations in LGI4 (leucine-rich glioma-inactivated 4).

170 Leucine-rich glioma-inactivated1 (LGI1) encephalitis is an antibody-a

171 the healthy brain is one hallmark of diffuse gliomas, including glioblastomas.

172 atients with astrocytic and oligodendroglial gliomas, including glioblastomas.

173 llular matrix protein prominent in malignant glioma, increases NOTCH activity in BTIC to promote thei

174 he sexual dimorphic differences in Nf1 optic glioma-induced retinal dysfunction by operating at the l

175 The data underscore the complexity of glioma infiltration.

176 Self-renewing, highly tumorigenic glioma-initiating cells (GIC) have been linked to glioma

177 et of malignant gliomas, its sufficiency for glioma initiation has not been evaluated.

178 ndings demonstrate a pathogenic role for NPC:glioma interactions and potential therapeutic targets to

179 and pleiotrophin knock down starkly reduced glioma invasion of the SVZ in the murine brain.

180 s and potential therapeutic targets to limit glioma invasion.

181 a-initiating cells (GIC) have been linked to glioma invasive properties, immunomodulation, and increa

182 nation of POL5551 and B20-4.1.1 reduced both glioma invasiveness by 16% to 39% and vascular density c

183 Malignant glioma is a formidable disease that commonly leads to de

184 iagnostic work-up of patients with suspected glioma is mainly done using MRI.

185 The presence of these mutations in glioma is prognostic for better clinical outcomes with l

186 GBM, the most aggressive of the gliomas, is characterized by extensive angiogenesis and

187 und to be expressed in a subset of malignant gliomas, its sufficiency for glioma initiation has not b

188 sis imaging (DKI) to differentiate low-grade glioma (LGG) (World Health Organization [WHO] grade II)

189 served during the development of lower-grade glioma (LGG).

190 These pediatric low-grade gliomas (LGGs) are fundamentally different from IDH-muta

191 Infiltrating low grade gliomas (LGGs) are heterogeneous in their behavior and t

192 ncreased the capacity of these cells to form glioma-like tumors in an oncogene-driven mouse brain tum

193 Gliomas maintain an acidic extracellular pH (pHe), which

194 K activity in glioma specimens and grades of glioma malignancy.

195 ene, individuals with NF1 are prone to optic gliomas, malignant gliomas, neurofibromas, and malignant

196 th brain-penetrant inhibitors in IDH1 mutant gliomas may have substantial patient benefit.

197 ve technique enables characterization of the glioma microenvironment with respect to the disease-driv

198 serve as specific imaging biomarkers of the glioma microenvironment.

199 Tests in the normal brain and in the F98 glioma model in vivo demonstrated that this controller e

200 strated in vitro against an aggressive human glioma model, with involvement of MMPs confirmed using p

201 ations modestly extended survival of a mouse glioma model.

202 activity in two independent syngeneic mouse glioma models by promoting migration of CAR T cells to t

203 In glioma models, the glia-specific architecture is present

204 human astrocytes (NHAs) and syngeneic mouse glioma models, the introduction of mutant IDH1 or treatm

205 rcoma and invasive F98 (28-fold improvement) glioma models.

206 ant human tissue, glioma atlases, and murine glioma models.

207 density compared to B20-4.1.1 alone in both glioma models.

208 Using a PDGF-B-driven proneural glioma mouse model, we assessed a panel of tyrosine kina

209 Using a glioma mouse model, we demonstrate that doxorubicin-load

210 rvation and validating their expression in a glioma mouse model.

211 V5 and Sox2-mCherry); and (4) engineering of glioma mutations (TP53 deletion; H3F3A point mutations).

212 th NF1 are prone to optic gliomas, malignant gliomas, neurofibromas, and malignant peripheral nerve s

213 in clinical outcome, we leveraged Nf1 optic glioma (Nf1-OPG) mice.

214 ith NF1 are at risk for developing low-grade gliomas of the optic pathway and brainstem, individuals

215 malignant progression (MP) to an anaplastic glioma or secondary glioblastoma (GBM).

216 rful new approach for the treatment invasive gliomas, particularly for preventing and controlling rec

217 ar morphology in a diffuse intrinsic pontine glioma patient was performed.

218 in enhancing the sphere-forming capacity of glioma patient-derived BTIC.

219 ction of survival in amino acid PET-positive glioma patients was highly accurate using computer-suppo

220 Epileptic activity, frequently occurring in glioma patients, can influence MRI findings.

221 with longer survival in medulloblastoma and glioma patients, suggesting their tumors may have been m

222 ng axis as a candidate therapeutic target in glioma patients.

223 bstantial proportion of pediatric high-grade gliomas (pHGG), often in association with TP53 loss and

224 Pediatric low-grade gliomas (PLGGs) are commonly associated with BRAF gene f

225 Patients with glioma present with complex palliative care needs throug

226 The majority of pediatric gliomas present as benign, slow-growing lesions classifi

227 imulating factor-1 receptor (CSF-1R), blocks glioma progression, markedly suppresses tumor cell proli

228 of the tumour microenvironment that promote glioma progression.

229 ous conditions and markedly increased during glioma progression.

230 Furthermore, the role of CNTFRalpha in glioma proliferation and apoptosis through the PI3K/AKT

231 olecule neuroligin-3 (NLGN3), which promotes glioma proliferation through the PI3K-mTOR pathway.

232 Together, these findings uncover a glioma-promoting role of BCL6 and provide the rationale

233 to improve care for pediatric patients with glioma range from increasing quality of life and prevent

234 Mice bearing orthotopic CT-2A or GL261 gliomas received POL5551 and/or anti-VEGF antibody B20-4

235 nd metalloproteinase, MMP-9, in murine optic gliomas relative to normal non-neoplastic optic nerve.

236 regulation and its clinical significance in glioma remain largely unknown.

237 nding how to increase immune infiltration of gliomas represents a key first step in achieving tumor d

238 complex with the binding partners, activated glioma Rho/ROCK signaling, and ROCK inhibition decreased

239 ood glucose levels were inversely related to glioma risk (AMORIS, P trend = 0.002; Me-Can, P trend =

240 that netrin-1 was significantly increased in glioma samples and positively correlated with cell proli

241 Results Low-grade (WHO grade II) glioma showed areas with increased OEF (+18%, P < .001,

242 data derived from a set of high-grade human gliomas, shows that high Caspase-8 expression levels cor

243 positively correlates with AMPK activity in glioma specimens and grades of glioma malignancy.

244 nd consequential site of pediatric and adult glioma spread, but the cellular and molecular mechanisms

245 Here we show that targeting glioma stem cell (GSC)-derived pericytes specifically di

246 Glioma stem cells (GSCs) have a central role in glioblas

247 ion of endolysosome levels by Qki loss helps glioma stem cells (GSCs) maintain their stemness in subo

248 ete abundant pleiotrophin (PTN) to stimulate glioma stem cells (GSCs) through its receptor PTPRZ1 thu

249 ltiple glioma cell lines and patient-derived glioma stem cells (GSCs), EGFR signaling promotes H3K23

250 ulation of self-renewing, highly tumorigenic glioma stem cells (GSCs), which contributes to tumor ini

251 tractable glioblastoma (grade IV glioma) and glioma stem cells (GSCs).

252 lls, macrophage/microglial cells (MGCs), and glioma stem cells (GSCs).

253 nfection of transformed breast carcinoma and glioma stem cells similarly inhibited EMT and induced ME

254 racellular, autocrine/paracrine mediators of glioma stem-like cell self-renewal could potentially con

255 Notch signaling is implicated in maintaining glioma stem-like cells (GSCs) within the hypoxic niche,

256 pically implanted with gliosarcoma tumors or glioma stem-like cells, respectively.

257 ce allografted with S100beta-v-erbB/p53(-/-) glioma stem-like cells.

258 , HIF-1alpha levels are greatly increased in glioma stem-like cells.

259 xRNA complexes isolated from patient-derived glioma stem-like cultures exhibit distinct compositions,

260 e statistical heterogeneity was explained by glioma subtype, echo time, and the proportion of recurre

261 (GWAS) have transformed our understanding of glioma susceptibility, but individual studies have had l

262 ed from IDH1 mutant, but not IDH1 wild type, gliomas systematically deleted IDH1 in vitro and in vivo

263 in normal tissues and longer in sarcomas and gliomas than in other cancers.

264 demonstrate how known genomic alterations in glioma that induce constitutive activation of MAPK are t

265 With gliomas, the recruitment of CD8+ T cells to the tumor is

266 For gliomas, the tumor-associated inflammatory response is p

267 ve the potential to be applied clinically in glioma therapy.

268 thetic liabilities that can be exploited for glioma therapy.

269 re-affected cortex (n = 2) and compared with glioma tissues (n = 3).

270 ficantly upregulated in both human and mouse glioma tissues.

271 s differentially expressed across high-grade glioma TMEs.

272 l communication underpins this propensity of glioma to colonize the SVZ through secretion of chemoatt

273 We found the most invasive gliomas to be characterized by Wnt5a overexpression, whi

274 tein structure of the myxoid matrix in optic gliomas to identify novel therapeutic targets.

275 sed to phenotype microvascular structures in gliomas to predict survival, and to explore the molecula

276 sible coadjuvant agent in clinical trials of glioma treatment.SIGNIFICANCE STATEMENT In this work, we

277 , these reduced immune infiltrates in muIDH1 glioma tumors may contribute in part to the differences

278 Here, using human astrocyte and glioma tumorsphere systems, we generate a large-scale at

279 the differences in aggressiveness of the two glioma types.

280 the systemic circulation into orthotopic F98 gliomas using MRgFUS, where they elicited a significant

281 ancer was approximately 10-fold smaller than glioma vasculature.

282 , echo time, and the proportion of recurrent glioma versus primary glioma.

283 In murine models of glioma, we demonstrated that oleandrin significantly inc

284 In an orthotopic mouse model of glioma, we found that Cic loss potentiated the formation

285 For glioma, when comparing those in the highest quartile of

286 y diagnosed 1p/19q non-co-deleted anaplastic gliomas, which are associated with lower sensitivity to

287 id chromatography-mass spectrometry on optic gliomas, which varied in the amount of myxoid matrix.

288 d Methods Seventeen patients with high-grade gliomas who had received 10-44 administrations of the ma

289 (+18%, P < .001, n = 20), whereas anaplastic glioma (WHO grade III) and glioblastoma (WHO grade IV) s

290 CMRO2 was decreased (P = .037) in low-grade glioma with a mutated IDH gene, and MTI was significantl

291 f pilomyxoid astrocytoma, a subtype of optic glioma with abundant myxoid matrix, is characterized by

292 Low-grade gliomas with favorable characteristics are slow-growing

293 ion may be a viable therapeutic strategy for gliomas with IDH mutations.Significance: These findings

294 lic liabilities created by IDH1 mutations in glioma, with possible implications to leverage its thera

295 r the palliative care of adult patients with glioma, with the aim to reduce symptom burden and improv

296 o the development of low-grade brain tumors (gliomas) within the optic pathway (optic gliomas).

297 The main diagnosis was glioma World Health Organization grade II-IV (n = 8); 2

298 mean age +/- SD, 48 +/- 14 y) with cerebral gliomas (World Health Organization [WHO] grade II: 10 [i

299 significantly suppressed the progression of glioma xenografts in mice.

300 aging of mice bearing PC3 (prostate) or U87 (glioma) xenografts using 5-[(18)F]-fluorohomoleucine sho