ライフサイエンスコーパス: glioma

1 r distance-dependent manner in patients with glioma.

2 s like esophageal squamous-cell carcinoma or glioma.

3 effects by mainly activating mTOR pathway in Glioma.

4 ciated with favourable outcome in high-grade glioma.

5 reprogramming may be a fundamental driver of glioma.

6 dehydrogenase (IDH) status in patients with glioma.

7 as a powerful therapeutic tool for treating glioma.

8 ssessment criteria for paediatric high-grade glioma.

9 and chemoresistant diffuse intrinsic pontine glioma.

10 HG and tumor metabolism in IDH-mutated human glioma.

11 nse to temozolomide treatment in mutant IDH1 glioma.

12 malignant clinical and molecular subtypes of glioma.

13 aluable imaging marker for IDH-mutated human glioma.

14 te with integrin alpha6 in patient malignant glioma.

15 ide support for cancer stem cell theories of glioma.

16 ated NTRK2 splice variant, TrkB.T1, in human glioma.

17 ompared with 14 of 31 (45.2%) with enhancing glioma.

18 rognosis and is the most aggressive grade of glioma.

19 nd management of adult patients with diffuse gliomas.

20 awn to differentiate grade II from grade III gliomas.

21 maging methods used to diagnose and classify gliomas.

22 as a robust biomarker for poor prognosis in gliomas.

23 ik3ca(H1047R) to generate high-grade diffuse gliomas.

24 e and CCR2 inhibition in anti-PD-1-resistant gliomas.

25 and follow-up of adult patients with diffuse gliomas.

26 may result in a worse prognosis for IDH(wt) gliomas.

27 are consumed in relatively large amounts by gliomas.

28 tial therapeutic target for the treatment of gliomas.

29 Altered cellular metabolism is a hallmark of gliomas.

30 response assessment in paediatric low-grade gliomas.

31 al outcomes in 56 patients with WHO grade IV gliomas.

32 e use of Ras pathway inhibitors in low-grade gliomas.

33 composition and gene regulation in malignant gliomas.

34 f mutational burden and signatures in 10,294 gliomas.

35 RNA-21 (miR-21) as a prognostic biomarker in gliomas.

36 patients diagnosed with high-risk low-grade gliomas.

37 trophic tyrosine receptor kinases (NTRKs) in gliomas.

38 rol samples from different mouse models with gliomas.

39 well as methylation-based classification of gliomas.

40 trials and clinical practice for high-grade gliomas.

41 ity within the first 2 wk after resection of gliomas.

42 o identify cancer stem cells in leukemia and gliomas.

43 tions with overall survival for only IDH(wt) gliomas.

44 is closely associated with highly malignant gliomas.

45 l burden (hypermutation) is observed in some gliomas(1-5); however, the mechanisms by which hypermuta

46 with white matter in both participants with glioma (2.36 mumol/g/min +/- 0.22 vs 0.75 mumol/g/min +/

47 _INST: 17 patients, 17 lesions, 10 low-grade glioma, 3 cavernoma, 4 focal cortical dysplasia; NEL_INS

48 In patients with gliomas 40 mm or less from the IHM region, seeding the n

49 d), the classification accuracy was 40 of 49 gliomas (82%; 95% CI: 71%, 92%) for model A and 42 of 49

50 ; 95% CI: 71%, 92%) for model A and 42 of 49 gliomas (86%; 95% CI: 76%, 96%) for model B.

51 Methods: Forty-three patients with cerebral gliomas (9 low-grade, 34 high-grade; 9 primary tumors, 3

52 rty of 35 patients (85.7%) with nonenhancing glioma achieved stable disease compared with 14 of 31 (4

53 riments on diseases including breast cancer, glioma and colorectal cancer.

54 induced pig model of high-grade spinal cord glioma and may potentially be used in preclinical therap

55 Glioma and renal cell carcinoma were prioritized because

56 +/- 18 [standard deviation]; nine men) with glioma and three healthy volunteers (mean age, 44 years

57 young adults with diffuse intrinsic pontine glioma and to develop a consensus on recommendations for

58 A high percentage of pediatric gliomas and bone tumors reportedly harbor missense mutat

59 cancers, including low-grade and high-grade gliomas and brain metastases (BrMs) originating from div

60 ain cancer pathophysiology, both for primary gliomas and for brain metastases.

61 ptember 2018, participants with IDH1-mutated gliomas and healthy participants were prospectively scan

62 Diffuse midline gliomas and posterior fossa type A ependymomas contain t

63 inine/valine (G34R/V) mutations drive deadly gliomas and show exquisite regional and temporal specifi

64 ion and increased EGFR expression in primary glioma, and employ a glioma cell line LN229 to identify

65 tures that are distinct from adult low-grade gliomas, and the developing paediatric brain is more sus

66 Diverse genetic subtypes of malignant glioma are sensitive to selective inhibition of the NAD(

67 Brainstem gliomas are a heterogeneous group of tumors that encompa

68 Malignant gliomas are central nervous system tumors and remain amo

69 Gliomas are currently classified through integration of

70 Although lower grade gliomas are driven by mutations in the isocitrate dehydr

71 te the immunosuppressive properties of human gliomas are essential to assess immune-based therapies.

72 Diffuse gliomas are malignant brain tumors that include lower-gr

73 G34R/V gliomas are neuronal malignancies where interneuron prog

74 Gliomas are one of the most common types of brain tumors

75 Posttreatment high-grade gliomas are usually monitored with contrast-enhanced MRI

76 Brain tumors (gliomas) are heterogeneous cellular ecosystems, where no

77 xtracellular acidity of WHO grade II and III gliomas associated with 1p/19q co-deletion.

78 diologist-FISH discordances, there were nine gliomas associated with a consensus neuroradiologist con

79 Whether truncated glioma-associated oncogene homolog 1 (TGLI1), a transcri

80 hile the dramatic heterogeneity of malignant gliomas at the genetic and immunological levels remains

81 ed median survival as a monotherapy in KR158 glioma-bearing animals and further increased median and

82 Serum isolated from glioma-bearing mice potently inhibited proliferation and

83 Treatment of glioma-bearing mice with proapoptotic PL3-guided NWs imp

84 oups derived from the brain and the blood of glioma-bearing mice.

85 and lactate in the brains of unaffected and glioma-bearing rats following the administration of (2)H

86 Glioma-bearing WT and Pd-1-/- mice survived significantl

87 -GFP), VSV-EBOVDeltaMLD without GFP targeted glioma but yielded only a modest extension of survival.

88 oncohistone, occurring frequently in midline gliomas but also identified in haematopoietic malignanci

89 hod for 1p/19q codeletion testing in diffuse gliomas but occasionally renders erroneous results.

90 in isocitrate dehydrogenase 1-mutated human glioma by using a super-resolution framework to upsample

91 prehensive functional characterization of 96 gliomas by genome-wide piggyBac insertional mutagenesis

92 ardiac glycosides in human glioblastomas and glioma cancer stem-like cells via inhibition of DNA repa

93 Here we show that a subset of recurrent gliomas carries MGMT genomic rearrangements that lead to

94 s into glioma etiology and the chronology of glioma-causing somatic alterations.

95 oint to a novel role of C4S and C6S in human glioma cell functions, thus possibly representing target

96 lating p120-catenin further prevents diffuse glioma cell infiltration of the mouse brain with margina

97 r goal is to study how the morphology of the glioma cell influences the formation of patterns of coll

98 R expression in primary glioma, and employ a glioma cell line LN229 to identify relevant proteins and

99 he identification of AltProts in NCH82 human glioma cell line.

100 ates with susceptibility to this drug across glioma cell lines, revealing ribosomal protein subunit R

101 ers of viable tumor cells, thereby promoting glioma cell proliferation.

102 1, and Nav3 demonstrates heightened EGFRvIII-glioma cell proliferation.

103 latory element in the HOTAIR locus increases glioma cell sensitivity to TMZ and alters transcription

104 element and that both function in regulating glioma cell sensitivity to TMZ.

105 propose a new regulatory mechanism governing glioma cell TMZ sensitivity.

106 nerated some of these MGMT rearrangements in glioma cells and demonstrated that the MGMT genomic rear

107 o rat models of glioblastoma (GBM; U87 human glioma cells and patient-derived human glioblastoma canc

108 Contacts between moving glioma cells are adaptive epithelial-like or filamentous

109 Diffuse brain infiltration by glioma cells causes detrimental disease progression, but

110 at mutant isocitrate-dehydrogenase (mIDH)1/2 glioma cells convert alpha-KG to D-2-hydroxyglutarate (D

111 cing analysis of post-treatment hypermutated glioma cells identified microsatellite mutations.

112 We show here that glioma cells infiltrate the brain collectively as multic

113 ular cross-sectional area) and tracked human glioma cells that spontaneously migrated within channels

114 These results are consistent with glioma cells utilizing a motor-clutch system to migrate

115 come both BBB and multidrug resistance (MDR) glioma cells while providing site-specific magnetic targ

116 Treatment of cultured glioma cells with C4S and C6S enhanced cell viability, m

117 proliferation of primary adult and pediatric glioma cells, but not the viability of normal brain cell

118 s obtained by overexpression of GLS2 in T98G glioma cells, including downregulation of oncogene c-Myc

119 stand the dynamic nature of brain tumors and glioma cells, including their invasion of normal brain.

120 In rat C6 glioma cells, leptin pre-treatment enhanced Ca(2+) mobil

121 In healthy volunteers and participants with glioma, CMRO(2) values in gray matter and white matter v

122 icantly lower MTR(asym) in 1p/19q co-deleted gliomas (co-deleted, 1.17% +/- 0.32%; non-co-deleted, 1.

123 Cox concordance index of ~ 0.85 for the TCGA glioma cohort, however, the gene-level model has twice a

124 9 months) for the nonenhancing and enhancing glioma cohorts, respectively.

125 (MEGENA), were applied on publicly available glioma, control brain and stem cell gene expression RNA-

126 hermore, a disturbed SPPL3-B3GNT5 pathway in glioma correlated with decreased patient survival.

127 nalysis of the miR-21 expression in the TCGA glioma dataset revealed that overexpression of miR-21 wa

128 ysis to assess miR-21 expression in the TCGA glioma dataset to validate the relationship between miR-

129 y chromatin regulatory pathways disrupted in gliomas, delineating their physiological function and ou

130 of this study was to explore the effects of glioma development and Temozolomide (TMZ) on fecal micro

131 Glioma development leads to gut dysbiosis in a mouse-mod

132 We highlight how classes of glioma differ in their cellular architecture and relate

133 Extensive genomic sequencing of gliomas, different cell types, brain tissue regions and

134 Diffuse intrinsic pontine glioma (DIPG) is a lethal pediatric brain cancer whose m

135 r the treatment of diffuse intrinsic pontine glioma (DIPG), an aggressive pediatric cancer resident i

136 Diffuse intrinsic pontine gliomas (DIPGs) are aggressive pediatric brain tumors fo

137 H3K27M diffuse intrinsic pontine gliomas (DIPGs) are fatal and lack treatments.

138 characteristic of pediatric diffuse midline gliomas (DMGs).

139 road map for the discovery of potential new glioma drug targets is suggested, with the goal of trans

140 T as a direct metabolic imaging technique in glioma enabled quantitative visualization of the Warburg

141 been observed in various cancers, including glioma, endometrial cancer, ovarian cancer, and breast c

142 nomic analysis provides unique insights into glioma etiology and the chronology of glioma-causing som

143 We explore EGFR-mutant glioma evolution in conditional mutant mice by whole-exo

144 For decades, it has been known that gliomas follow a non-random spatial distribution, appear

145 tions for the management of adult high-grade glioma, for paediatrics there is inclusion of diffusion-

146 he management of adult patients with diffuse gliomas, for patients and caregivers, and for health-car

147 Using this map, we demonstrated that glioma frequency is elevated in association cortex and c

148 dendrocyte precursor cells, exhibited a high glioma frequency.

149 Chemogenomic analysis of mutated glioma genes reveals potential drug targets, with severa

150 iptome data, including data from the Chinese Glioma Genome Atlas RNAseq, the Cancer Genome Atlas RNAs

151 ting of associations between ADC metrics and glioma genotypes, including Bonferroni correction for mu

152 ound A readily implemented MRI biomarker for glioma genotyping is currently lacking.

153 HIF2alpha expression increased with glioma grade, with over half of GBM specimens HIF2alpha

154 ics and immune escape signature by comparing glioma growth in immunocompetent versus immunodeficient

155 letion blocks distant dispersal, restricting glioma growth in the SVZ.

156 ripples recruitment, dramatically suppresses glioma growth, and increases survival.

157 ng of innate and adaptive responses inhibits glioma growth, but also activates immune checkpoint.

158 e of neurons and immune cells in controlling glioma growth, relevant to future therapeutic targeting.

159 Clinical trials of treatments for high-grade gliomas have traditionally relied on measures of respons

160 rvival or clinical benefit, with the complex glioma heterogeneity often being the reason to blame.

161 High-grade gliomas (HGG) afflict both children and adults and respo

162 (TMZ) is a frequently used chemotherapy for glioma; however, chemoresistance is a major problem limi

163 tent and reproducible growth of a high-grade glioma in all animals.

164 Sporadic gliomas in companion dogs provide a window on the intera

165 thways to induce the formation of high-grade gliomas in rodent models.

166 TrkB.T1 enhances PDGF-driven gliomas in vivo, augments PDGF-induced Akt and STAT3 sig

167 We generated gliomas in WT mice via in utero deletion of key tumor su

168 antly recurrent somatic alterations in these gliomas including mutant EGFR amplifications and Sub1, T

169 We report that radiation induces a glioma-initiating cell phenotype, and we have identified

170 alter the intrinsic radiation sensitivity of glioma-initiating cells (GICs).

171 Diffuse intrinsic pontine glioma is an aggressive pediatric cancer for which no ef

172 Malignant glioma is rapidly fatal, and ionizing radiation is part

173 Glioma is the most common intrinsic brain tumor and also

174 In patients with mIDH1 advanced glioma, ivosidenib 500 mg once per day was associated wi

175 between the increased survival in low-grade glioma (LGG) and complementarity of IDH1 mutants to the

176 o govern Neurofibromatosis-1 (NF1) low-grade glioma (LGG) growth.

177 roglioma is an important type of lower-grade glioma (LGG), which is a slowly progressing brain tumor.

178 anging study for patients with WHO low-grade glioma (LGG, grade II), as it was the first to demonstra

179 Diffuse low-grade gliomas (LGG) have been reclassified based on molecular

180 ignant brain tumors that include lower-grade gliomas (LGGs) and glioblastomas.

181 ch into neuropsychiatric disease and cancer, gliomas may be expected to localize to brain regions cha

182 Results Data in a total of 45 patients with glioma (mean age, 51.3 years +/- 14.3 [standard deviatio

183 Results Three participants with IDH1-mutated gliomas (mean age, 50 years +/- 21 [standard deviation];

184 hts into the molecular mechanisms underlying glioma metabolism are rapidly emerging.

185 goal of translating these new insights about glioma metabolism into clinical benefits for patients.

186 tifies isocitrate dehydrogenase (IDH)-mutant gliomas misassigned to 1p/19q codeletion status with FIS

187 t the production of a high-grade spinal cord glioma model in pigs using lentiviral gene transfer.

188 notherapy for efficacy in a mouse orthotopic glioma model.

189 inotecan chemotherapy to the brain and a rat glioma model.

190 ne transfer represents a feasible pathway to glioma modeling in higher order species.

191 tends survival in clinically relevant murine glioma models and provides the basis on which to advance

192 In an immunocompetent orthotopic glioma mouse model overexpressing truncated O-linked gly

193 hatase and tensin homologue (PTEN)-deficient glioma mouse models, mRNA-containing exosomes restored t

194 In patients with nonenhancing glioma (n = 35), the objective response rate was 2.9%, w

195 id tumors (n = 229) and pediatric high-grade gliomas (n = 401), we show significant associations with

196 Collective glioma networks infiltrating the brain thus depend on ad

197 populated with putative cells of origin for glioma, neural stem cells and oligodendrocyte precursor

198 In the test sample of 49 gliomas (nine IDH wild type, 21 IDH mutant/1p19q intact,

199 d on their expression in adult and pediatric gliomas, nine of these hits are prioritized as lncRNA Gl

200 Results: For IDH(wt) and IDH(m-noncodel) gliomas, nSUV demonstrated significant positive correlat

201 us in World Health Organization grade II/III gliomas on the basis of standard clinical MRI sequences

202 atosis type 1 (NF1)-associated optic pathway gliomas (OPGs) and a follow-up period of at least 10 yea

203 Grade 4 glioma or GBM has poor prognosis and is the most aggress

204 ures often herald the clinical appearance of gliomas or appear at later stages.

205 and peritumoural regions of grade II and III gliomas (p = 0.02 and p =0.001, respectively).

206 allenge in follow-up of diffuse infiltrating gliomas, particularly high grade, which leads to a poten

207 wn about the roles of neurons and T cells in glioma pathobiology.

208 g new insight into the mechanisms that drive glioma pathogenesis.

209 novel prognostic biomarker for WHO grade IV glioma patient outcomes.

210 diagnosed and histomolecularly characterized glioma patients (glioblastoma, 90%; age range, 20-79 y)

211 y significant HR was reported for PFS in the glioma patients (HR = 1.23, 95% CI: 0.41, 3.72).

212 e ((18)F-FET) PET for response assessment in glioma patients after adjuvant temozolomide chemotherapy

213 Compared to healthy controls, mice and glioma patients demonstrated significant differences in

214 hnique to stain microglia from epileptic and glioma patients to examine responses to purines.

215 the effect of TET1 expression on survival in glioma patients using open-access data from the Genomic

216 We included 76 glioma patients who received amine chemical exchange sat

217 Methods: Sixty-eight treatment-naive glioma patients who underwent (18)F-FDOPA PET and physio

218 ient data identified as diffuse infiltrating glioma patients whose disease progressed/recurred were u

219 Glioma patients with increased AVIL expression have a wo

220 In glioma patients, differentiation between tumor progressi

221 When applied to glioma patients, transcripts of neutrophils exposed to I

222 from treatment-related changes in high-grade glioma patients.

223 and a predictor of poor clinical outcome in glioma patients.

224 and treatment-related changes in high-grade glioma patients.

225 2 correlated with worse clinical outcomes in glioma patients..

226 as significantly associated with worse OS in glioma patients; for the other study, which provided dat

227 showed high similarity with human pediatric gliomas per robust aneuploidy, mutational rates, relativ

228 Pediatric low-grade gliomas (pLGG) are frequently driven by genetic alterati

229 characterized cohort of pediatric low-grade gliomas (pLGGs) published to date.

230 acles that the intra-tumour heterogeneity of glioma present.

231 enase (IDH) mutations are highly frequent in glioma, producing high levels of the oncometabolite D-2-

232 pression of miR-21 is correlated with poorer glioma prognosis.

233 hesis that glutamine may be a key marker for glioma progression and indicate that inflammation is ass

234 cells and their microenvironment to promote glioma progression, and it is also a potential therapeut

235 ucial role of astrocytes in edema, ischemia, glioma progression, stroke, and epilepsy.

236 may offer an unanticipated strategy to halt glioma progression.

237 nine of these hits are prioritized as lncRNA Glioma Radiation Sensitizers (lncGRS).

238 t and the injected dose of gadopiclenol in a glioma rat model compared with those of conventional GBC

239 ril and July 2012, 32 rats implanted with C6 glioma received two intravenous injections at a 24-hour

240 tial treatment delay for patients with early glioma recurrence.

241 useful to detect residual tumor tissue after glioma resection.

242 lighted, providing important clues as to how gliomas respond to and adapt to their changing tissue an

243 utamine metabolism and inflammation in human glioma samples and explore the use of glutamine as a pot

244 In total, 1633 glioma samples with transcriptome data, including data f

245 In general, paediatric low-grade gliomas show clinical and biological features that are d

246 Conclusion: IDH(m-codel) gliomas showed distinctive patterns of correlations betw

247 Canine gliomas showed high similarity with human pediatric glio

248 microsatellite instability in MMR-deficient gliomas, single-cell whole-genome sequencing analysis of

249 These studies identify lncGRS-1 as a glioma-specific therapeutic target and establish a gener

250 IL-33 expression in a large subset of human glioma specimens and murine models correlates with incre

251 mpacts cancer-relevant phenotypes in GBM and glioma stem cell lines.

252 poxia by a simple isoform switch to regulate glioma stem cell self-renewal, tumorigenicity, and progr

253 suppressor genes that feeds back to regulate glioma stem cell survival.

254 lastoma (GBM), maintains stem-like features (glioma stem cell, GSC) through hypoxia-induced responses

255 The interplay between glioma stem cells (GSCs) and the tumor microenvironment

256 pregulates genes critical for maintenance of glioma stem cells (GSCs).

257 shift towards mesenchymal cellular state of glioma stem cells, promoting both invasive and prolifera

258 Glioma stem-like cells (GSC) in glioblastoma (GBM) struc

259 at one such conjugate shows efficacy against glioma stem-like cells.

260 iptomic profiles defined four transcriptomic glioma subgroups with 91.4% concordance with the WHO-def

261 of applying VERDICT in a range of different glioma subtypes.

262 alterations shared between canine and human gliomas such as the receptor tyrosine kinases, TP53 and

263 unable to preserve VHL function and lacking glioma suppression activity.

264 ven by MMR defects in chemotherapy-sensitive gliomas that recur after treatment with the chemotherapy

265 In six (66.7%) of these nine gliomas, the 1p/19q codeletion status as determined with

266 In multiple solid tumours, including gliomas, the mechanical properties change as the disease

267 Gliomas, the most common malignant primary brain tumours

268 Three subregions of glioma-the necrotic and nonenhancing tumor core, the per

269 tions, thus possibly representing targets in glioma therapy.

270 resonance spectra were acquired from ex vivo glioma tissue (n = 16, grades II-IV) to quantify metabol

271 omas with those of human pediatric and adult gliomas to characterize evolutionarily conserved mammali

272 ifier confidently classified all but 17 TCGA gliomas to one of the four transcriptomic profile (TP) g

273 essing the response of paediatric high-grade gliomas to various treatments.

274 Six pediatric patients with glioma tolerated this combination without significant ad

275 ains bromodomain-containing protein BRD9 and glioma tumor suppressor candidate region 1 (GLTSCR1) or

276 Human (Homo sapiens) glioma tumor-suppressor candidate region gene2 (GLTSCR2)

277 n signaling axis as a critical mechanism for glioma tumorigenesis that may serve as a new therapeutic

278 (v)beta(3), moderate in alpha(5)beta(1)) and glioma U87MG (very high in alpha(v)beta(3), moderate/hig

279 functional driver landscapes of EGFR-mutant gliomas, uncovering potential therapeutic strategies, an

280 resents a non-invasive analysis of low-grade gliomas using imaging features based on the updated clas

281 Response criteria for paediatric high-grade glioma vary historically and across different cooperativ

282 To investigate the role of PIEZO1 in gliomas, we analysed PIEZO1 gene expression at the trans

283 ome, and methylation sequencing of 83 canine gliomas, we found alterations shared between canine and

284 s that confer susceptibility to this drug in gliomas, we performed a genome-scale CRISPR knockout scr

285 ix patients with recurrent PDGFRalpha-driven glioma were treated with dasatinib and everolimus.

286 MMR-deficient gliomas were characterized by a lack of prominent T cell

287 Diffuse gliomas were classified into grade II and grade III.

288 In conclusion, 1p/19q co-deleted gliomas were less acidic, which may be related to better

289 f post-mortem gene expression, we found that gliomas were localized to brain regions enriched with ex

290 s demonstrated in a patient with mutant-IDH1 glioma where it enables imaging of D-2-hydroxyglutarate

291 For gliomas where (a) consensus neuroradiologist 1p/19q pred

292 In glioma WHO grade II, it is unclear whether the extent of

293 atients (20 male and 16 female) with diffuse gliomas, who underwent ASL and DWI.

294 r molecular testing should be considered for gliomas with discordant neuroimaging and FISH results.

295 es a robust and objective method to classify gliomas with high agreement to the current WHO guideline

296 hematologic malignancies, solid tumors, and gliomas with mIDH1.

297 We compared the molecular profiles of canine gliomas with those of human pediatric and adult gliomas

298 ng these are frequently altered in patients' gliomas, with prognostic implications.

299 ents from five institutions with lower-grade gliomas (World Health Organization grade II and III) wer

300 Data in patients with IDH-mutant lower-grade gliomas (World Health Organization grade II/III) and 1p/