ライフサイエンスコーパス: high-grade glioma

1 response assessment criteria for paediatric high-grade glioma.

2 ion is associated with favourable outcome in high-grade glioma.

3 16 of these 18 genes were down-regulated in high-grade glioma.

4 followed an alternative evolutionary path to high-grade glioma.

5 ted with decreased survival of patients with high-grade glioma.

6 stic value for OS in patients with suspected high-grade glioma.

7 ssion from true progression in patients with high-grade glioma.

8 ations during treatment for 44 patients with high-grade glioma.

9 quent association of PTEN mutations in human high-grade glioma.

10 gery, and photodynamic therapy for recurrent high-grade glioma.

11 en shown to improve gross-total resection of high-grade glioma.

12 iated with an increased risk of developing a high-grade glioma.

13 ssing intraoperative MRI in the treatment of high-grade glioma.

14 cost-effective modality in the treatment of high-grade glioma.

15 odel was constructed to follow patients with high-grade glioma.

16 a multicenter trial involving patients with high-grade glioma.

17 inded radiology review for 133 patients with high-grade glioma.

18 inhibits the progression of KrasG12V-driven high-grade glioma.

19 al receptor involved in the proliferation of high-grade glioma.

20 the delayed brain tumor (DBT) mouse model of high-grade glioma.

21 ults in hyperactivity of this conductance in high grade gliomas.

22 has been associated with the development of high grade gliomas.

23 clinically-annotated and genetically-defined high grade gliomas.

24 mal and malignant tissue during resection of high grade gliomas.

25 very of boronophenylalanine in patients with high-grade gliomas.

26 neutron capture therapy for the treatment of high-grade gliomas.

27 es efficacy in differentiating the low- from high-grade gliomas.

28 ism contributing to the growth of aggressive high-grade gliomas.

29 d A-to-I editing and cancer, particularly in high-grade gliomas.

30 ve angiogenesis that is a typical feature of high-grade gliomas.

31 use of MRI and PET for surgical resection of high-grade gliomas.

32 MRI alone to plan the surgical resection of high-grade gliomas.

33 n 4 months were observed among patients with high-grade gliomas.

34 Bumex as adjuvant therapy for patients with high-grade gliomas.

35 l alkylating agent used for the treatment of high-grade gliomas.

36 es in the imaging of gliomas with a focus on high-grade gliomas.

37 mendations for updated response criteria for high-grade gliomas.

38 s significantly increased in the majority of high-grade gliomas.

39 PET tracers for the treatment evaluation of high-grade gliomas.

40 ve therapeutic strategy for radiosensitizing high-grade gliomas.

41 nic therapies may have activity in recurrent high-grade gliomas.

42 at antiangiogenic therapies have activity in high-grade gliomas.

43 r glioblastoma (GBM) results in formation of high-grade gliomas.

44 for improving the outcomes for patients with high-grade gliomas.

45 to current trials and clinical practice for high-grade gliomas.

46 uptake is a distinguishing characteristic of high-grade gliomas.

47 a pharmaceutical agent has maximum access to high-grade gliomas.

48 er as a surrogate marker of proliferation in high-grade gliomas.

49 ill likely improve survival in patients with high-grade gliomas.

50 ing (MRI) during a course of radiotherapy of high-grade gliomas.

51 e in histology-independent classification of high-grade gliomas.

52 ntitumor activity in patients with recurrent high-grade gliomas.

53 GFR) is commonly amplified and/or mutated in high-grade gliomas.

54 carmustine (BCNU) in patients with recurrent high-grade gliomas.

55 dency to undergo malignant transformation to high-grade gliomas.

56 adults with previously irradiated, recurrent high-grade gliomas.

57 ity in a minority of patients with recurrent high-grade gliomas.

58 sets from 16 patients aged 21-71 years with high-grade gliomas.

59 valuable for tumor-specific gene transfer to high-grade gliomas.

60 0 are the most common genetic alterations in high-grade gliomas.

61 imal morbidity in patients with intracranial high-grade gliomas.

62 tumour immune microenvironment in paediatric high-grade gliomas.

63 existing tumor suppressor losses to generate high-grade gliomas.

64 ging biomarker of macrophages in adults with high-grade gliomas.

65 ed with patient prognosis in MES, but not PN high-grade gliomas.

66 ts receptor CSF1R are overexpressed in human high-grade gliomas.

67 l of Ras* mice and promoted the formation of high-grade gliomas.

68 s is low compared with other tumours such as high-grade gliomas.

69 Differences in SUV(max) between high-grade gliomas (1.89 +/- 0.78 [mean +/- standard dev

70 in a number of freshly resected and cultured high grade gliomas, 2) syntaxin 1A inhibited ASIC curren

71 t common diagnoses were meningioma (37%) and high-grade glioma (20%).

72 low-grade glioma (n = 93), ependymoma (32), high-grade glioma (25), medulloblastoma (22), gangliogli

73 57.8; germ cell tumors, 63.5; ependymoma or high-grade glioma, 69.8; low-grade glioma, 71.5; and oth

74 (rCBV) and VSI(MRI) in eleven patients with high-grade glioma (7 WHO grade III and 4 WHO grade IV).

75 rain tumor specimens of 213 patients (mostly high-grade gliomas [89%]) included in the Vienna Cancer

76 tients after a median latency of 12.6 years (high-grade gliomas, 9.1 years; meningiomas, 19 years).

77 gliomas, we found TAX-1 to be amplified in 2 high-grade gliomas among a group of 26 gliomas investiga

78 p Study 945, the largest cohort of childhood high-grade gliomas analyzed to date.

79 ause the INK4a-ARF locus is often deleted in high-grade gliomas (anaplastic oligodendroglioma and gli

80 data from 157 unpublished cases of pediatric high-grade glioma and diffuse intrinsic pontine glioma a

81 erved in four of 14 assessable patients with high-grade glioma and in two of six with primitive neuro

82 Patients with a histologic diagnosis of high-grade glioma and radiographic evidence of tumor pro

83 of genome-wide association studies (GWAS) of high-grade glioma and replication data (1,644 cases and

84 s to target surface GRP78 as a biomarker for high-grade glioma and to develop effective cell-specific

85 tosis-were compared in the solid parts of 17 high-grade gliomas and 11 low-grade gliomas (P<.05 signi

86 alyzed 28 pediatric gliomas consisting of 14 high-grade gliomas and 14 low-grade gliomas.

87 risk; HR, 3.86; 95% CI, 1.59-9.35; P = .003) high-grade gliomas and 191 glioblastomas (global log-ran

88 survival ranged from 0-19.5% for subsequent high-grade gliomas and 57.3-100% for meningiomas, which

89 metastatic cancers, including low-grade and high-grade gliomas and brain metastases (BrMs) originati

90 For other types of tumors, such as malignant high-grade gliomas and brainstem gliomas, new approaches

91 e 1 (NTRK1), is a potent oncogenic driver of high-grade gliomas and confers sensitivity to the experi

92 cterizing genetically engineered mouse (GEM) high-grade gliomas and evaluating the pharmacokinetics i

93 n many tumor types including the majority of high-grade gliomas and expression of activated RAS or RA

94 PI(3)K/Akt pathway, are found in almost all high-grade gliomas and MAPK signaling is necessary for c

95 is a rational strategy for the treatment of high-grade gliomas and may be an effective adjuvant ther

96 is well tolerated by patients with recurrent high-grade gliomas and may have efficacy in this disease

97 nctions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mut

98 l blood volumes in the peritumoral region in high-grade gliomas and metastases were 1.31 +/- 0.97 (me

99 al blood volume and metabolic ratios between high-grade gliomas and metastases.

100 The peritumoral LNR exceeded 2.0 in seven high-grade gliomas and no metastases (P = .02).

101 , we examined expression array data of human high-grade gliomas and performed RT-PCR on glioblastoma

102 old significant promise for the treatment of high-grade gliomas and provide a rationale for proceedin

103 gh levels of SLFN5 expression correlate with high-grade gliomas and shorter overall survival in patie

104 inositide 3-kinase/Akt pathway for growth of high-grade gliomas and suggest that multiple molecular a

105 hat COX-2 is up-regulated in the majority of high-grade gliomas and that a potential role of COX-2 in

106 le polymers following resection of recurrent high-grade gliomas and the systemic BCNU exposure with i

107 ion is the most common genetic alteration in high-grade glioma, and approximately 50% of EGFR-amplifi

108 ainst nonprogressive high-grade meningiomas, high-grade gliomas, and nontumor brain specimens.

109 Pediatric high-grade gliomas are among the deadliest of childhood

110 riteria for assessing response to therapy in high-grade gliomas are based on two-dimensional tumor me

111 High-grade gliomas are brain tumors associated with a de

112 High-grade gliomas are characterized by exuberant vascul

113 High-grade gliomas are lethal brain cancers whose progre

114 though therapies for patients with recurrent high-grade gliomas are limited, there has been important

115 High-grade gliomas are the most aggressive malignant bra

116 Posttreatment high-grade gliomas are usually monitored with contrast-e

117 lowed clear differentiation between low- and high-grade glioma (area under the receiver operating cha

118 with relapsed or progressive, biopsy-proven, high-grade glioma (arm A) and progressive, diffuse, intr

119 l genes that are differentially expressed in high-grade glioma as a prognostic molecular signature.

120 on and pseudopalisades, elements that define high-grade gliomas as SHH-producing microenvironments.

121 was performed on 10 patients with recurrent high-grade glioma at 5 different institutions within the

122 in low-grade glioma (AUC, 0.818) and MTI in high-grade glioma (AUC, 0.854) and for all WHO grades (A

123 were tested for differences between low- and high-grade gliomas based on one-way ANOVA.

124 R traits that are associated with some known high-grade glioma biomarkers and association with genomi

125 vement in the poor prognosis for humans with high-grade glioma brain tumors, alternative therapeutic

126 ajor up-regulated isoform of this protein in high-grade gliomas but is absent in a specific subset of

127 ptor (EGFR) is amplified or overexpressed in high-grade gliomas but is low or undetectable in normal

128 group developed response criteria for adult high-grade glioma, but these were not created to meet th

129 Notably, human high-grade gliomas carry focal hemizygous deletions of t

130 f 275,895 autosomal variants among 692 adult high-grade glioma cases (622 from the San Francisco Adul

131 Data from 855 high-grade glioma cases and 1,160 controls from 4 geogra

132 h P < 10(-6) using independent data from 176 high-grade glioma cases and 174 controls from the Mayo C

133 the Children's Cancer Group (CCG) trial for high-grade gliomas (CCG-945).

134 s channel activity promotes a reversion of a high grade glioma cell to a phenotype resembling that of

135 rain tumors, we stably transfected the human high-grade glioma cell line SNB19 and the human low-grad

136 expression of uPAR has been correlated with high-grade glioma cell lines and tumors We report here t

137 ries of these agents against a panel of five high-grade glioma cell lines to identify a promising com

138 -expressed GRP78 as a target for suppressing high-grade glioma cell lines.

139 to detect surface-localized GRP78 in diverse high-grade glioma cell lines.

140 ing Hsc70 expression promotes reversion of a high-grade glioma cell to a more normal astrocytic pheno

141 High grade glioma cells derived from patient biopsies ex

142 e hypothesis that the conductance pathway in high grade glioma cells is comprised of ENaC/DEG subunit

143 High grade glioma cells possess a voltage-independent, a

144 53-, p14(ARF)-, and p16(Ink4a)/pRb-deficient high grade glioma cells that lacked the p16(Ink4a)-depen

145 utively activated sodium currents present in high grade glioma cells.

146 xpression of amiloride-sensitive currents in high grade glioma cells.

147 that kill proliferative and nonproliferative high-grade glioma cells by programmed necrosis.

148 High-grade glioma cells express subunits of the ENaC/Deg

149 We have previously shown that high-grade glioma cells functionally express this curren

150 31 with glioblastoma) were enrolled into the high-grade glioma cohort and 13 patients were enrolled i

151 inotecan (BEV/IR) in patients with recurrent high-grade glioma compared with MR imaging alone from th

152 amino acid PET for the surgical resection of high-grade gliomas, compared with MRI alone, from the pe

153 High-grade gliomas defined by histone 3 K27M driver muta

154 gulated in malignant glioma specimens and in high-grade glioma-derived primary cultures, whereas rema

155 brain tumors (ie, medulloblastoma, low- and high-grade gliomas, diffuse intrinsic pontine glioma, an

156 gistically and safely with radiation against high-grade gliomas, drugs must pass the endothelial junc

157 thologic diagnoses were made in 24 cases (13 high-grade gliomas, eight metastases to the brain, and t

158 Despite multimodality treatment, most high-grade gliomas eventually recur and are ultimately i

159 Current therapies for high-grade gliomas extend survival only modestly.

160 respectively, for differentiating low- from high-grade gliomas for ADC, D and f, and differentiating

161 recommendations for the management of adult high-grade glioma, for paediatrics there is inclusion of

162 o differentiation, and induced both low- and high-grade glioma formation in vivo.

163 ), and clinical patient data profiles of 543 high-grade gliomas from US medical centers and The Cance

164 grade glioma (LGG) and all four subtypes of high grade glioma (GBM).

165 c mutations of H3F3A in aggressive pediatric high-grade gliomas generate K27M or G34R/V mutant histon

166 therapeutic anticoagulation in patients with high-grade gliomas given the increased risk of ICH and p

167 xpression profiles in brain tumors including high-grade gliomas [glioblastoma multiforme (GBM) and an

168 The median survival was 18 +/- 4.7 mo in the high-grade glioma group and 58 +/- 27 mo in the low-grad

169 On the other hand, all high-grade gliomas had various degrees of LOH affecting

170 The diagnosis and management of high-grade glioma has profound effects on patients and t

171 py on survival and recurrence in adults with high-grade glioma have had inconclusive results.

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

173 In one case of the high grade glioma (HGG) only the left hemisphere Broca's

174 High grade gliomas (HGG) are classified into four subgro

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

176 Pediatric high-grade glioma (HGG) is a devastating disease with a

177 High-grade glioma (HGG) is a group of primary malignant

178 Tumor heterogeneity of high-grade glioma (HGG) is recognized by four clinically

179 me, phosphoproteome and transcriptome in two high-grade glioma (HGG) mouse models driven by mutated R

180 survival benefit was associated with maximal high-grade glioma (HGG) resection and analysed this lite

181 ediatric brain tumors, focusing on pediatric high-grade glioma (HGG), a subgroup with universally poo

182 High-grade glioma (HGG), one of the most lethal human ne

183 different therapeutic regimens in astrocytic high-grade glioma (HGG), the prognosis for patients rema

184 n alkylating agent licensed for treatment of high-grade glioma (HGG).

185 ve myristoylated form of Akt1 did not induce high-grade glioma (HGG).

186 rsor cells, the putative cellular origins of high-grade glioma (HGG).

187 ompared with patients with primary pediatric high-grade glioma (HGG; median, 25 mutations per exome;

188 High-grade gliomas (HGG) afflict both children and adult

189 High-grade gliomas (HGG) are a devastating group of canc

190 Patients with high-grade gliomas (HGG) are frequently excluded from fi

191 The outcome for children with high-grade gliomas (HGG) remains dismal, with a 2-year s

192 llow-up MR imaging in 2 patients revealed 66 high-grade gliomas (HGG), 77 low-grade gliomas (LGG), 2

193 In high-grade gliomas (HGG), distinct hierarchical cell pop

194 e uptake of (90)Y-DOTATOC in meningiomas and high-grade gliomas (HGGs) and a feasibility study of the

195 High-grade gliomas (HGGs) are incurable brain tumors tha

196 Salvage options for recurrent high-grade gliomas (HGGs) are limited by cumulative toxi

197 High-grade gliomas (HGGs) are the most common malignant

198 Pediatric and adult high-grade gliomas (HGGs) frequently harbor PDGFRA alter

199 High-grade gliomas (HGGs) include the most common and th

200 Diffuse brainstem gliomas (BSGs) and other high-grade gliomas (HGGs) of childhood carry a dismal pr

201 Medulloblastomas (MBs), but not high-grade gliomas (HGGs), demonstrated spatially homoge

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

203 oversial: the value of maximal resection for high-grade gliomas (HGGs).

204 High-grade gliomas (HGGs; WHO grades 3-4) are highly div

205 Among high-grade gliomas, histologically classic glioblastomas

206 rate consistent and reproducible growth of a high-grade glioma in all animals.

207 GF-beta1 on the growth of the SMA 560 murine high-grade glioma in vivo is growth inhibition.

208 ction methodology, could be used to classify high-grade gliomas in a manner more objective, explicit,

209 present the molecular landscape of low- and high-grade gliomas in patients affected by NF1 (NF1-glio

210 and p53 pathways to induce the formation of high-grade gliomas in rodent models.

211 te complex breaks, we found that DSBs induce high-grade gliomas in these mice which, otherwise, do no

212 ted through MEK, leads to the development of high-grade gliomas in vivo and suggest that MEK may be a

213 r Ink4a/Arf loss leads to the development of high-grade gliomas in vivo.

214 on transcripts were more frequently found in high-grade gliomas, in the classical subtype of gliomas,

215 PC) were discovered at the invasive front of high-grade gliomas, in which they exhibited a unique per

216 ological consequences of p16 inactivation in high-grade gliomas included facilitating invasiveness, w

217 High grade gliomas, including glioblastoma (GBM), are th

218 Pediatric high grade glioma is refractory to conventional multimod

219 High-grade glioma is a highly malignant and metastatic b

220 High-grade glioma is the most common primary brain cance

221 High-grade glioma is undoubtedly a challenging research

222 r the degree of expression of p53 protein in high-grade gliomas is associated with progression-free s

223 The prognosis of children with high-grade gliomas is uncertain, even when clinical and

224 expression) and with a separate group of 180 high-grade gliomas (log-rank P = .00003; HR, 0.476; 95%

225 teristics of solitary metastases and primary high-grade gliomas may sometimes be similar, perfusion-w

226 High-grade gliomas, metastases, and benign lesions can b

227 Specifically in high-grade gliomas, miR-376a* accumulated entirely in an

228 Diagnoses included high-grade glioma (n = 10), brainstem glioma (n = 7), me

229 after MT were glioblastoma (n = 7) and other high-grade gliomas (n = 4).

230 nant rhabdoid tumors (n = 229) and pediatric high-grade gliomas (n = 401), we show significant associ

231 hat temozolomide has minimal activity in the high-grade gliomas of childhood.

232 eloid leukemia, cutaneous melanoma, low- and high-grade gliomas of the brain, and adenocarcinomas of

233 High-grade gliomas of the CNS are characterized by poor

234 High-grade gliomas often possess an impaired blood-brain

235 Twenty-two brain tumors (10 high-grade gliomas, one low-grade glioma, and 11 meningi

236 Twenty-seven patients with either high-grade glioma or metastases were enrolled in a bicen

237 ress has been made in the treatment of adult high-grade gliomas over the last two decades, thus neces

238 In a panel of low-grade and high-grade glioma patient samples, we show for the first

239 ociated with a shorter survival in pediatric high-grade glioma patient samples.

240 to predict the overall survival (OS) time of high-grade gliomas patient.

241 and surgically resected tumour samples from high-grade glioma patients demonstrates the clinical app

242 ontaining 24 image-localized biopsies from 7 high-grade glioma patients to validate the model.

243 The proportion of high-grade glioma patients with cognitive deterioration

244 ed metric maps derived from rs-fMRI) from 68 high-grade glioma patients with different survival time.

245 data from healthy fetal tissue and pediatric high-grade glioma patients, illustrates the potential of

246 To assess the cognitive performance of high-grade glioma patients, prospectively collected cogn

247 tion methods were used to collect data in 22 high-grade glioma patients, with informed written consen

248 progression and treatment-related changes in high-grade glioma patients.

249 rogression from treatment-related changes in high-grade glioma patients.

250 Pediatric high-grade glioma (pHGG) and diffuse intrinsic pontine g

251 und in a substantial proportion of pediatric high-grade gliomas (pHGG), often in association with TP5

252 ing to Response Assessment in Neuro-Oncology High-Grade Glioma (RANO-HGG) criteria, the overall respo

253 d strongly upregulated in both low-grade and high-grade gliomas, reduces glioma cell growth by cell-c

254 Five of 18 patients (28%) with high-grade gliomas remain free of disease at 39+, 44+, 4

255 The prognosis for children with high-grade gliomas remains somewhat unpredictable.

256 High-grade gliomas represent a significant source of can

257 In three patients with high-grade glioma, responses included one complete remis

258 evated protein levels of HDAC6 were found in high grade glioma samples, in contrast to the decreased

259 nchmark for comparison with future pediatric high-grade glioma studies, in addition to identifying at

260 High grade gliomas such as glioblastoma multiforme expre

261 Clinical findings in high-grade glioma suggest that PTEN gene alterations are

262 e highest frequency of mutations detected in high-grade gliomas, T-lineage acute lymphoblastic leukae

263 rane localization, and its expression in all high-grade gliomas tested to date suggest that it may pl

264 noreactive score was significantly higher in high-grade glioma than low-grade glioma and normal brain

265 d (18)F-FDG PET were significantly higher in high-grade gliomas than in low-grade gliomas (2.15 +/- 0

266 axial kurtosis were significantly higher in high-grade gliomas than in low-grade gliomas (P = .02, P

267 All medulloblastomas, ependymomas, and high-grade gliomas that abutted a CSF space were detecta

268 f Ink4 and Arf tumor suppressors to generate high-grade gliomas that are commonly driven by Met ampli

269 anscriptional regulatory mechanism active in high-grade gliomas that drives poor outcomes.

270 peutic option in the subset of patients with high-grade gliomas that express both functional p53 and

271 d late toxicity, while in selected groups of high-grade gliomas the use of adjuvant or neo-adjuvant c

272 Within high-grade gliomas, the precise identities and functiona

273 here has been progress in treating recurrent high-grade gliomas, the prognosis remains poor and much

274 treatment resistance rates, particularly for high grade gliomas, there is a need for specific biomark

275 37 proteins differentially expressed across high-grade glioma TMEs.

276 nges in assessing the response of paediatric high-grade gliomas to various treatments.

277 in the management of patients with recurrent high-grade glioma treated with BEV/IR may be cost-effect

278 treatment outcome in patients with recurrent high-grade glioma treated with fresolimumab.

279 on of cultured cells originally derived from high grade gliomas (U87-MG and SK-MG1) with ASIC2 abolis

280 Adult patients with recurrent high-grade gliomas underwent tumor resection, implantati

281 stigate the fresolimumab uptake in recurrent high-grade gliomas using (89)Zr-fresolimumab PET and to

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

283 (89)Zr-fresolimumab penetrated recurrent high-grade gliomas very well but did not result in clini

284 131I-TM-601 in adult patients with recurrent high-grade glioma was performed to determine the biodist

285 BPND of (11)C-(R)PK11195 in high-grade gliomas was significantly higher than in low-

286 em/initiating cell (BTSC) lines derived from high-grade gliomas, we show that BTSCs are subject to im

287 e role of this pathway in the development of high-grade gliomas, we used the established RCAS/TVA gli

288 Sixty patients with high-grade glioma were enrolled onto a study of intratre

289 Twelve patients with recurrent high-grade glioma were included: 10 glioblastomas, 1 ana

290 thods In this prospective study, adults with high-grade gliomas were enrolled between July 2015 and J

291 years +/- 12 [age range, 32-74 years]) with high-grade gliomas were included.

292 10, updated response assessment criteria for high-grade gliomas were published.

293 t EGR1-expressing cells are more frequent in high grade gliomas where the nuclear expression of EGR1

294 ocesses compared with nonbrainstem pediatric high-grade gliomas, whereas expression signatures of low

295 MRI accurately reflect vessel caliber within high-grade gliomas, while traditional measures of rCBV a

296 s were negative in 5 patients with recurrent high-grade glioma who subsequently suffered tumor progre

297 aterials and Methods Seventeen patients with high-grade gliomas who had received 10-44 administration

298 Low-grade tumors progress to high-grade gliomas with aggressive biological behavior a

299 summarizes current treatments for recurrent high-grade gliomas with an emphasis on more novel approa

300 combination of activated Ras and Akt induces high-grade gliomas with the histological features of hum