ライフサイエンスコーパス: malignant glioma

1 ng the levels of 5hmC are also prognostic in malignant glioma.

2 tivity in unselected patients with recurrent malignant glioma.

3 tal growth factor in patients with recurrent malignant glioma.

4 d TEAD in driving the MES differentiation of malignant glioma.

5 tential therapeutic targets for treatment of malignant glioma.

6 ing molecular alteration in large subsets of malignant glioma.

7 tate personalised medicine in the setting of malignant glioma.

8 ough apoptosis, is used for the treatment of malignant glioma.

9 og pathway activity has been demonstrated in malignant glioma.

10 activates expression of mesenchymal genes in malignant glioma.

11 a viable potential target for the therapy of malignant glioma.

12 and we revisit the developmental origins of malignant glioma.

13 dy against VEGF--for patients with recurrent malignant glioma.

14 rucial to improve outcomes for patients with malignant glioma.

15 nvasion may provide an effective therapy for malignant glioma.

16 ion-free survival in patients with recurrent malignant glioma.

17 ive and well tolerated options for recurrent malignant glioma.

18 ing outcome in patients with newly diagnosed malignant glioma.

19 ay be developed into a potential therapy for malignant glioma.

20 nce imaging (MRI) in patients with recurrent malignant glioma.

21 h and are thus promising in the treatment of malignant glioma.

22 hat underlies this schizophrenic behavior in malignant glioma.

23 ssible clinical application in patients with malignant glioma.

24 oring therapy to the individual patient with malignant glioma.

25 creening of epigenetically silenced genes in malignant glioma.

26 e heterogeneous mass of cells that compose a malignant glioma.

27 Forkhead box M1 (FoxM1) is overexpressed in malignant glioma.

28 and is particularly severe in patients with malignant glioma.

29 d be a target for combinatorial treatment of malignant glioma.

30 co-segregate with integrin alpha6 in patient malignant glioma.

31 ed that CypB is upregulated in many cases of malignant glioma.

32 syndromes are well-defined risk factors for malignant glioma.

33 t have been linked to the risk of developing malignant glioma.

34 for use in clinical trials for patients with malignant glioma.

35 clinical trials for patients with recurrent malignant glioma.

36 n low levels of 5hmC and reduced survival in malignant glioma.

37 expression is closely associated with highly malignant gliomas.

38 antitative imaging markers of macrophages in malignant gliomas.

39 to the heterogeneous populations observed in malignant gliomas.

40 urons in the brains of mice can give rise to malignant gliomas.

41 that replication-competent HCMV may exist in malignant gliomas.

42 and accelerated radiation in newly diagnosed malignant gliomas.

43 y-ICLC) in HLA-A2(+) patients with recurrent malignant gliomas.

44 rs in the assessment and management of adult malignant gliomas.

45 oapoptotic therapies to improve treatment of malignant gliomas.

46 IDH2 occur in a majority of several types of malignant gliomas.

47 pression of link proteins in human brain and malignant gliomas.

48 ult in poor effectiveness of chemotherapy in malignant gliomas.

49 hog signaling regulates the growth of select malignant gliomas.

50 survival outcomes in patients with recurrent malignant gliomas.

51 y virus 1-associated dementia, and growth of malignant gliomas.

52 that have been demonstrated to be active in malignant gliomas.

53 hown to have promising activity in recurrent malignant gliomas.

54 uidance to physicians treating patients with malignant gliomas.

55 COX-2 expression with tumor angiogenesis in malignant gliomas.

56 ajor obstacles to successful chemotherapy of malignant gliomas.

57 ng of this therapy approach in patients with malignant gliomas.

58 factor receptors is a frequent occurrence in malignant gliomas.

59 apeutic targets for the treatment of diffuse malignant gliomas.

60 in a variety of cancer cell types, including malignant gliomas.

61 zone may be of potential use in treatment of malignant gliomas.

62 abolic imaging in the clinical management of malignant gliomas.

63 holds promise as a therapeutic agent against malignant gliomas.

64 ated in a variety of cancer types, including malignant gliomas.

65 tment for patients suffering from high-grade malignant gliomas.

66 peutic agents in clinical studies focused on malignant gliomas.

67 ith strong activating effect on NF-kappaB in malignant gliomas.

68 logs are considered as promising therapy for malignant gliomas.

69 n treatment of murine syngeneic intracranial malignant gliomas.

70 a central role in the treatment of childhood malignant gliomas.

71 ated receptors as potential targets to treat malignant gliomas.

72 he clonal composition and gene regulation in malignant gliomas.

73 plified, mutated, and overexpressed in human malignant gliomas.

74 develop potential therapeutic strategies for malignant gliomas.

75 d that these cells consistently give rise to malignant gliomas.

76 process that turns slowly dividing OPCs into malignant gliomas.

77 date therapeutic target for the treatment of malignant gliomas.

78 nostic biomarker and a therapeutic target of malignant gliomas.

79 and therapeutic procedures for patients with malignant gliomas.

80 ondrial membrane protein highly expressed in malignant gliomas.

81 fy QPRT as a potential therapeutic target in malignant gliomas.

82 -FLT PET is associated with OS in high-grade malignant gliomas.

83 Vs) currently in clinical trial for treating malignant gliomas.

84 Among malignant gliomas, 60%-80% show loss of P14ARF tumor sup

85 iated with prolonged survival in adults with malignant gliomas, although the association between MGMT

86 y 2013 using the terms glioblastoma, glioma, malignant glioma, anaplastic astrocytoma, anaplastic oli

87 trocyte elevated gene-1 (AEG-1) increases in malignant glioma and AEG-1 regulates in vitro invasion a

88 T cells recognize NKG2D ligands expressed on malignant glioma and are cytotoxic to glioma cell lines

89 minimal efficacy in children with recurrent malignant glioma and brainstem glioma.

90 ption factor-5 (ATF5) is highly expressed in malignant glioma and has a key role in promoting cell su

91 n developing therapeutic agents for treating malignant glioma and other human cancers.

92 rrent or progressive, temozolomide-resistant malignant glioma and to evaluate the safety of administe

93 ody of literature on PDGF autocrine loops in malignant glioma and with more recent observations on th

94 ine its effect on the intracranial growth of malignant gliomas and further study its antitumor mechan

95 e stabilizing factor HuR is overexpressed in malignant gliomas and linked to RNA stabilization of ang

96 Malignant gliomas and metastatic tumors are the most com

97 peutic target for improving the treatment of malignant gliomas and other brain tumors.

98 ant activation are frequent abnormalities in malignant gliomas and other human cancers and have been

99 Recent evidence from studies in malignant gliomas and other types of cancers points to a

100 dentify a novel chemoresistance mechanism in malignant gliomas and show that combination of drugs cap

101 expression is dramatically reduced in human malignant gliomas and that reexpression of functional me

102 ent experience of angiogenesis inhibitors in malignant gliomas and to highlight both the promise and

103 2014, using the terms glioblastoma, glioma, malignant glioma, and brain neoplasm, as well as by sear

104 high levels of spatial heterogeneity in MB, malignant glioma, and renal cell carcinoma (RCC).

105 files of 10 normal human brain specimens, 10 malignant gliomas, and 7 human glioma cell lines.

106 Diverse genetic subtypes of malignant glioma are sensitive to selective inhibition o

107 e cellular origins of stem-like cells within malignant glioma are still contended.

108 Malignant gliomas are aggressive brain tumors with limit

109 Malignant gliomas are almost uniformly fatal and display

110 Malignant gliomas are central nervous system tumors and

111 Malignant gliomas are characterized by an intrinsic resi

112 Malignant gliomas are highly aggressive brain tumors tha

113 Malignant gliomas are highly aggressive tumors of the ce

114 Malignant gliomas are highly invasive and chemoresistant

115 Malignant gliomas are highly invasive brain tumors that

116 Malignant gliomas are highly invasive tumours that use t

117 Malignant gliomas are highly invasive, proliferative, an

118 Malignant gliomas are highly lethal neoplasms with limit

119 Malignant gliomas are lethal brain tumors for which nove

120 Malignant gliomas are lethal cancers in the brain and he

121 Malignant gliomas are lethal cancers that display striki

122 Malignant gliomas are locally aggressive, highly vascula

123 Malignant gliomas are the most common and the most letha

124 Malignant gliomas are the most common primary intrinsic

125 Glioblastomas and malignant gliomas are the most common primary malignant

126 Malignant gliomas are treated with a combination of surg

127 Malignant gliomas are vascular tumours that produce vasc

128 GBM), the most common and aggressive type of malignant glioma, are characterized by increased invasio

129 Vs), in clinical trials for the treatment of malignant gliomas, are assumed to be selective for tumor

130 How malignant gliomas arise in a mature brain remains a myst

131 olved in the pathogenesis and progression of malignant gliomas as the centre of a splicing oncogenic

132 ificity, while the dramatic heterogeneity of malignant gliomas at the genetic and immunological level

133 man cytomegalovirus (HCMV) has been found in malignant gliomas at variable frequencies with efforts t

134 were high in low grade tumors and reduced in malignant glioma, but did not exhibit any correlation wi

135 gs)) are greatly diminished in patients with malignant glioma, but T(regs) frequently represent an in

136 ed in brain tumor-initiating cells (BTIC) in malignant glioma, but the mechanism of its activation is

137 Temozolomide is used widely to treat malignant glioma, but the overall response to this agent

138 e hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsibl

139 While amiloride reduces pH(i) of malignant gliomas by inhibiting isoform 1 of sodium-prot

140 of TTP via p38/MAPK promotes progression of malignant gliomas by negatively regulating its RNA desta

141 Thus, EGFR activation in malignant gliomas can transcriptionally activate COX-2 e

142 ozolomide, commonly used in the treatment of malignant glioma, causes cellular cytotoxicity by formin

143 has been reported to selectively kill human malignant glioma cell lines but not primary astrocytes.

144 r and atazanavir cause cell death in various malignant glioma cell lines in vitro.

145 t, IRES insertion permits HSV propagation in malignant glioma cell lines that do not support replicat

146 ated in malignant glioma specimens and human malignant glioma cell lines, correlating with their rate

147 e sought to establish a role for stathmin in malignant glioma cell motility, migration, and invasion

148 expression lead to significant decreases in malignant glioma cell motility, migration, and invasion.

149 However, it is estimated that only 5-15% of malignant glioma cells are in mitosis at any one time.

150 First, malignant glioma cells are stimulated to invade brain th

151 regulates in vitro invasion and migration of malignant glioma cells by activating the nuclear factor-

152 time of mice inoculated intracranially with malignant glioma cells compared with that of untreated m

153 e translation initiation at the HRV2 IRES in malignant glioma cells differ from those in normal centr

154 ow T-oligos exert antitumor effects on human malignant glioma cells in vitro and in vivo.

155 onal overexpression of TTP as a transgene in malignant glioma cells led to RNA destabilization of IL-

156 Malignant glioma cells maintain an elevated intracellula

157 Another possible mechanism of resistance of malignant glioma cells might be upregulation of pro-inva

158 Here we show that malignant glioma cells suppress NK immune surveillance b

159 that T-oligos inhibited the proliferation of malignant glioma cells through induction of nonapoptotic

160 hat ACSVL3 maintains oncogenic properties of malignant glioma cells via a mechanism that involves, in

161 uropathogenic properties but highly lytic in malignant glioma cells was accomplished by exchange of t

162 Importantly, not only rapamycin-sensitive malignant glioma cells with PTEN mutations but also rapa

163 PTEN mutations but also rapamycin-resistant malignant glioma cells with wild-type PTEN were sensitiz

164 tral role in regulating the proliferation of malignant glioma cells, and mTOR-specific inhibitors suc

165 Human malignant glioma cells, but not nonneoplastic astrocytes

166 3D) multicellular spheroids established with malignant glioma cells, unlike conventional two-dimensio

167 oblastoma multiforme (GBM) cell line, highly malignant glioma cells, was first injected into 5-week-o

168 ential for the proliferation and survival of malignant glioma cells, which suggests that inhibition o

169 esulted in significant radiosensitization of malignant glioma cells, which will guide the development

170 icity in normal cells, in U87-MG and U373-MG malignant glioma cells.

171 PV but has no effect on viral propagation in malignant glioma cells.

172 ociates with the IRES in neuronal but not in malignant glioma cells.

173 nhances the antitumor effect of rapamycin on malignant glioma cells.

174 133 and nestin and differentiation status of malignant glioma cells.

175 multiforme (GBM) is the most common form of malignant glioma, characterized by unpredictable clinica

176 er surgery and increase the effectiveness of malignant glioma chemotherapy.

177 , the largest randomized trial for childhood malignant gliomas completed to date.

178 , R3659, were serially passaged within human malignant glioma D54-MG cell lines in vitro or flank tum

179 d molecular events that initiate and promote malignant glioma development are not completely understo

180 Malignant gliomas especially glioblastoma (GBM) are poor

181 rongly suppresses the intracranial growth of malignant gliomas, even in the presence of the strong pr

182 Malignant gliomas exhibit extensive heterogeneity and po

183 Patients with malignant gliomas experience frequent clinical complicat

184 r-initiating cells isolated from fresh human malignant gliomas express the neurotrophin receptors Trk

185 erapies for these cancers, and patients with malignant glioma fare poorly, even after aggressive surg

186 Grade 4 malignant glioma (GBM) is a fatal disease despite aggres

187 Malignant gliomas/GBMs grow as a single mass (Type 1) an

188 ype, generating highly genetically divergent malignant gliomas/GBMs in distant brain regions.

189 esults demonstrate that ATF5 is essential in malignant glioma genesis and reveal that the ATF5-mediat

190 Knowledge of malignant glioma genetics has already impacted clinical

191 amic model and inhibit tumor growth in a U87 malignant glioma glioblastoma xenograft model.

192 expression in glioma stem cells and inhibits malignant glioma growth in cell culture and mouse models

193 Similarly, in human malignant gliomas harbouring IDH1 mutations, we find mar

194 T expression status and outcome in pediatric malignant gliomas has not been defined.

195 Gene therapy of malignant gliomas has shown a lack of clinical success t

196 herapy, and chemotherapy, most patients with malignant glioma have a poor prognosis.

197 Immunotherapeutic strategies for malignant glioma have to overcome the immunomodulatory a

198 Malignant gliomas have a distinctive ability to infiltra

199 Several new agents targeting angiogenesis in malignant gliomas have become available and have been in

200 Malignant gliomas have been shown to release glutamate,

201 trials are now in progress for patients with malignant gliomas; however, a better understanding of ho

202 In malignant gliomas, IDH1(R132H) expression induces widesp

203 fection occurs in a high percentage of human malignant gliomas in vivo, as the HCMV immediate early-1

204 prevent or promote regression/eradication of malignant gliomas in vivo.

205 Malignant gliomas, including glioblastoma multiforme, co

206 Malignant gliomas, including the most common subtype, gl

207 an extracellular matrix protein prominent in malignant glioma, increases NOTCH activity in BTIC to pr

208 In addition, in mice bearing orthotopic malignant gliomas, inhibition with bevacizumab of vascul

209 Malignant glioma is a consistently fatal brain cancer.

210 Malignant glioma is a formidable disease that commonly l

211 Malignant glioma is rapidly fatal, and ionizing radiatio

212 Malignant glioma is the most common central nervous syst

213 te aggressive therapies, median survival for malignant gliomas is less than 15 months.

214 tors alone in the treatment of patients with malignant gliomas is only modest, potentially because th

215 The role of AQP4 aggregation into OAP in malignant gliomas is still unclear.

216 Overexpression of MGMT in childhood malignant gliomas is strongly associated with an adverse

217 urrently, the most efficacious treatment for malignant gliomas is temozolomide; however, gliomas expr

218 A common pathobiological feature of malignant gliomas is the insidious infiltration of singl

219 A distinct feature of malignant gliomas is the intrinsic ability of single tum

220 most aggressive and least treatable form of malignant glioma, is the most common human brain tumor.

221 as been found to be expressed in a subset of malignant gliomas, its sufficiency for glioma initiation

222 ied highly tumorigenic subpopulations within malignant gliomas, known generally as cancer stem cells.

223 therapeutic agent of choice for treatment of malignant gliomas, leads to induction of CHOP, a major p

224 s embedded within fresh surgical isolates of malignant gliomas lent support to a new paradigm in canc

225 xtent of tumor resection in this subgroup of malignant gliomas located adjacent to eloquent areas fro

226 Metastatic tumors and malignant gliomas make up the majority of cancers in the

227 alpha2 (IL-13Ralpha2) in a majority of human malignant gliomas makes this protein an attractive vacci

228 ese findings suggest that 5hmC regulation in malignant glioma may represent an important determinant

229 The probe delineates malignant glioma, medulloblastoma, prostate cancer, inte

230 Malignant gliomas metastasize throughout the brain by in

231 11) was conducted in children with recurrent malignant glioma (MG) and intrinsic brainstem glioma (BS

232 Malignant glioma (MG) is the most lethal primary brain t

233 CED to deliver CB in patients with recurrent malignant glioma (MG).

234 Malignant gliomas (MG), including grades III and IV astr

235 ), atypical teratoid/rhabdoid tumor (n = 1), malignant glioma (n = 1), and choroid plexus carcinoma,

236 g nude mice (mouse angiosarcoma, n = 18; rat malignant glioma, n = 10).

237 posttreatment tumor tissue of patients with malignant gliomas, NDRG1 was induced and predictive of p

238 viduals with NF1 are prone to optic gliomas, malignant gliomas, neurofibromas, and malignant peripher

239 tcome predictions in patients with recurrent malignant glioma on bevacizumab therapy.

240 overall survival in patients with recurrent malignant glioma on bevacizumab therapy.

241 tly, the ICD of p75NTR was commonly found in malignant glioma patient specimens, suggesting that the

242 With the dismal prognosis for malignant glioma patients, survival predictions become k

243 urgically created resection cavity (SCRC) of malignant glioma patients.

244 de novel therapeutic strategies for treating malignant glioma patients.

245 de novel therapeutic strategies for treating malignant glioma patients.Oncogene advance online public

246 generates a penetrant acute-onset high-grade malignant glioma phenotype with notable clinical, pathol

247 es a fully penetrant, rapid-onset high-grade malignant glioma phenotype with prominent pathological a

248 r and activator of transcription (Stat)3 and malignant glioma phenotype.

249 LD22-4 inhibits the rate of malignant gliomas prepared from U87MG cells in an orthot

250 ged as the treatment of choice for recurrent malignant gliomas, prolonging progression-free survival

251 of rapamycin complex 1 (mTORC1) activity in malignant gliomas promote tumor progression, suggesting

252 tegies, the prognosis for patients harboring malignant gliomas remains dismal.

253 ces and in vivo testing in orthotopic murine malignant glioma revealed preserved nanoparticle diffusi

254 Analysis of human malignant glioma samples indicates that ATF5 expression

255 A variety of cancers, including malignant gliomas, show aberrant activation of STAT3, wh

256 dult brain, but is significantly elevated in malignant glioma specimens and human malignant glioma ce

257 TRIM11 expression levels were upregulated in malignant glioma specimens and in high-grade glioma-deri

258 as found to be markedly elevated in clinical malignant glioma specimens but nearly undetectable in no

259 are linked to acute inflammatory responses, malignant glioma stem cell metastasis, and chronic infla

260 les in the etiology of primary and recurrent malignant gliomas, suggesting that patient therapy shoul

261 the rationale for targeting angiogenesis in malignant gliomas, summarizes relevant clinical trial re

262 molecular mechanisms by which astrocytes and malignant gliomas suppress monocyte/microglial function

263 ast 20 years, with only 30% of patients with malignant glioma surviving 5 years after diagnosis.

264 controlling magnetic particles for treating malignant glioma that should be applicable to treat a wi

265 Malignant glioma, the most common primary brain tumor, i

266 In primary malignant gliomas, the amplification/alteration of the e

267 nvolves the role of cytomegalovirus (CMV) in malignant gliomas, the most common form of primary brain

268 Malignant gliomas, the most common type of primary brain

269 ocused on immunotherapy for the treatment of malignant gliomas, the prognosis for this disease remain

270 ntiangiogenic drugs are increasingly used in malignant glioma therapy.

271 uing debates around cytoreductive surgery in malignant gliomas, there is broad consensus that increas

272 Here, we show that human malignant glioma tissues and also tumor-initiating cells

273 P) is also ubiquitously expressed in primary malignant glioma tissues and cell lines.

274 dy was undertaken in patients with recurrent malignant glioma to determine the efficacy and safety of

275 shifts, allowing T cells from patients with malignant glioma to function in vitro at levels equivale

276 lar pathways involved in the pathogenesis of malignant glioma transformation and progression.

277 ll proliferation, in patients with recurrent malignant gliomas treated with bevacizumab in combinatio

278 Patients with recurrent malignant gliomas treated with biweekly cycles of bevaci

279 (V) compared with MB(C) for angiosarcoma and malignant glioma tumors (P < .001).

280 Glioblastoma multiforme (GBM) is the most malignant glioma type with diffuse borders due to extens

281 cantly more potent and active, against human malignant glioma U87-MG and U373-MG cells in vitro and i

282 xpressed in several solid cancers, including malignant gliomas, upon adoption of metastatic or invasi

283 Here, we reexamined the HCMV prevalence in malignant gliomas using different methods and began to d

284 dels to investigate the complex ecosystem of malignant gliomas using the Cre/loxP recombination syste

285 efficacy and selectivity of virotherapy for malignant glioma, we designed a strategy to amplify aden

286 es can induce specific CTLs in patients with malignant gliomas, we have examined whether analogue epi

287 Fifty participants with malignant glioma were randomly assigned to either a verb

288 Orthotopic malignant gliomas were established in syngeneic immunoco

289 ults reveal an essential survival pathway in malignant glioma, whereby activation of a RAS-mitogen-ac

290 at develop in the central nervous system are malignant gliomas, which are essentially incurable.

291 aping embryonal tumor formation present with malignant gliomas, which are typically identified in the

292 rty seven patients presumably suffering from malignant gliomas (WHO grade III or IV) according to rad

293 ther knowledge of the molecular pathology of malignant gliomas will result in novel therapies.

294 he kinetics of (18)F-FLT during treatment of malignant glioma with bevacizumab and irinotecan.

295 vir inhibits the growth of xenografted human malignant glioma, with concomitant induction of the proa

296 chemotherapeutic agent for the treatment of malignant gliomas, with significant growth inhibition.

297 tion may be useful in limiting the spread of malignant gliomas within the brain, and that nitrosourea

298 e Hedgehog pathway in established orthotopic malignant glioma xenografts confers a survival advantage

299 <0.001) inhibited the growth of subcutaneous malignant glioma xenografts during the 30-day follow-up

300 their receptors are frequently expressed in malignant gliomas, yet their functions are largely unkno