ライフサイエンスコーパス: glioma cell

1 omide or irradiation increases cell death in glioma cells.

2 developed a model of HuR multimerization in glioma cells.

3 on confer chemosensitization in IDH1-mutated glioma cells.

4 icrotube (TM)-mediated brain colonization by glioma cells.

5 tion for multikinase inhibitor resistance in glioma cells.

6 to promote the survival of murine proneural glioma cells.

7 ed tsA201 cells and in glial cell-derived C6 glioma cells.

8 for the in vitro and in vivo destruction of glioma cells.

9 ion of stem cell markers and self-renewal in glioma cells.

10 ive effects and triggered apoptosis of human glioma cells.

11 lly bound to cervical, lung, esophageal, and glioma cells.

12 matrix stiffness and fibronectin density in glioma cells.

13 ivity and feedforward expression of NLGN3 in glioma cells.

14 p-regulates SK1 expression during hypoxia in glioma cells.

15 ss of EGFRvIII-driven Met phosphorylation in glioma cells.

16 c interaction between EGFRwt and EGFRvIII in glioma cells.

17 l cells treated with conditioned medium from glioma cells.

18 tion of the Fas receptor pathway in p53(+/+) glioma cells.

19 ng NK immune surveillance that can eradicate glioma cells.

20 w role for Myc in the proficient division of glioma cells.

21 TR) is a novel mediator of invasion of human glioma cells.

22 H1 into Ras-transformed cells or established glioma cells.

23 maitotoxin-elicited Ca(2+) influx in rat C6 glioma cells.

24 uman colonic T84 epithelial cells or U251-MG glioma cells.

25 nvasion by stimulating amoeboid migration of glioma cells.

26 revent vascular microthrombosis triggered by glioma cells.

27 lC-3 colocalize to the invading processes of glioma cells.

28 emozolomide, and irradiation induced QPRT in glioma cells.

29 l signaling proteins that are deregulated in glioma cells.

30 orescent protein (GFP) expressing human U251 glioma cells.

31 miR-145 in glial tumors and its function in glioma cells.

32 PD-L1-induced caspase-dependent apoptosis of glioma cells.

33 ntly decreased the migration and invasion of glioma cells.

34 s, and fibroblasts, cortical tubers, and U87 glioma cells.

35 toma and UVW/noradrenaline transporter (NAT) glioma cells.

36 alleles are required for D-2HG production in glioma cells.

37 stin and differentiation status of malignant glioma cells.

38 silencing of CTGF decreased the migration of glioma cells.

39 C12 cells, cultured cortical neurons, and C6 glioma cells.

40 am of the PDGFRalpha-PI3K/SHP-2 signaling in glioma cells.

41 of the mevalonate pathway in densely-plated glioma cells.

42 between presynaptic neurons and postsynaptic glioma cells.

43 eness, migration, and apoptotic potential in glioma cells.

44 and downregulation of DNA repair pathways in glioma cells.

45 f TRL-derived lipid nutrients by surrounding glioma cells.

46 gregation into OAP influences the biology of glioma cells.

47 n tumor characterized by highly infiltrative glioma cells.

48 and provides a source of lipid nutrients for glioma cells.

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

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

51 come together during HuR multimerization in glioma cells.

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

53 nd are associated with the transformation of glioma cells along the very aggressive mesenchymal pheno

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

55 rs compared to normal brain specimens and in glioma cells and glioma stem cells (GSCs) compared to no

56 al activity of GPC1 expression in both human glioma cells and normal astrocytes in vitro.

57 cells were analyzed in coculture with human glioma cells and normal rat astrocytes: CNS coculture ca

58 sely reflect the oxygenation status of donor glioma cells and patient tumors, and that the exosomal p

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

60 exchanger NHE5 is abundantly expressed in C6 glioma cells and plays an important part in regulating c

61 cytotoxic effects of temozolomide therapy on glioma cells and significantly prolonged time to tumor r

62 In vitro hypoxia experiments with glioma cells and studies with patient materials reveal t

63 e differences in channel activity between C6 glioma cells and tsA201 cells expressing L166Q and A167V

64 nant cells, larger pools of undifferentiated glioma cells, and an increase in macrophage over microgl

65 er65, protein synthesis and proliferation in glioma cells, and reduced tumor growth in an orthotopic

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

67 onstrated that galectin-1-deficient GL26-Cit glioma cells are approximately 3-fold more sensitive to

68 In-vitro studies on glioma cells are used to compare the efficiency of the C

69 GL261 murine glioma cells are widely used as a syngeneic animal model

70 S2, also known as iNOS) originating from the glioma cells as a driving stimulus in the control of mic

71 e diverse pathways followed by invading U251 glioma cells as observed by our multimodal imaging appro

72 relevant mouse model of glioma and find that glioma cells, as they populate the perivascular space of

73 4 (AQP4-OAP) triggered cell shape changes in glioma cells associated with alterations to the F-actin

74 This approach permits in situ analysis of glioma cells at the molecular and genomic level as well

75 as a niche supporting the growth of invasive glioma cells away from the primary tumor.

76 myelin (SM) levels, which is markedly low in glioma cells before treatment.

77 These findings suggest that glioma cells benefit from TIGAR expression by (i) improv

78 directs adenovirus to IL13Ralpha2 expressing glioma cells both in vitro and in vivo.

79 eration of chemosensitive and chemoresistant glioma cells but did not display toxicity against non-ca

80 eventually leading to necrotic death of U251 glioma cells but not primary astrocytes.

81 ated in CD133-ve glioma stem cells (GSC) and glioma cells but unmethylated in CD133+ve ones.

82 Fibulin-3 is a protein secreted by glioma cells, but absent in normal brain, that promotes

83 Human malignant glioma cells, but not nonneoplastic astrocytes, expresse

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

85 PEAMOtecan kills glioma cells by mitotic catastrophe with p53 mutant/knoc

86 l activity can foster malignant behaviour of glioma cells by non-synaptic paracrine and autocrine mec

87 roliferative and nonproliferative high-grade glioma cells by programmed necrosis.

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

89 d anchorage-independent growth, and rendered glioma cells chemosensitive.

90 s, including extensive lipid droplets within glioma cells, collagen deposition in gliosarcoma, and ir

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

92 s derived from microglial cells treated with glioma cell-conditioned medium to induce angiogenesis.

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

94 "mis-trafficking" caused by UCD38B in human glioma cells corresponds to mitochondrial depolarization

95 Conversely, galectin-1-deficient glioma cells could be eradicated by host NK cells before

96 of infection was positively correlated with glioma cell death.

97 lacked PD-L1 and were defective in inducing glioma cell death; this effect was reversed on PD-L1 gen

98 er, these findings illustrate a mechanism of glioma cell defense against an incoming infection by oHS

99 Thus, indolent human glioma cells deficient for TF remain viable but permanen

100 U1242MG glioma cells depleted of NPM1 presented with altered sil

101 y, we found that in mouse brain slices, U251 glioma cells do not follow white matter tracts but rathe

102 uced proliferation and increased death of C6 glioma cells, effects that can be partially rescued by o

103 enograft studies show that DcR1 depletion in glioma cells enhances the efficacy of temozolomide.

104 nant progression in glioblastoma multiforme, glioma cells exhibit intrinsic resistance toward many ki

105 Human glioma cells expressing both a caspase-3 sensor as a sur

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

107 m7GTP to enrich for initiation complexes in glioma cells followed by mass spectrometry-based quantit

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

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

110 Our work showed that ribavirin inhibits glioma cell growth and migration, and increases cell cyc

111 mpact on patient survival, primarily because glioma cells have an inherent propensity to invade into

112 Most therapeutic approaches targeting glioma cells have failed.

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

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

115 Migration of human glioma cells (hGCs) within the brain parenchyma makes gl

116 tion of chemoattractant signals toward which glioma cells home.

117 OPCs and highly proliferative Olig2-positive glioma cells identified all the transcripts associated w

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

119 Expression profiling in glioma cells identified SAT1 target genes that distingui

120 e study of the in vivo radiation response of glioma cells in a mouse model of proneural glioblastoma.

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

122 ct communication channel between neurons and glioma cells in different disease models and human tumou

123 combined profiling and functional studies of glioma cells in glioblastoma multiforme (GBM) models est

124 roach has been used to assess the density of glioma cells in murine orthotopic xenografts models and

125 y reduce TM-associated brain colonization by glioma cells in patients.SIGNIFICANCE STATEMENT In this

126 I efficiently inhibited the proliferation of glioma cells in the presence of serum by activating the

127 rest and mitigated the proliferation rate of glioma cells in vitro and in vivo.

128 nti-tumoral effects in vivo, despite killing glioma cells in vitro, suggesting a TME-mediated resista

129 glioblastoma cell lines and patient-derived glioma cells in vitro.

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

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

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

133 s of great importance as the highly invasive glioma cells infiltrated into normal brain tissue are re

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

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

136 Collectively, our findings show how glioma cells influence the tumor microenvironment to rec

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

138 Overexpression of IGFBP3 in glioma cells inhibited cell proliferation in vitro and i

139 Dock180(WT), protein in EGFRvIII-expressing glioma cells inhibited receptor-stimulated cell prolifer

140 These findings were corroborated in GL261 glioma cells intracranially transplanted in mice express

141 Glioma cells invade in distinct patterns, possibly deter

142 ic acid (NA), an essential vitamin, inhibits glioma cell invasion in vitro and in vivo.

143 ts its function from inhibiting to promoting glioma cell invasion.

144 Functionally, miR-491-3p inhibited glioma cell invasion; overexpression of both miR-491-5p

145 egulates Id-1 gene expression and associated glioma cell invasiveness and self-renewal.

146 expression levels positively correlate with glioma cell invasiveness in culture and with histopathol

147 is unable to aggregate into OAP, ameliorated glioma cell invasiveness, improved cell migration, and i

148 ose that oncogenic activation of EGFRvIII in glioma cells is driven by co-expressed activated EGFR wi

149 ced variant initially described within human glioma cells is the glioma BK (gBK) channel.

150 the contrary, the overexpression of IL-8 in glioma cells lacking DeltaEGFR potently enhanced their t

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

152 ing of CIC protein to the nucleus in a human glioma cell line expressing IDH1(R132H) and overexpressi

153 sts were found to inhibit proliferation of a glioma cell line in vitro.

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

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

156 FIA axis suppresses tumorigenesis in a human glioma cell line.

157 rase activity and CD133 levels in GSC and in glioma cell line.

158 ll gliomas or robust 53BP1 gene silencing in glioma cell lines (but not 53BP1 heterozygous tumors or

159 ects of VP without light activation on human glioma cell lines (LN229 and SNB19).

160 eutic target in a panel of diverse pediatric glioma cell lines (SF188, KNS42, UW479 and RES186) using

161 y and late endosomes in four different human glioma cell lines after UCD38B treatment, followed by ca

162 ntration of alpha-ketoglutarate substrate in glioma cell lines and could be suppressed by ectopic ove

163 ents and GICs derived from xenografted human glioma cell lines and determined that miR-33a promotes G

164 In glioma cell lines and glioma-stem-like cells, HDAC6 inhi

165 iR-491-5p and -3p inhibited proliferation of glioma cell lines and impaired the propagation of glioma

166 Glioma cell lines and low passage primary cultures were

167 prone H-Ras(12V) knock-in mice as well as in glioma cell lines and patient-derived GBM specimens exhi

168 ha-driven glioma EMT, invasion and growth in glioma cell lines and patient-derived glioma stem cells

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

170 ted glioma EMT, tumor growth and invasion in glioma cell lines and patient-derived GSCs.

171 pression and was directly induced by Sox2 in glioma cell lines and patient-derived neurospheres.

172 sed on malignant glioma and are cytotoxic to glioma cell lines and primary GBM explants.

173 pha was expressed in a subset of established glioma cell lines and primary glioblastoma cell cultures

174 We then used human glioma cell lines as model astroglial cells to represent

175 Suppression of BCAT1 in glioma cell lines blocked the excretion of glutamate and

176 ectopic expression of DeltaEGFR in different glioma cell lines caused up to 60-fold increases in the

177 Glioma cell lines expressing the M23-AQP4 isoform, which

178 GBMs and glioma cell lines had low levels of NPTX2 transcripts, w

179 GBM and glioma cell lines had low levels of ULK2 transcripts, wh

180 g HLA-G gene expression were investigated in glioma cell lines U251MG, D247MG, and U138MG.

181 By treating glioma cell lines with the polyclonal N-20 antibody agai

182 Rodent (C6) and human (U251) glioma cell lines, and non-tumor human astrocytes (HA) a

183 th and migration of several human and murine glioma cell lines, as well as human glioblastoma stem-li

184 ctive of the drug sensitivities of different glioma cell lines, in comparison with other existing met

185 tured murine (GL261) and human (U251, U87MG) glioma cell lines, increased by approximately 25% when t

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

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

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

189 Functional analysis of ECONEXIN in glioma cell lines, U87 and U251, showed it was dominantl

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

191 face GRP78 to the survival and growth of the glioma cell lines.

192 urface-localized GRP78 in diverse high-grade glioma cell lines.

193 esses c-Myc expression and activity in human glioma cell lines.

194 osis in otherwise highly apoptosis-resistant glioma cell lines.

195 n of CD133 promoter in glioma stem cells and glioma cell lines.

196 tial flow promotes cell invasion in multiple glioma cell lines.

197 In rat 9L glioma cells loaded with nanoemulsion, the local pH of n

198 ith the maximal levels found in the invading glioma cells located within normal brain tissue; and (ii

199 n of Akt, Erk1/2, Rac1 and Cdc42 activities, glioma cell migration and survival in vitro and tumor gr

200 In addition miR-145 regulates glioma cell migration by targeting CTGF which downregula

201 ckdown of SGEF expression by shRNA decreases glioma cell migration in vitro and invasion ex vivo.

202 as well as Fn14 overexpression can stimulate glioma cell migration, invasion and resistance to chemot

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

204 n of Dock180, stimulates Rac1 activation and glioma cell migration.

205 brogated the inhibitory effect of miR-145 on glioma cell migration.

206 Here we analyze rat C6 and patient-derived glioma cell motility in vitro using micropatterned linea

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

208 ECFNs; optimum approximately 1 kPa) and U251 glioma cells (optimum approximately 100 kPa).

209 efficient replication and oncolysis in MO59J gliomas cells; other gliomas tested required the entire

210 opic tumor tissue occurred preferentially in glioma cells over microglial cells.

211 LuIII selectively infected glioma cells over normal glial cells in vitro.

212 cultured astrocytes (control condition) and glioma cells (pathological condition) clearly distinguis

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

214 blockade alone is inefficient in stimulating glioma cell phagocytosis.

215 ss-associated NKG2D ligands on TMZ-resistant glioma cells, potentially rendering them vulnerable to g

216 In contrast, silencing expression of MCSF in glioma cells prevented tube formation of human umbilical

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

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

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

220 (pY481) dramatically attenuates EGF-promoted glioma cell proliferation, tumor growth and resistance t

221 1, and Nav3 demonstrates heightened EGFRvIII-glioma cell proliferation.

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

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

224 Glioma cells recruit and exploit microglia (the resident

225 endothelial cell motility and association to glioma cells, reduced endothelial cell sprouting, and in

226 molecular consequences of NLGN3 secretion in glioma cells remain unknown.

227 as a way to deliver cytotoxic agents to the glioma cells remaining after surgical resection while sp

228 ectively, our results suggest that stem-like glioma cells reprogram their metabolism to self-renew an

229 Stem-like glioma cells reside within a perivascular niche and disp

230 ype; (ii) Fn14 expression can be detected in glioma cells residing in both the tumor core and invasiv

231 rvival were affected upon AEBP1 silencing in glioma cells, resulting in cell death.

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

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

234 In vitro uptake assays in mouse DBT gliomas cells revealed that (S)-[(18)F]FAMPe enters cell

235 d the formation of cell-cell junctions by C6 glioma cells seeded on top of electrodes.

236 -mediated gliovascular coupling is lost, and glioma cells seize control over the regulation of vascul

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

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

239 therefore be a valuable strategy to enhance glioma cell sensitivity toward spontaneously occurring o

240 In BDNF-deficient mice (bdnftm1Jae/J) and in glioma cells silenced for TrkB receptor expression, olea

241 Glioma-cell-specific genetic perturbation of AMPA recept

242 omoting inhibition of adenylyl cyclase in C6 glioma cells stably expressing the P2Y14-R was shifted t

243 e examined the roles of miR-124 and SNAI2 in glioma cell stem-like traits.

244 el and targetable molecular circuit by which glioma cell stemness and tumor-propagating capacity are

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

246 Here we show that malignant glioma cells suppress NK immune surveillance by overexpr

247 ing macrophages secrete SPP1, which sustains glioma cell survival and stimulates angiogenesis.

248 g 2 (ID2), which we found to be required for glioma cell survival.

249 significant impact against the infiltrative glioma cells that are a major source of recurrence.

250 In contrast, neither causes changes in glioma cells that have higher cholesterol content.

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

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

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

254 entry oHSVs are preferentially taken up into glioma cells through the endosomal pathway rather than v

255 LX5-WNT5A axis governs the diffuse spread of glioma cells throughout the brain parenchyma, contributi

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

257 r the response of three different subsets of glioma cells to a clinically relevant chemotherapeutic a

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

259 Olig2 deletion further sensitizes glioma cells to EGFR inhibitors and extends the lifespan

260 tumors or partial gene knockdown) sensitizes glioma cells to ionizing radiation (IR), both in vitro a

261 ully repair the damaged DNA upon exposure of glioma cells to IR with a consequent prolonged cell-cycl

262 ght be an important determinant in orienting glioma cells to persist or perish.

263 ectively decrease tumor growth and sensitize glioma cells to radiation therapy.

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

265 teracting Ser/Thr kinase 1 (MNK1) sensitizes glioma cells to the mTORC1 inhibitor rapamycin through a

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

267 The underlying molecular mechanism used by glioma cells to transform microglia into a tumor-support

268 and consequently restores the sensitivity of glioma cells to tyrosine kinase inhibitors in vivo in pr

269 inhibitor protein PME-1 drives resistance of glioma cells to various multikinase inhibitors.

270 ic antidepressant treatment of rats or of C6 glioma cells, tracks with the delayed onset of therapeut

271 actor (CTGF) as a novel target of miR-145 in glioma cells; transfection of the cells with this miRNA

272 We used time-course RNA-seq data from glioma cells treated with dbcAMP (a cAMP activator) as a

273 These effects were also observed in glioma cells treated with the Aurora-A inhibitor TC-A231

274 ellular spheroids established with malignant glioma cells, unlike conventional two-dimensional (2D) c

275 re, we show that NF1-loss in patient-derived glioma cells using shRNA increases self-renewal, heighte

276 Treatments of glioma cells using the PKA inhibitors H-89 and KT5720, o

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

278 NDI/2DG-induced death of glioma cells was partly prevented by lysosomal cathepsin

279 multiforme (GBM) cell line, highly malignant glioma cells, was first injected into 5-week-old athymic

280 Glioma cells were evaluated for CXCR4 expression and pol

281 As a proof-of-concept demonstration, human glioma cells were labeled with liposomes with or without

282 C6 glioma cells were treated with 10 uM ketamine for 15 min

283 In contrast, differentiated glioma cells were unaffected by the targeting of purine

284 Sustained treatment of C6 glioma cells, which lack 5-hydroxytryptamine transporter

285 ULK2 also inhibited the growth of glioma cells, which required autophagy induction as kina

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

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

288 Here, we demonstrate that human glioma cells whose migration is guided by bradykinin gen

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

290 Transfection of glioma cells with miR-145 mimic or transduction with a l

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

292 Glioma cells with one or two TMs were mainly responsible

293 t synaptic communication between neurons and glioma cells with potential clinical implications.

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

295 Glioma cells with stem cell traits are thought to be res

296 role in balancing the division properties of glioma cells with stemness properties.

297 ctive activity (EC50 = 0.26-1.8 muM) against glioma cells with the IDH1 R132H mutation.

298 a relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed

299 llular Ca(2+) concentration in 1321N1 and C6 glioma cells without altering TRAP-6 and carbachol Ca(2+

300 owth of IDH1-mutant--but not IDH1-wild-type--glioma cells without appreciable changes in genome-wide