ライフサイエンスコーパス: oligodendroglioma

1 malignantly transformed oligodendroglioma (m-oligodendroglioma).

2 a potential clinical strategy for treating m-oligodendroglioma.

3 These mice developed low-grade oligodendroglioma.

4 man chromosome 1p, which is commonly lost in oligodendroglioma.

5 in some tumor types, particularly anaplastic oligodendroglioma.

6 tional repressor mutated in the brain cancer oligodendroglioma.

7 r surgical strategies for LGGs, particularly oligodendroglioma.

8 he pathogenesis and therapeutic targeting of oligodendroglioma.

9 d Huntington's disease and one had a grade 2 oligodendroglioma.

10 elet-derived growth factor-induced malignant oligodendroglioma.

11 ntribute to the distinctive biology of human oligodendroglioma.

12 FBP2-mediated progression of PDGFB-initiated oligodendroglioma.

13 eness to therapy in patients with anaplastic oligodendroglioma.

14 which is observed in over 50% of anaplastic oligodendrogliomas.

15 to transduce primary human astrocytomas and oligodendrogliomas.

16 errant methylation in human astrocytomas and oligodendrogliomas.

17 in a specific subset of low-grade, indolent oligodendrogliomas.

18 grade and is required to sustain high-grade oligodendrogliomas.

19 osome, a locus that is deleted in 50%-80% of oligodendrogliomas.

20 view of the genes and mechanisms underlying oligodendrogliomas.

21 gliomas, 28 glioblastomas and 22 anaplastic oligodendrogliomas.

22 ression profiling in morphologically classic oligodendrogliomas.

23 predictor of chemosensitivity in anaplastic oligodendrogliomas.

24 analyzed these three genes in 72 anaplastic oligodendrogliomas.

25 including astrocytic neoplasms and low-grade oligodendrogliomas.

26 ssion from well-differentiated to anaplastic oligodendrogliomas.

27 erapeutic response and prolonged survival in oligodendrogliomas.

28 ese cases were among the 24 (42%) anaplastic oligodendrogliomas.

29 primary central nervous system lymphoma and oligodendrogliomas.

30 of adult patients with recurrent hemispheric oligodendrogliomas.

31 in adult patients with recurrent hemispheric oligodendrogliomas.

32 ould contribute to the observed formation of oligodendrogliomas.

33 tes into survival benefits for patients with oligodendrogliomas.

34 survival curves separated after 6-8 years in oligodendrogliomas.

35 and grade 2 or 3 IDH-mutant, 1p19q-codeleted oligodendrogliomas.

36 ations to classify tumors as astrocytomas or oligodendrogliomas.

37 than in low-grade astrocytomas and low-grade oligodendrogliomas.

38 on the chromosome arms frequently deleted in oligodendrogliomas.

39 arly genetic alterations in astrocytomas and oligodendrogliomas.

40 ut are distinct from the 1p abnormalities in oligodendrogliomas.

41 apy and improved prognosis for patients with oligodendrogliomas.

42 ad glioblastoma multiforme, 2 had anaplastic oligodendroglioma, 1 had anaplastic ependymoma, and 1 ha

43 anaplastic gliomas [n = 48; astrocytoma, 28; oligodendroglioma, 14; mixed glioma, six]) received trea

44 microsatellite markers was detected in four oligodendrogliomas (17.4%), one pituitary adenoma (3.2%)

45 Thirty-three oligodendrogliomas (25 with 1p/19q loss) and 53 oligoast

46 mas met the inclusion criteria, including 19 oligodendrogliomas, 26 astrocytomas, and 11 mixed glioma

47 umours (256 glioblastoma, 89 astrocytoma, 58 oligodendroglioma; 338 primary, 65 recurrence).

48 glioblastomas, 3 of 4 mixed gliomas, 4 of 11 oligodendrogliomas, 6 of 8 astrocytomas, 2 of 2 meningio

49 previously demonstrated chemosensitivity of oligodendrogliomas, a combined approach of histologic an

50 nd mechanisms contributing to the genesis of oligodendrogliomas, a subtype of primary brain tumors.

51 Like neuroblastoma, oligodendrogliomas also show a high frequency of deletio

52 t glioma, anaplastic astrocytoma, anaplastic oligodendroglioma, anaplastic oligoastrocytoma, and brai

53 ecific domains were identified in anaplastic oligodendrogliomas, anaplastic astrocytomas, glioblastom

54 endroglioma), intermediate-grade (anaplastic oligodendroglioma and anaplastic astrocytoma), and high-

55 /total N-acetylaspartate [tNAA], P = .0054), oligodendroglioma and astrocytoma (eg, tumoral Gln/tNAA,

56 ytoma (eg, tumoral Gln/tNAA, P = .0033), and oligodendroglioma and glioblastoma (eg, tumoral Glu/tNAA

57 en deleted in high-grade gliomas (anaplastic oligodendroglioma and glioblastoma), we investigated the

58 es of infiltrating astrocytic brain cancers (oligodendroglioma and high-grade astrocytoma) and found

59 Co-deletion of 1p/19q is a hallmark of oligodendroglioma and predicts better survival.

60 ined loss of 1p and 19q in 64% (21 of 32) of oligodendrogliomas and 67% (6 of 9) of oligoastrocytomas

61 as an objective, ancillary tool for grading oligodendrogliomas and a potential approach for classify

62 The cells of origin for oligodendrogliomas and astrocytomas are not known but ar

63 otal 1p and 19q are found in the majority of oligodendrogliomas and considered as a diagnostic marker

64 cally relevant tissues from 20 patients with oligodendrogliomas and grade II-IV astrocytomas.

65 70% of WHO grade II and III astrocytomas and oligodendrogliomas and in glioblastomas that developed f

66 (21 low-grade astrocytomas and 14 low-grade oligodendrogliomas and low-grade mixed oligoastrocytomas

67 FAP-V(12)Ha-ras;GFAP-EGFRvIII mice developed oligodendrogliomas and mixed oligoastrocytoma tumors, in

68 n data clearly delineated PAs from low-grade oligodendrogliomas and normal white matter.

69 the molecular analysis of 1p and 19q loss in oligodendrogliomas and oligoastrocytomas in archival rou

70 TNAP2 expression decreased by tumor grade in oligodendrogliomas and PTPRD expression also in IDH-muta

71 omas, or tumors with characteristics seen in oligodendrogliomas and small-cell astrocytomas, indicati

72 IDHi on the cellular hierarchies that drive oligodendrogliomas and suggests a genetic modifier that

73 ression is specifically decreased in primary oligodendrogliomas and up-regulated in glioma cell lines

74 ration decreased rapidly in 1p/19q codeleted oligodendrogliomas and with a slower time course in astr

75 ere included: 10 glioblastomas, 1 anaplastic oligodendroglioma, and 1 anaplastic astrocytoma.

76 nd paediatric glioblastoma (GBM), anaplastic oligodendroglioma, and diffuse intrinsic pontine glioma

77 gliomas including glioblastoma, astrocytoma, oligodendroglioma, and NF1-related low-grade neuroglioma

78 s with supratentorial low-grade astrocytoma, oligodendroglioma, and oligoastrocytoma found somewhat l

79 gulator of cell fate in neurodevelopment and oligodendroglioma, and suggest that its loss contributes

80 arrangement displayed histologic features of oligodendroglioma, and the gene products of both rearran

81 There were 21 low-grade astrocytomas, 64 oligodendrogliomas, and 16 mixed oligoastrocytomas.

82 in 162 diffuse gliomas (79 astrocytomas, 52 oligodendrogliomas, and 31 mixed oligoastrocytomas), col

83 ss II tumors are similar to 1p/19q codeleted oligodendrogliomas, and class III represents infiltrativ

84 ligodendrogliomas, in 18/23 (83%) anaplastic oligodendrogliomas, and in 3/8 (38%) oligoastrocytomas g

85 pulation of low-grade gliomas (astrocytomas, oligodendrogliomas, and mixed gliomas) to improve our un

86 w-grade gliomas (LGGs) include astrocytomas, oligodendrogliomas, and mixed oligoastrocytomas (WHO gra

87 /19q intact gliomas, including astrocytomas, oligodendrogliomas, and oligoastrocytomas, formed a thir

88 tomas, a second grouped the 1p/19q codeleted oligodendrogliomas, and the mixture of remaining 1p/19q

89 oastrocytomas with 1p/19q LOH are related to oligodendrogliomas, and those with p53 mutations are rel

90 Anaplastic oligodendroglioma, another type of malignant glioma, pro

91 Anaplastic oligodendroglioma (AO) are rare primary brain tumours th

92 lastic oligoastrocytoma (AOA) and anaplastic oligodendroglioma (AO)] remain subjective, and the exist

93 aplastic astrocytoma [AA], n = 6; anaplastic oligodendroglioma [AO], n = 2; gliosarcoma [GS], n = 1;

94 Anaplastic oligodendroglioma are chemotherapy-sensitive tumors.

95 ted with angiogenesis and proliferation in m-oligodendroglioma are not well understood.

96 These anaplastic oligodendrogliomas are characterized by increased cellul

97 Oligodendrogliomas are the second most common malignant

98 Oligodendrogliomas are the second most common type of gl

99 Oligodendrogliomas are typically associated with the mos

100 plus chemotherapy and histologic findings of oligodendroglioma as favorable prognostic variables for

101 e model, a decreased incidence of anaplastic oligodendroglioma as well as prolonged survival was obse

102 r-derived glioma stem-like cells (GSCs) from oligodendroglioma as well as proneural and mesenchymal g

103 t including also IDH-mutant astrocytomas and oligodendrogliomas as well as in normal brain samples fr

104 gliomas, meningiomas, medulloblastomas, and oligodendrogliomas, as well as peripheral nervous system

105 The samples analyzed included oligodendroglioma, astrocytoma, and meningioma tumors of

106 ed out on 36 human glioma samples, including oligodendroglioma, astrocytoma, and oligoastrocytoma, al

107 senting various human brain tumors including oligodendroglioma, astrocytoma, pilocytic astrocytoma, o

108 a from IDH1/2 mutant acute myeloid leukemia, oligodendroglioma, astrocytoma, solid papillary breast c

109 alities, can serve as the cell of origin for oligodendrogliomas, astrocytomas, or mixed gliomas.

110 s was 2-fold lower (P < 0.03), and for mixed oligodendroglioma-astrocytomas, the mean was 4-fold lowe

111 de insight into the cellular architecture of oligodendrogliomas at single-cell resolution and support

112 particular MIB-1, may be useful in assessing oligodendroglioma behavior, whereas their role in malign

113 DH-wildtype astrocytomas and 1p19q-codeleted oligodendrogliomas but not in IDH-mutant astrocytomas.

114 for modelling more diffuse astrocytomas and oligodendrogliomas, but could be tuned to improve the re

115 ua (CIC) occur in approximately 50% of human oligodendrogliomas, but mechanistic links to pathogenesi

116 ma, and suggest that its loss contributes to oligodendroglioma by promoting proliferation and an OPC-

117 gle cells from six IDH1 or IDH2 mutant human oligodendrogliomas by RNA sequencing (RNA-seq) and recon

118 profiles between IDH-mutant astrocytoma and oligodendroglioma can be primarily explained by distinct

119 servation of uncertain significance in human oligodendroglioma, can initiate oligodendroglioma in the

120 ligodendroglia circRNA landscapes in the HOG oligodendroglioma cell line, distinct from neuronal circ

121 n, we generated Cic-deficient mice and human oligodendroglioma cell models.

122 Human oligodendroglioma cells also demonstrated calcium mobili

123 fficient to abolish self-renewal capacity of oligodendroglioma cells and downregulate genes involved

124 Transplanting wild-type oligodendroglioma cells into the brain generated lethal

125 Intact human oligodendroglioma cells specifically bound [3H]SQ29,548

126 s in neonatal rat oligodendrocytes and human oligodendroglioma cells was investigated using immunocyt

127 2 is essential for tumor initiation by mouse oligodendroglioma cells, and they illustrated a Sox2-dir

128 In patient-derived oligodendroglioma cells, CIC re-expression or ETV5 block

129 r protein on both oligodendrocytes and human oligodendroglioma cells.

130 of myelinated fibers in areas infiltrated by oligodendroglioma cells.

131 ular pH and attenuates acid load recovery in oligodendroglioma cells.

132 0 GAP domain caused a decreased incidence of oligodendrogliomas compared with that observed with PDGF

133 mors were diagnosed as glioblastomas with an oligodendroglioma component before the World Health Orga

134 Upon culture, one oligodendroglioma contained an unbalanced 45,XX,t(1;19)(

135 t human OLIG genes are expressed strongly in oligodendroglioma, contrasting absent or low expression

136 s clear that p73 is not a candidate gene for oligodendroglioma despite its location in the frequently

137 orted by the fact that human astrocytoma and oligodendroglioma display a high degree of overlap in gl

138 oligodendroglioma (or oligoastrocytoma with oligodendroglioma dominant) in 68%.

139 More than 80% of oligodendrogliomas exhibit LOH for 1 p and 19q alleles.

140 , including an exon defined by an anaplastic oligodendroglioma expressed sequence tag, and spans at l

141 7 of 12 glioblastoma multiforme, and 2 of 6 oligodendrogliomas) expressed EGFRvIII, as determined by

142 gically classic glioblastomas and anaplastic oligodendrogliomas follow markedly different clinical co

143 Oligodendroglioma frequently (> or = 70%) responds to ra

144 ii) codeletion of 1p and 19q differentiating oligodendrogliomas from astrocytomas; (iii) IDH1/2 mutat

145 ngle-nucleus RNA-sequencing three IDH-mutant oligodendrogliomas from patients who derived clinical be

146 rocytoma, anaplastic astrocytoma, anaplastic oligodendroglioma, glioblastoma multiforme, gliomatosis

147 subsequently induced angiogenesis to promote oligodendroglioma growth and malignant transformation.

148 f ISL2 in regulating angiogenesis to promote oligodendroglioma growth and malignant transformation.

149 overall degree of enzyme activation, whereas oligodendrogliomas had the least.

150 Most oligodendrogliomas have chromosomes 1p/19q co-deletion a

151 H-mutated genotypes, between astrocytoma and oligodendroglioma histologies, as well as for tumors tha

152 (P < .01), large tumor volume (P < .01), and oligodendroglioma histopathologic type (P = .02).

153 We profiled >200 metabolites in human oligodendroglioma (HOG) cells to determine the effects o

154 toma, isocitrate dehydrogenase (IDH) mutant; oligodendroglioma, IDH mutant and 1p/19q codeleted; and

155 ularly confirmed glioblastoma, IDH-wildtype; oligodendroglioma, IDH-mutant and 1p/19q codeleted; and

156 g to the 2016 WHO classification system: (1) oligodendroglioma, IDH-mutant and 1p19q co-deleted (n =

157 mbers of methylated CpG sites were found for oligodendroglioma, IDH-mutant and 1p19q co-deleted.

158 arily responsible for fuelling the growth of oligodendroglioma in humans.

159 nce in human oligodendroglioma, can initiate oligodendroglioma in the mouse.

160 neural progenitors induced the formation of oligodendrogliomas in about 60% of mice by 12 wk of age;

161 was seen in 17/23 (74%) well-differentiated oligodendrogliomas, in 18/23 (83%) anaplastic oligodendr

162 enomenon was found with grade III anaplastic oligodendrogliomas, in which stronger EGFR expression wa

163 of prolonged survival in patients with pure oligodendroglioma, independent of tumor grade.

164 with 24 primary glioma tissues of low-grade (oligodendroglioma), intermediate-grade (anaplastic oligo

165 Oligodendroglioma is an important type of lower-grade gl

166 Oligodendroglioma is characterized by mutations of IDH a

167 archies, suggesting that the architecture of oligodendroglioma is primarily dictated by developmental

168 Adults with newly diagnosed oligodendroglioma, isocitrate dehydrogenase (IDH)-mutant

169 rolonged survival of patients with low-grade oligodendroglioma (LGO) and oligoastrocytoma (LGOA), the

170 ed overall survival among patients with pure oligodendroglioma (log-rank, P =.03) and remained a sign

171 a characteristic of malignantly transformed oligodendroglioma (m-oligodendroglioma).

172 ivated angiogenesis through VEGFA to promote oligodendroglioma malignant transformation.

173 ein-2 (2.2-fold increase, P = .019), and the oligodendroglioma markers oligodendrocyte lineage transc

174 We present evidence that some low-grade oligodendrogliomas may be comprised of proliferating gli

175 umor, Astrocytoma, Ependymoma, Glioblastoma, Oligodendroglioma, Medulloblastoma, Germinoma, and Schwa

176 the first report of ALT in medulloblastomas, oligodendrogliomas, meningiomas, schwannomas, and pediat

177 Inefficient removal of O6MeGua in oligodendrogliomas might also account for their response

178 rimitive neuroectodermal tumor, astrocytoma, oligodendroglioma, mixed glioma, and tumors of the perip

179 on prevalence was 55%, 47%, and 0% among the oligodendrogliomas, mixed oligoastrocytomas, and astrocy

180 naplastic gliomas with mixed astrocytoma and oligodendroglioma morphological features.

181 3), ependymoma (n = 2), meningioma (n = 3), oligodendroglioma (n = 1), and melanoma (n = 12) tumor s

182 30 745), astrocytoma (n=5402; n=10 631), and oligodendroglioma (n=3977; n=9187).

183 7; anaplastic astrocytoma, n = 4; anaplastic oligodendroglioma, n = 2).

184 malignant brain tumors (astrocytoma, n = 17; oligodendroglioma, n = 3) and in nine healthy volunteers

185 as showed that primary MMRD was absent among oligodendrogliomas (none of 67) and uncommon in BRAF(V60

186 nts with IDH-mutant 1p/19q-codeleted grade 3 oligodendroglioma (O3(IDHmt/Codel)) benefit from adding

187 at a third resection had transformed into an oligodendroglioma of WHO grade III.

188 Oligodendrogliomas of all grades overexpress epidermal g

189 , had his diagnosis changed to an anaplastic oligodendroglioma on subsequent central neuropathologic

190 unger than 40 years and in patients who have oligodendroglioma or oligo-dominant histology.

191 ffuse tumor margin on T2-weighted MR images, oligodendroglioma or oligoastrocytoma histopathologic ty

192 o astrocytes induced the formation of either oligodendrogliomas or mixed oligoastrocytomas in about 4

193 Patients with recurrent anaplastic oligodendrogliomas or oligoastrocytomas and recurrent lo

194 9%; anaplastic astrocytomas, 11%; anaplastic oligodendrogliomas or oligoastrocytomas, 25%; and gliobl

195 astrocytoma dominant) in 32% of patients and oligodendroglioma (or oligoastrocytoma with oligodendrog

196 survivors of WHO grade I or II astrocytoma, oligodendroglioma, or oligoastrocytoma with clinically a

197 f astrocytomas (10/55) and in 73% (24/33) of oligodendrogliomas (P < 0.0001), and loss of the 19q13.3

198 (6/55) of astrocytomas and in 64% (21/33) of oligodendrogliomas (P < 0.0001).

199 % (21/55) of astrocytomas and 73% (24/33) of oligodendrogliomas (P = 0.0017).

200 glioblastomas, lower grade astrocytomas and oligodendrogliomas (P<0.00001).

201 We then established novel oligodendroglioma patient tumor-derived orthotopic xenog

202 response and overall survival in anaplastic oligodendroglioma patients treated with procarbazine, lo

203 nd postoperative TV <= 4.6 mL in addition to oligodendroglioma patients with either preoperative TV >

204 V <= 4.6 mL who received no chemotherapy and oligodendroglioma patients with preoperative TV <= 43.1

205 study suggests that ISL2 is a biomarker for oligodendroglioma progression and that anti-ISL2 therapy

206 AAV-ISL2-shRNA with temozolomide suppressed oligodendroglioma progression more effectively than eith

207 Anaplastic oligodendrogliomas, pure (AO) and mixed (anaplastic olig

208 patients (379 with astrocytoma and 349 with oligodendroglioma) received no first-line treatment beyo

209 To characterize the changes associated with oligodendroglioma recurrence and progression, we analyze

210 Today, the diagnosis of anaplastic oligodendroglioma requires the presence of both IDH-mt a

211 ta provide evidence that neoplastic cells of oligodendroglioma resemble oligodendrocytes or their pro

212 Anaplastic progression in oligodendrogliomas resulted in a larger number of cells

213 on of Tax1 in primary human astrocytomas and oligodendrogliomas resulted in significantly higher leve

214 Examination of 27 additional oligodendrogliomas revealed 12 and 3 more tumors with mu

215 el predicts for two major groups of gliomas (oligodendroglioma-rich and glioblastoma-rich groups) sep

216 verexpression of OLIG2 was not only found in oligodendroglioma samples and normal neural tissue but a

217 ssion of glypican-1 in human astrocytoma and oligodendroglioma samples compared with nonneoplastic gl

218 Twenty oligodendroglioma samples with 1p36.3 deletions were scr

219 We found that NHE-1 on 1p is silenced in oligodendrogliomas secondary to IDH-associated hypermeth

220 These included 33 astrocytic tumors, 23 oligodendrogliomas, six gangliogliomas, 41 meningiomas,

221 The observed requirement of oligodendroglioma stem cells for Sox2 suggested its rele

222 gy Group (RTOG) clinical trial in anaplastic oligodendroglioma suggested a progression-free survival

223 es DAOY (medulloblastoma), SWB61 (anaplastic oligodendroglioma), SWB40 (anaplastic astrocytoma), and

224 a risk-stratified approach to patients with oligodendrogliomas that optimizes treatment efficacy and

225 Among Mayo Clinic oligodendrogliomas, the prevalence of fusion was 81%.

226 In anaplastic oligodendroglioma, therefore, PTEN is a target of 10q lo

227 yielding a spontaneous model of infiltrating oligodendroglioma, this study demonstrates that astrocyt

228 tor expression in tissue from seven of seven oligodendrogliomas, three of three pilocytic astrocytoma

229 rease in tumor volume did not differ between oligodendrogliomas treated with temozolomide or carmusti

230 or gene involved in astrocytoma, and perhaps oligodendroglioma, tumorigenesis.

231 e and progression, we analyzed two recurrent oligodendroglioma tumors upon diagnosis and after tumor

232 Most tumors including low-grade oligodendrogliomas use telomerase reverse transcriptase

233 rnofsky performance score, cytological type (oligodendroglioma vs astrocytoma), and, potentially, the

234 The median OS for patients with low-grade oligodendroglioma was 9.1 years without fusion and 13.0

235 assic glioblastoma and nonclassic anaplastic oligodendroglioma was not significantly different (P = 0

236 The mean for oligodendrogliomas was 2-fold lower (P < 0.03), and for

237 latelet-derived growth factor (PDGF)-induced oligodendrogliomas was accelerated in mice lacking the c

238 ing the development of growth-factor-induced oligodendroglioma, we identified a critical role for the

239 ppressor gene involved in the development of oligodendrogliomas, we performed mutation analysis of p7

240 ntegrated genetic and epigenetic analysis of oligodendrogliomas, we show that aberrant CpG island met

241 me, and those with anaplastic astrocytoma or oligodendroglioma were 54, 52, and 116 wk, respectively.

242 Unlike astrocytomas, oligodendrogliomas were found consistently to contain fe

243 ), with recurrent supratentorial hemispheric oligodendrogliomas were treated.

244 th grade 2 astrocytoma, oligoastrocytoma, or oligodendroglioma who were younger than 40 years of age

245 ients with astrocytoma, and 74 patients with oligodendroglioma) who underwent two consecutive multimo

246 P is a young woman with a previously treated oligodendroglioma, WHO grade II, with loss of heterozygo

247 onsisting primarily of a moderately cellular oligodendroglioma with distinct areas of a fibrillary as

248 Recent research suggests that oligodendrogliomas with and without the -1p/-19q genotyp

249 as, we performed mutation analysis of p73 in oligodendrogliomas with chromosome 1 p-arm deletions.

250 subset of 14 glioblastomas and 7 anaplastic oligodendrogliomas with classic histology.

251 TP2a is characterized as IDHmut-codel, oligodendrogliomas with high tumor purity.

252 Oligodendrogliomas with loss of heterozygosity on chromo

253 However, grade II oligodendrogliomas with strong EGFR expression and 1p/19

254 ydrogenase (IDH)-mutant and 1p/19q-codeleted oligodendrogliomas with the best prognosis; IDH-mutant a

255 alysis provides information about aggressive oligodendrogliomas with worse prognosis and suggests tha

256 I) glioma (astrocytoma, oligoastrocytoma, or oligodendroglioma) with at least one high-risk feature (

257 I) glioma (astrocytoma, oligoastrocytoma, or oligodendroglioma) with at least one high-risk feature (

258 oma, vestibular schwannoma, astrocytoma, and oligodendroglioma, with information on tumour size and s

259 omal region that may contain a suppressor of oligodendrogliomas, yet its expression is elevated in so