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1               These mice developed low-grade oligodendroglioma.
2 man chromosome 1p, which is commonly lost in oligodendroglioma.
3 in some tumor types, particularly anaplastic oligodendroglioma.
4 d Huntington's disease and one had a grade 2 oligodendroglioma.
5 elet-derived growth factor-induced malignant oligodendroglioma.
6 ntribute to the distinctive biology of human oligodendroglioma.
7 he pathogenesis and therapeutic targeting of oligodendroglioma.
8 FBP2-mediated progression of PDGFB-initiated oligodendroglioma.
9 eness to therapy in patients with anaplastic oligodendroglioma.
10 osome, a locus that is deleted in 50%-80% of oligodendrogliomas.
11  view of the genes and mechanisms underlying oligodendrogliomas.
12  gliomas, 28 glioblastomas and 22 anaplastic oligodendrogliomas.
13 ression profiling in morphologically classic oligodendrogliomas.
14  predictor of chemosensitivity in anaplastic oligodendrogliomas.
15  analyzed these three genes in 72 anaplastic oligodendrogliomas.
16 including astrocytic neoplasms and low-grade oligodendrogliomas.
17 ssion from well-differentiated to anaplastic oligodendrogliomas.
18 erapeutic response and prolonged survival in oligodendrogliomas.
19 ese cases were among the 24 (42%) anaplastic oligodendrogliomas.
20  primary central nervous system lymphoma and oligodendrogliomas.
21 of adult patients with recurrent hemispheric oligodendrogliomas.
22 in adult patients with recurrent hemispheric oligodendrogliomas.
23 ould contribute to the observed formation of oligodendrogliomas.
24 than in low-grade astrocytomas and low-grade oligodendrogliomas.
25 on the chromosome arms frequently deleted in oligodendrogliomas.
26 arly genetic alterations in astrocytomas and oligodendrogliomas.
27 ut are distinct from the 1p abnormalities in oligodendrogliomas.
28 apy and improved prognosis for patients with oligodendrogliomas.
29  which is observed in over 50% of anaplastic oligodendrogliomas.
30  to transduce primary human astrocytomas and oligodendrogliomas.
31 errant methylation in human astrocytomas and oligodendrogliomas.
32  in a specific subset of low-grade, indolent oligodendrogliomas.
33  grade and is required to sustain high-grade oligodendrogliomas.
34 ad glioblastoma multiforme, 2 had anaplastic oligodendroglioma, 1 had anaplastic ependymoma, and 1 ha
35 anaplastic gliomas [n = 48; astrocytoma, 28; oligodendroglioma, 14; mixed glioma, six]) received trea
36  microsatellite markers was detected in four oligodendrogliomas (17.4%), one pituitary adenoma (3.2%)
37                                 Thirty-three oligodendrogliomas (25 with 1p/19q loss) and 53 oligoast
38 glioblastomas, 3 of 4 mixed gliomas, 4 of 11 oligodendrogliomas, 6 of 8 astrocytomas, 2 of 2 meningio
39  previously demonstrated chemosensitivity of oligodendrogliomas, a combined approach of histologic an
40 nd mechanisms contributing to the genesis of oligodendrogliomas, a subtype of primary brain tumors.
41                          Like neuroblastoma, oligodendrogliomas also show a high frequency of deletio
42 t glioma, anaplastic astrocytoma, anaplastic oligodendroglioma, anaplastic oligoastrocytoma, and brai
43 ecific domains were identified in anaplastic oligodendrogliomas, anaplastic astrocytomas, glioblastom
44 endroglioma), intermediate-grade (anaplastic oligodendroglioma and anaplastic astrocytoma), and high-
45 en deleted in high-grade gliomas (anaplastic oligodendroglioma and glioblastoma), we investigated the
46 es of infiltrating astrocytic brain cancers (oligodendroglioma and high-grade astrocytoma) and found
47 ined loss of 1p and 19q in 64% (21 of 32) of oligodendrogliomas and 67% (6 of 9) of oligoastrocytomas
48  as an objective, ancillary tool for grading oligodendrogliomas and a potential approach for classify
49                      The cells of origin for oligodendrogliomas and astrocytomas are not known but ar
50 otal 1p and 19q are found in the majority of oligodendrogliomas and considered as a diagnostic marker
51 cally relevant tissues from 20 patients with oligodendrogliomas and grade II-IV astrocytomas.
52 70% of WHO grade II and III astrocytomas and oligodendrogliomas and in glioblastomas that developed f
53  (21 low-grade astrocytomas and 14 low-grade oligodendrogliomas and low-grade mixed oligoastrocytomas
54 FAP-V(12)Ha-ras;GFAP-EGFRvIII mice developed oligodendrogliomas and mixed oligoastrocytoma tumors, in
55 n data clearly delineated PAs from low-grade oligodendrogliomas and normal white matter.
56 the molecular analysis of 1p and 19q loss in oligodendrogliomas and oligoastrocytomas in archival rou
57 omas, or tumors with characteristics seen in oligodendrogliomas and small-cell astrocytomas, indicati
58 ression is specifically decreased in primary oligodendrogliomas and up-regulated in glioma cell lines
59 ration decreased rapidly in 1p/19q codeleted oligodendrogliomas and with a slower time course in astr
60 ere included: 10 glioblastomas, 1 anaplastic oligodendroglioma, and 1 anaplastic astrocytoma.
61 nd paediatric glioblastoma (GBM), anaplastic oligodendroglioma, and diffuse intrinsic pontine glioma
62 s with supratentorial low-grade astrocytoma, oligodendroglioma, and oligoastrocytoma found somewhat l
63 arrangement displayed histologic features of oligodendroglioma, and the gene products of both rearran
64     There were 21 low-grade astrocytomas, 64 oligodendrogliomas, and 16 mixed oligoastrocytomas.
65  in 162 diffuse gliomas (79 astrocytomas, 52 oligodendrogliomas, and 31 mixed oligoastrocytomas), col
66 ss II tumors are similar to 1p/19q codeleted oligodendrogliomas, and class III represents infiltrativ
67 ligodendrogliomas, in 18/23 (83%) anaplastic oligodendrogliomas, and in 3/8 (38%) oligoastrocytomas g
68 pulation of low-grade gliomas (astrocytomas, oligodendrogliomas, and mixed gliomas) to improve our un
69 w-grade gliomas (LGGs) include astrocytomas, oligodendrogliomas, and mixed oligoastrocytomas (WHO gra
70 /19q intact gliomas, including astrocytomas, oligodendrogliomas, and oligoastrocytomas, formed a thir
71 tomas, a second grouped the 1p/19q codeleted oligodendrogliomas, and the mixture of remaining 1p/19q
72 oastrocytomas with 1p/19q LOH are related to oligodendrogliomas, and those with p53 mutations are rel
73                                   Anaplastic oligodendroglioma, another type of malignant glioma, pro
74                                   Anaplastic oligodendroglioma (AO) are rare primary brain tumours th
75 lastic oligoastrocytoma (AOA) and anaplastic oligodendroglioma (AO)] remain subjective, and the exist
76 aplastic astrocytoma [AA], n = 6; anaplastic oligodendroglioma [AO], n = 2; gliosarcoma [GS], n = 1;
77                                   Anaplastic oligodendroglioma are chemotherapy-sensitive tumors.
78                             These anaplastic oligodendrogliomas are characterized by increased cellul
79                                              Oligodendrogliomas are the second most common malignant
80                                              Oligodendrogliomas are the second most common type of gl
81 plus chemotherapy and histologic findings of oligodendroglioma as favorable prognostic variables for
82 e model, a decreased incidence of anaplastic oligodendroglioma as well as prolonged survival was obse
83 r-derived glioma stem-like cells (GSCs) from oligodendroglioma as well as proneural and mesenchymal g
84  gliomas, meningiomas, medulloblastomas, and oligodendrogliomas, as well as peripheral nervous system
85                The samples analyzed included oligodendroglioma, astrocytoma, and meningioma tumors of
86 ed out on 36 human glioma samples, including oligodendroglioma, astrocytoma, and oligoastrocytoma, al
87 senting various human brain tumors including oligodendroglioma, astrocytoma, pilocytic astrocytoma, o
88 alities, can serve as the cell of origin for oligodendrogliomas, astrocytomas, or mixed gliomas.
89 s was 2-fold lower (P < 0.03), and for mixed oligodendroglioma-astrocytomas, the mean was 4-fold lowe
90 de insight into the cellular architecture of oligodendrogliomas at single-cell resolution and support
91 particular MIB-1, may be useful in assessing oligodendroglioma behavior, whereas their role in malign
92 ua (CIC) occur in approximately 50% of human oligodendrogliomas, but mechanistic links to pathogenesi
93 gle cells from six IDH1 or IDH2 mutant human oligodendrogliomas by RNA sequencing (RNA-seq) and recon
94  profiles between IDH-mutant astrocytoma and oligodendroglioma can be primarily explained by distinct
95 servation of uncertain significance in human oligodendroglioma, can initiate oligodendroglioma in the
96 n, we generated Cic-deficient mice and human oligodendroglioma cell models.
97                                        Human oligodendroglioma cells also demonstrated calcium mobili
98                      Transplanting wild-type oligodendroglioma cells into the brain generated lethal
99                                 Intact human oligodendroglioma cells specifically bound [3H]SQ29,548
100 s in neonatal rat oligodendrocytes and human oligodendroglioma cells was investigated using immunocyt
101 2 is essential for tumor initiation by mouse oligodendroglioma cells, and they illustrated a Sox2-dir
102 r protein on both oligodendrocytes and human oligodendroglioma cells.
103 ular pH and attenuates acid load recovery in oligodendroglioma cells.
104 of myelinated fibers in areas infiltrated by oligodendroglioma cells.
105 0 GAP domain caused a decreased incidence of oligodendrogliomas compared with that observed with PDGF
106                            Upon culture, one oligodendroglioma contained an unbalanced 45,XX,t(1;19)(
107 t human OLIG genes are expressed strongly in oligodendroglioma, contrasting absent or low expression
108 s clear that p73 is not a candidate gene for oligodendroglioma despite its location in the frequently
109 orted by the fact that human astrocytoma and oligodendroglioma display a high degree of overlap in gl
110  oligodendroglioma (or oligoastrocytoma with oligodendroglioma dominant) in 68%.
111                             More than 80% of oligodendrogliomas exhibit LOH for 1 p and 19q alleles.
112 , including an exon defined by an anaplastic oligodendroglioma expressed sequence tag, and spans at l
113  7 of 12 glioblastoma multiforme, and 2 of 6 oligodendrogliomas) expressed EGFRvIII, as determined by
114 gically classic glioblastomas and anaplastic oligodendrogliomas follow markedly different clinical co
115                                              Oligodendroglioma frequently (> or = 70%) responds to ra
116 ii) codeletion of 1p and 19q differentiating oligodendrogliomas from astrocytomas; (iii) IDH1/2 mutat
117 rocytoma, anaplastic astrocytoma, anaplastic oligodendroglioma, glioblastoma multiforme, gliomatosis
118 overall degree of enzyme activation, whereas oligodendrogliomas had the least.
119                                         Most oligodendrogliomas have chromosomes 1p/19q co-deletion a
120 H-mutated genotypes, between astrocytoma and oligodendroglioma histologies, as well as for tumors tha
121 (P < .01), large tumor volume (P < .01), and oligodendroglioma histopathologic type (P = .02).
122        We profiled >200 metabolites in human oligodendroglioma (HOG) cells to determine the effects o
123 arily responsible for fuelling the growth of oligodendroglioma in humans.
124 nce in human oligodendroglioma, can initiate oligodendroglioma in the mouse.
125  neural progenitors induced the formation of oligodendrogliomas in about 60% of mice by 12 wk of age;
126  was seen in 17/23 (74%) well-differentiated oligodendrogliomas, in 18/23 (83%) anaplastic oligodendr
127 enomenon was found with grade III anaplastic oligodendrogliomas, in which stronger EGFR expression wa
128  of prolonged survival in patients with pure oligodendroglioma, independent of tumor grade.
129 with 24 primary glioma tissues of low-grade (oligodendroglioma), intermediate-grade (anaplastic oligo
130                                              Oligodendroglioma is characterized by mutations of IDH a
131 archies, suggesting that the architecture of oligodendroglioma is primarily dictated by developmental
132 rolonged survival of patients with low-grade oligodendroglioma (LGO) and oligoastrocytoma (LGOA), the
133 ed overall survival among patients with pure oligodendroglioma (log-rank, P =.03) and remained a sign
134 ein-2 (2.2-fold increase, P = .019), and the oligodendroglioma markers oligodendrocyte lineage transc
135      We present evidence that some low-grade oligodendrogliomas may be comprised of proliferating gli
136 the first report of ALT in medulloblastomas, oligodendrogliomas, meningiomas, schwannomas, and pediat
137            Inefficient removal of O6MeGua in oligodendrogliomas might also account for their response
138 rimitive neuroectodermal tumor, astrocytoma, oligodendroglioma, mixed glioma, and tumors of the perip
139 on prevalence was 55%, 47%, and 0% among the oligodendrogliomas, mixed oligoastrocytomas, and astrocy
140 naplastic gliomas with mixed astrocytoma and oligodendroglioma morphological features.
141  3), ependymoma (n = 2), meningioma (n = 3), oligodendroglioma (n = 1), and melanoma (n = 12) tumor s
142 7; anaplastic astrocytoma, n = 4; anaplastic oligodendroglioma, n = 2).
143 malignant brain tumors (astrocytoma, n = 17; oligodendroglioma, n = 3) and in nine healthy volunteers
144 at a third resection had transformed into an oligodendroglioma of WHO grade III.
145                                              Oligodendrogliomas of all grades overexpress epidermal g
146 , had his diagnosis changed to an anaplastic oligodendroglioma on subsequent central neuropathologic
147 unger than 40 years and in patients who have oligodendroglioma or oligo-dominant histology.
148 ffuse tumor margin on T2-weighted MR images, oligodendroglioma or oligoastrocytoma histopathologic ty
149 o astrocytes induced the formation of either oligodendrogliomas or mixed oligoastrocytomas in about 4
150           Patients with recurrent anaplastic oligodendrogliomas or oligoastrocytomas and recurrent lo
151 9%; anaplastic astrocytomas, 11%; anaplastic oligodendrogliomas or oligoastrocytomas, 25%; and gliobl
152 astrocytoma dominant) in 32% of patients and oligodendroglioma (or oligoastrocytoma with oligodendrog
153  survivors of WHO grade I or II astrocytoma, oligodendroglioma, or oligoastrocytoma with clinically a
154 f astrocytomas (10/55) and in 73% (24/33) of oligodendrogliomas (P < 0.0001), and loss of the 19q13.3
155 (6/55) of astrocytomas and in 64% (21/33) of oligodendrogliomas (P < 0.0001).
156 % (21/55) of astrocytomas and 73% (24/33) of oligodendrogliomas (P = 0.0017).
157  glioblastomas, lower grade astrocytomas and oligodendrogliomas (P<0.00001).
158  response and overall survival in anaplastic oligodendroglioma patients treated with procarbazine, lo
159                                   Anaplastic oligodendrogliomas, pure (AO) and mixed (anaplastic olig
160           Today, the diagnosis of anaplastic oligodendroglioma requires the presence of both IDH-mt a
161 ta provide evidence that neoplastic cells of oligodendroglioma resemble oligodendrocytes or their pro
162                    Anaplastic progression in oligodendrogliomas resulted in a larger number of cells
163 on of Tax1 in primary human astrocytomas and oligodendrogliomas resulted in significantly higher leve
164                 Examination of 27 additional oligodendrogliomas revealed 12 and 3 more tumors with mu
165 el predicts for two major groups of gliomas (oligodendroglioma-rich and glioblastoma-rich groups) sep
166 verexpression of OLIG2 was not only found in oligodendroglioma samples and normal neural tissue but a
167 ssion of glypican-1 in human astrocytoma and oligodendroglioma samples compared with nonneoplastic gl
168                                       Twenty oligodendroglioma samples with 1p36.3 deletions were scr
169     We found that NHE-1 on 1p is silenced in oligodendrogliomas secondary to IDH-associated hypermeth
170      These included 33 astrocytic tumors, 23 oligodendrogliomas, six gangliogliomas, 41 meningiomas,
171                  The observed requirement of oligodendroglioma stem cells for Sox2 suggested its rele
172 gy Group (RTOG) clinical trial in anaplastic oligodendroglioma suggested a progression-free survival
173 es DAOY (medulloblastoma), SWB61 (anaplastic oligodendroglioma), SWB40 (anaplastic astrocytoma), and
174  a risk-stratified approach to patients with oligodendrogliomas that optimizes treatment efficacy and
175                            Among Mayo Clinic oligodendrogliomas, the prevalence of fusion was 81%.
176                                In anaplastic oligodendroglioma, therefore, PTEN is a target of 10q lo
177 yielding a spontaneous model of infiltrating oligodendroglioma, this study demonstrates that astrocyt
178 tor expression in tissue from seven of seven oligodendrogliomas, three of three pilocytic astrocytoma
179 rease in tumor volume did not differ between oligodendrogliomas treated with temozolomide or carmusti
180 or gene involved in astrocytoma, and perhaps oligodendroglioma, tumorigenesis.
181 rnofsky performance score, cytological type (oligodendroglioma vs astrocytoma), and, potentially, the
182    The median OS for patients with low-grade oligodendroglioma was 9.1 years without fusion and 13.0
183 assic glioblastoma and nonclassic anaplastic oligodendroglioma was not significantly different (P = 0
184                                 The mean for oligodendrogliomas was 2-fold lower (P < 0.03), and for
185 latelet-derived growth factor (PDGF)-induced oligodendrogliomas was accelerated in mice lacking the c
186 ing the development of growth-factor-induced oligodendroglioma, we identified a critical role for the
187 ppressor gene involved in the development of oligodendrogliomas, we performed mutation analysis of p7
188 ntegrated genetic and epigenetic analysis of oligodendrogliomas, we show that aberrant CpG island met
189 me, and those with anaplastic astrocytoma or oligodendroglioma were 54, 52, and 116 wk, respectively.
190                         Unlike astrocytomas, oligodendrogliomas were found consistently to contain fe
191 ), with recurrent supratentorial hemispheric oligodendrogliomas were treated.
192 th grade 2 astrocytoma, oligoastrocytoma, or oligodendroglioma who were younger than 40 years of age
193 P is a young woman with a previously treated oligodendroglioma, WHO grade II, with loss of heterozygo
194 onsisting primarily of a moderately cellular oligodendroglioma with distinct areas of a fibrillary as
195                Recent research suggests that oligodendrogliomas with and without the -1p/-19q genotyp
196 as, we performed mutation analysis of p73 in oligodendrogliomas with chromosome 1 p-arm deletions.
197  subset of 14 glioblastomas and 7 anaplastic oligodendrogliomas with classic histology.
198                                              Oligodendrogliomas with loss of heterozygosity on chromo
199                            However, grade II oligodendrogliomas with strong EGFR expression and 1p/19
200 I) glioma (astrocytoma, oligoastrocytoma, or oligodendroglioma) with at least one high-risk feature (
201 I) glioma (astrocytoma, oligoastrocytoma, or oligodendroglioma) with at least one high-risk feature (
202 omal region that may contain a suppressor of oligodendrogliomas, yet its expression is elevated in so

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