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1 the mathematical diagnosis of brain cancer (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 tate personalised medicine in the setting of malignant glioma.
7 og pathway activity has been demonstrated in malignant glioma.
8 activates expression of mesenchymal genes in malignant glioma.
9 a viable potential target for the therapy of malignant glioma.
10 and we revisit the developmental origins of malignant glioma.
11 dy against VEGF--for patients with recurrent malignant glioma.
12 rucial to improve outcomes for patients with malignant glioma.
13 ion-free survival in patients with recurrent malignant glioma.
14 ive and well tolerated options for recurrent malignant glioma.
15 ing outcome in patients with newly diagnosed malignant glioma.
16 nce imaging (MRI) in patients with recurrent malignant glioma.
17 h and are thus promising in the treatment of malignant glioma.
18 d be a target for combinatorial treatment of malignant glioma.
19 hat underlies this schizophrenic behavior in malignant glioma.
20 ssible clinical application in patients with malignant glioma.
21 oring therapy to the individual patient with malignant glioma.
22 creening of epigenetically silenced genes in malignant glioma.
23 e heterogeneous mass of cells that compose a malignant glioma.
24 Forkhead box M1 (FoxM1) is overexpressed in malignant glioma.
25 and is particularly severe in patients with malignant glioma.
26 nvasion may provide an effective therapy for malignant glioma.
27 ed that CypB is upregulated in many cases of malignant glioma.
28 ay be developed into a potential therapy for malignant glioma.
29 syndromes are well-defined risk factors for malignant glioma.
30 t have been linked to the risk of developing malignant glioma.
31 for use in clinical trials for patients with malignant glioma.
32 clinical trials for patients with recurrent malignant glioma.
33 n low levels of 5hmC and reduced survival in malignant glioma.
34 ng the levels of 5hmC are also prognostic in malignant glioma.
35 ith strong activating effect on NF-kappaB in malignant gliomas.
36 and accelerated radiation in newly diagnosed malignant gliomas.
37 n treatment of murine syngeneic intracranial malignant gliomas.
38 y-ICLC) in HLA-A2(+) patients with recurrent malignant gliomas.
39 rs in the assessment and management of adult malignant gliomas.
40 oapoptotic therapies to improve treatment of malignant gliomas.
41 IDH2 occur in a majority of several types of malignant gliomas.
42 pression of link proteins in human brain and malignant gliomas.
43 ult in poor effectiveness of chemotherapy in malignant gliomas.
44 hog signaling regulates the growth of select malignant gliomas.
45 survival outcomes in patients with recurrent malignant gliomas.
46 y virus 1-associated dementia, and growth of malignant gliomas.
47 that have been demonstrated to be active in malignant gliomas.
48 hown to have promising activity in recurrent malignant gliomas.
49 uidance to physicians treating patients with malignant gliomas.
50 ated receptors as potential targets to treat malignant gliomas.
51 COX-2 expression with tumor angiogenesis in malignant gliomas.
52 ajor obstacles to successful chemotherapy of malignant gliomas.
53 ng of this therapy approach in patients with malignant gliomas.
54 factor receptors is a frequent occurrence in malignant gliomas.
55 apeutic targets for the treatment of diffuse malignant gliomas.
56 in a variety of cancer cell types, including malignant gliomas.
57 plified, mutated, and overexpressed in human malignant gliomas.
58 zone may be of potential use in treatment of malignant gliomas.
59 abolic imaging in the clinical management of malignant gliomas.
60 holds promise as a therapeutic agent against malignant gliomas.
61 ated in a variety of cancer types, including malignant gliomas.
62 tment for patients suffering from high-grade malignant gliomas.
63 peutic agents in clinical studies focused on malignant gliomas.
64 logs are considered as promising therapy for malignant gliomas.
65 a central role in the treatment of childhood malignant gliomas.
66 a new potential target of therapy for human malignant gliomas.
67 mprovements in the survival of patients with malignant gliomas.
68 I trials of these vaccines in patients with malignant gliomas.
69 naling is considered a promising therapy for malignant gliomas.
70 develop potential therapeutic strategies for malignant gliomas.
71 d that these cells consistently give rise to malignant gliomas.
72 process that turns slowly dividing OPCs into malignant gliomas.
73 date therapeutic target for the treatment of malignant gliomas.
74 nostic biomarker and a therapeutic target of malignant gliomas.
75 and therapeutic procedures for patients with malignant gliomas.
76 ondrial membrane protein highly expressed in malignant gliomas.
77 fy QPRT as a potential therapeutic target in malignant gliomas.
78 -FLT PET is associated with OS in high-grade malignant gliomas.
79 Vs) currently in clinical trial for treating malignant gliomas.
80 to the heterogeneous populations observed in malignant gliomas.
81 urons in the brains of mice can give rise to malignant gliomas.
82 that replication-competent HCMV may exist in malignant gliomas.
84 iated with prolonged survival in adults with malignant gliomas, although the association between MGMT
85 y 2013 using the terms glioblastoma, glioma, malignant glioma, anaplastic astrocytoma, anaplastic oli
86 ed cellular immune function in patients with malignant glioma and advance a role for T(regs) in facil
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
90 ption factor-5 (ATF5) is highly expressed in malignant glioma and has a key role in promoting cell su
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
98 ant activation are frequent abnormalities in malignant gliomas and other human cancers and have been
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
126 GBM), the most common and aggressive type of malignant glioma, are characterized by increased invasio
127 Vs), in clinical trials for the treatment of malignant gliomas, are assumed to be selective for tumor
129 olved in the pathogenesis and progression of malignant gliomas as the centre of a splicing oncogenic
130 man cytomegalovirus (HCMV) has been found in malignant gliomas at variable frequencies with efforts t
131 were high in low grade tumors and reduced in malignant glioma, but did not exhibit any correlation wi
132 gs)) are greatly diminished in patients with malignant glioma, but T(regs) frequently represent an in
133 ed in brain tumor-initiating cells (BTIC) in malignant glioma, but the mechanism of its activation is
135 e hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsibl
137 of TTP via p38/MAPK promotes progression of malignant gliomas by negatively regulating its RNA desta
140 ozolomide, commonly used in the treatment of malignant glioma, causes cellular cytotoxicity by formin
141 has been reported to selectively kill human malignant glioma cell lines but not primary astrocytes.
143 t, IRES insertion permits HSV propagation in malignant glioma cell lines that do not support replicat
144 ated in malignant glioma specimens and human malignant glioma cell lines, correlating with their rate
145 e sought to establish a role for stathmin in malignant glioma cell motility, migration, and invasion
146 expression lead to significant decreases in malignant glioma cell motility, migration, and invasion.
147 ls by inducing autophagy and suggest that in malignant glioma cells a disruption of the PI3K/Akt sign
148 However, it is estimated that only 5-15% of malignant glioma cells are in mitosis at any one time.
150 regulates in vitro invasion and migration of malignant glioma cells by activating the nuclear factor-
151 hat rapamycin exerts its antitumor effect on malignant glioma cells by inducing autophagy and suggest
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
155 onal overexpression of TTP as a transgene in malignant glioma cells led to RNA destabilization of IL-
157 Another possible mechanism of resistance of malignant glioma cells might be upregulation of pro-inva
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
166 oblastoma multiforme (GBM) cell line, highly malignant glioma cells, was first injected into 5-week-o
167 ential for the proliferation and survival of malignant glioma cells, which suggests that inhibition o
168 esulted in significant radiosensitization of malignant glioma cells, which will guide the development
174 multiforme (GBM) is the most common form of malignant glioma, characterized by unpredictable clinica
177 , R3659, were serially passaged within human malignant glioma D54-MG cell lines in vitro or flank tum
178 d molecular events that initiate and promote malignant glioma development are not completely understo
180 rongly suppresses the intracranial growth of malignant gliomas, even in the presence of the strong pr
183 r-initiating cells isolated from fresh human malignant gliomas express the neurotrophin receptors Trk
185 esults demonstrate that ATF5 is essential in malignant glioma genesis and reveal that the ATF5-mediat
188 expression in glioma stem cells and inhibits malignant glioma growth in cell culture and mouse models
194 Several new agents targeting angiogenesis in malignant gliomas have become available and have been in
196 trials are now in progress for patients with malignant gliomas; however, a better understanding of ho
198 fection occurs in a high percentage of human malignant gliomas in vivo, as the HCMV immediate early-1
202 an extracellular matrix protein prominent in malignant glioma, increases NOTCH activity in BTIC to pr
203 In addition, in mice bearing orthotopic malignant gliomas, inhibition with bevacizumab of vascul
209 tors alone in the treatment of patients with malignant gliomas is only modest, potentially because th
211 urrently, the most efficacious treatment for malignant gliomas is temozolomide; however, gliomas expr
214 most aggressive and least treatable form of malignant glioma, is the most common human brain tumor.
215 as been found to be expressed in a subset of malignant gliomas, its sufficiency for glioma initiation
216 ied highly tumorigenic subpopulations within malignant gliomas, known generally as cancer stem cells.
217 therapeutic agent of choice for treatment of malignant gliomas, leads to induction of CHOP, a major p
218 s embedded within fresh surgical isolates of malignant gliomas lent support to a new paradigm in canc
219 xtent of tumor resection in this subgroup of malignant gliomas located adjacent to eloquent areas fro
221 alpha2 (IL-13Ralpha2) in a majority of human malignant gliomas makes this protein an attractive vacci
222 ese findings suggest that 5hmC regulation in malignant glioma may represent an important determinant
225 11) was conducted in children with recurrent malignant glioma (MG) and intrinsic brainstem glioma (BS
230 ), atypical teratoid/rhabdoid tumor (n = 1), malignant glioma (n = 1), and choroid plexus carcinoma,
232 posttreatment tumor tissue of patients with malignant gliomas, NDRG1 was induced and predictive of p
233 viduals with NF1 are prone to optic gliomas, malignant gliomas, neurofibromas, and malignant peripher
236 tly, the ICD of p75NTR was commonly found in malignant glioma patient specimens, suggesting that the
237 ration of 100 mCi of 131I-m81C6 to recurrent malignant glioma patients followed by chemotherapy is as
242 de novel therapeutic strategies for treating malignant glioma patients.Oncogene advance online public
243 generates a penetrant acute-onset high-grade malignant glioma phenotype with notable clinical, pathol
244 es a fully penetrant, rapid-onset high-grade malignant glioma phenotype with prominent pathological a
247 ged as the treatment of choice for recurrent malignant gliomas, prolonging progression-free survival
248 of rapamycin complex 1 (mTORC1) activity in malignant gliomas promote tumor progression, suggesting
249 The poor survival of patients with human malignant gliomas relates partly to the inability to del
252 ces and in vivo testing in orthotopic murine malignant glioma revealed preserved nanoparticle diffusi
255 dult brain, but is significantly elevated in malignant glioma specimens and human malignant glioma ce
256 TRIM11 expression levels were upregulated in malignant glioma specimens and in high-grade glioma-deri
257 as found to be markedly elevated in clinical malignant glioma specimens but nearly undetectable in no
258 are linked to acute inflammatory responses, malignant glioma stem cell metastasis, and chronic infla
259 les in the etiology of primary and recurrent malignant gliomas, suggesting that patient therapy shoul
260 the rationale for targeting angiogenesis in malignant gliomas, summarizes relevant clinical trial re
261 molecular mechanisms by which astrocytes and malignant gliomas suppress monocyte/microglial function
262 ast 20 years, with only 30% of patients with malignant glioma surviving 5 years after diagnosis.
263 controlling magnetic particles for treating malignant glioma that should be applicable to treat a wi
266 nvolves the role of cytomegalovirus (CMV) in malignant gliomas, the most common form of primary brain
268 ocused on immunotherapy for the treatment of malignant gliomas, the prognosis for this disease remain
270 uing debates around cytoreductive surgery in malignant gliomas, there is broad consensus that increas
273 dy was undertaken in patients with recurrent malignant glioma to determine the efficacy and safety of
274 shifts, allowing T cells from patients with malignant glioma to function in vitro at levels equivale
276 ll proliferation, in patients with recurrent malignant gliomas treated with bevacizumab in combinatio
280 Glioblastoma multiforme (GBM) is the most malignant glioma type with diffuse borders due to extens
281 agy but not apoptosis in rapamycin-sensitive malignant glioma U87-MG and T98G cells by inhibiting the
282 cantly more potent and active, against human malignant glioma U87-MG and U373-MG cells in vitro and i
283 xpressed in several solid cancers, including malignant gliomas, upon adoption of metastatic or invasi
284 Here, we reexamined the HCMV prevalence in malignant gliomas using different methods and began to d
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
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
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
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