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1 a multicenter trial involving patients with high-grade glioma.
2 ted with decreased survival of patients with high-grade glioma.
3 stic value for OS in patients with suspected high-grade glioma.
4 ssion from true progression in patients with high-grade glioma.
5 inded radiology review for 133 patients with high-grade glioma.
6 inhibits the progression of KrasG12V-driven high-grade glioma.
7 ations during treatment for 44 patients with high-grade glioma.
8 quent association of PTEN mutations in human high-grade glioma.
9 gery, and photodynamic therapy for recurrent high-grade glioma.
10 iated with an increased risk of developing a high-grade glioma.
11 al receptor involved in the proliferation of high-grade glioma.
12 the delayed brain tumor (DBT) mouse model of high-grade glioma.
13 16 of these 18 genes were down-regulated in high-grade glioma.
14 followed an alternative evolutionary path to high-grade glioma.
15 ults in hyperactivity of this conductance in high grade gliomas.
16 has been associated with the development of high grade gliomas.
17 clinically-annotated and genetically-defined high grade gliomas.
18 mal and malignant tissue during resection of high grade gliomas.
19 use of MRI and PET for surgical resection of high-grade gliomas.
20 MRI alone to plan the surgical resection of high-grade gliomas.
21 n 4 months were observed among patients with high-grade gliomas.
22 Bumex as adjuvant therapy for patients with high-grade gliomas.
23 l alkylating agent used for the treatment of high-grade gliomas.
24 es in the imaging of gliomas with a focus on high-grade gliomas.
25 mendations for updated response criteria for high-grade gliomas.
26 s significantly increased in the majority of high-grade gliomas.
27 ve therapeutic strategy for radiosensitizing high-grade gliomas.
28 nic therapies may have activity in recurrent high-grade gliomas.
29 at antiangiogenic therapies have activity in high-grade gliomas.
30 for improving the outcomes for patients with high-grade gliomas.
31 uptake is a distinguishing characteristic of high-grade gliomas.
32 a pharmaceutical agent has maximum access to high-grade gliomas.
33 er as a surrogate marker of proliferation in high-grade gliomas.
34 ill likely improve survival in patients with high-grade gliomas.
35 ing (MRI) during a course of radiotherapy of high-grade gliomas.
36 e in histology-independent classification of high-grade gliomas.
37 ntitumor activity in patients with recurrent high-grade gliomas.
38 GFR) is commonly amplified and/or mutated in high-grade gliomas.
39 carmustine (BCNU) in patients with recurrent high-grade gliomas.
40 dency to undergo malignant transformation to high-grade gliomas.
41 adults with previously irradiated, recurrent high-grade gliomas.
42 ity in a minority of patients with recurrent high-grade gliomas.
43 sets from 16 patients aged 21-71 years with high-grade gliomas.
44 valuable for tumor-specific gene transfer to high-grade gliomas.
45 0 are the most common genetic alterations in high-grade gliomas.
46 imal morbidity in patients with intracranial high-grade gliomas.
47 ed with patient prognosis in MES, but not PN high-grade gliomas.
48 ts receptor CSF1R are overexpressed in human high-grade gliomas.
49 l of Ras* mice and promoted the formation of high-grade gliomas.
50 s is low compared with other tumours such as high-grade gliomas.
51 very of boronophenylalanine in patients with high-grade gliomas.
52 neutron capture therapy for the treatment of high-grade gliomas.
53 es efficacy in differentiating the low- from high-grade gliomas.
54 ism contributing to the growth of aggressive high-grade gliomas.
55 d A-to-I editing and cancer, particularly in high-grade gliomas.
56 ve angiogenesis that is a typical feature of high-grade gliomas.
58 in a number of freshly resected and cultured high grade gliomas, 2) syntaxin 1A inhibited ASIC curren
60 57.8; germ cell tumors, 63.5; ependymoma or high-grade glioma, 69.8; low-grade glioma, 71.5; and oth
61 rain tumor specimens of 213 patients (mostly high-grade gliomas [89%]) included in the Vienna Cancer
62 tients after a median latency of 12.6 years (high-grade gliomas, 9.1 years; meningiomas, 19 years).
63 gliomas, we found TAX-1 to be amplified in 2 high-grade gliomas among a group of 26 gliomas investiga
65 ause the INK4a-ARF locus is often deleted in high-grade gliomas (anaplastic oligodendroglioma and gli
66 data from 157 unpublished cases of pediatric high-grade glioma and diffuse intrinsic pontine glioma a
67 erved in four of 14 assessable patients with high-grade glioma and in two of six with primitive neuro
69 of genome-wide association studies (GWAS) of high-grade glioma and replication data (1,644 cases and
70 s to target surface GRP78 as a biomarker for high-grade glioma and to develop effective cell-specific
71 tosis-were compared in the solid parts of 17 high-grade gliomas and 11 low-grade gliomas (P<.05 signi
73 risk; HR, 3.86; 95% CI, 1.59-9.35; P = .003) high-grade gliomas and 191 glioblastomas (global log-ran
74 survival ranged from 0-19.5% for subsequent high-grade gliomas and 57.3-100% for meningiomas, which
75 For other types of tumors, such as malignant high-grade gliomas and brainstem gliomas, new approaches
76 e 1 (NTRK1), is a potent oncogenic driver of high-grade gliomas and confers sensitivity to the experi
77 cterizing genetically engineered mouse (GEM) high-grade gliomas and evaluating the pharmacokinetics i
78 n many tumor types including the majority of high-grade gliomas and expression of activated RAS or RA
79 PI(3)K/Akt pathway, are found in almost all high-grade gliomas and MAPK signaling is necessary for c
80 is a rational strategy for the treatment of high-grade gliomas and may be an effective adjuvant ther
81 is well tolerated by patients with recurrent high-grade gliomas and may have efficacy in this disease
82 nctions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mut
83 l blood volumes in the peritumoral region in high-grade gliomas and metastases were 1.31 +/- 0.97 (me
86 , we examined expression array data of human high-grade gliomas and performed RT-PCR on glioblastoma
87 old significant promise for the treatment of high-grade gliomas and provide a rationale for proceedin
88 gh levels of SLFN5 expression correlate with high-grade gliomas and shorter overall survival in patie
89 inositide 3-kinase/Akt pathway for growth of high-grade gliomas and suggest that multiple molecular a
90 hat COX-2 is up-regulated in the majority of high-grade gliomas and that a potential role of COX-2 in
91 le polymers following resection of recurrent high-grade gliomas and the systemic BCNU exposure with i
92 ion is the most common genetic alteration in high-grade glioma, and approximately 50% of EGFR-amplifi
94 riteria for assessing response to therapy in high-grade gliomas are based on two-dimensional tumor me
97 though therapies for patients with recurrent high-grade gliomas are limited, there has been important
98 lowed clear differentiation between low- and high-grade glioma (area under the receiver operating cha
99 with relapsed or progressive, biopsy-proven, high-grade glioma (arm A) and progressive, diffuse, intr
100 l genes that are differentially expressed in high-grade glioma as a prognostic molecular signature.
101 on and pseudopalisades, elements that define high-grade gliomas as SHH-producing microenvironments.
102 was performed on 10 patients with recurrent high-grade glioma at 5 different institutions within the
103 in low-grade glioma (AUC, 0.818) and MTI in high-grade glioma (AUC, 0.854) and for all WHO grades (A
105 R traits that are associated with some known high-grade glioma biomarkers and association with genomi
106 vement in the poor prognosis for humans with high-grade glioma brain tumors, alternative therapeutic
107 ajor up-regulated isoform of this protein in high-grade gliomas but is absent in a specific subset of
108 ptor (EGFR) is amplified or overexpressed in high-grade gliomas but is low or undetectable in normal
110 f 275,895 autosomal variants among 692 adult high-grade glioma cases (622 from the San Francisco Adul
112 h P < 10(-6) using independent data from 176 high-grade glioma cases and 174 controls from the Mayo C
114 s channel activity promotes a reversion of a high grade glioma cell to a phenotype resembling that of
115 rain tumors, we stably transfected the human high-grade glioma cell line SNB19 and the human low-grad
116 expression of uPAR has been correlated with high-grade glioma cell lines and tumors We report here t
117 ries of these agents against a panel of five high-grade glioma cell lines to identify a promising com
120 ing Hsc70 expression promotes reversion of a high-grade glioma cell to a more normal astrocytic pheno
122 e hypothesis that the conductance pathway in high grade glioma cells is comprised of ENaC/DEG subunit
124 53-, p14(ARF)-, and p16(Ink4a)/pRb-deficient high grade glioma cells that lacked the p16(Ink4a)-depen
130 inotecan (BEV/IR) in patients with recurrent high-grade glioma compared with MR imaging alone from th
131 amino acid PET for the surgical resection of high-grade gliomas, compared with MRI alone, from the pe
132 gulated in malignant glioma specimens and in high-grade glioma-derived primary cultures, whereas rema
133 brain tumors (ie, medulloblastoma, low- and high-grade gliomas, diffuse intrinsic pontine glioma, an
134 gistically and safely with radiation against high-grade gliomas, drugs must pass the endothelial junc
135 thologic diagnoses were made in 24 cases (13 high-grade gliomas, eight metastases to the brain, and t
138 respectively, for differentiating low- from high-grade gliomas for ADC, D and f, and differentiating
140 ), and clinical patient data profiles of 543 high-grade gliomas from US medical centers and The Cance
141 c mutations of H3F3A in aggressive pediatric high-grade gliomas generate K27M or G34R/V mutant histon
142 therapeutic anticoagulation in patients with high-grade gliomas given the increased risk of ICH and p
143 xpression profiles in brain tumors including high-grade gliomas [glioblastoma multiforme (GBM) and an
144 The median survival was 18 +/- 4.7 mo in the high-grade glioma group and 58 +/- 27 mo in the low-grad
154 survival benefit was associated with maximal high-grade glioma (HGG) resection and analysed this lite
156 different therapeutic regimens in astrocytic high-grade glioma (HGG), the prognosis for patients rema
160 ompared with patients with primary pediatric high-grade glioma (HGG; median, 25 mutations per exome;
164 llow-up MR imaging in 2 patients revealed 66 high-grade gliomas (HGG), 77 low-grade gliomas (LGG), 2
166 e uptake of (90)Y-DOTATOC in meningiomas and high-grade gliomas (HGGs) and a feasibility study of the
171 Diffuse brainstem gliomas (BSGs) and other high-grade gliomas (HGGs) of childhood carry a dismal pr
178 ction methodology, could be used to classify high-grade gliomas in a manner more objective, explicit,
179 te complex breaks, we found that DSBs induce high-grade gliomas in these mice which, otherwise, do no
180 ted through MEK, leads to the development of high-grade gliomas in vivo and suggest that MEK may be a
182 on transcripts were more frequently found in high-grade gliomas, in the classical subtype of gliomas,
183 PC) were discovered at the invasive front of high-grade gliomas, in which they exhibited a unique per
184 ological consequences of p16 inactivation in high-grade gliomas included facilitating invasiveness, w
188 r the degree of expression of p53 protein in high-grade gliomas is associated with progression-free s
190 expression) and with a separate group of 180 high-grade gliomas (log-rank P = .00003; HR, 0.476; 95%
191 teristics of solitary metastases and primary high-grade gliomas may sometimes be similar, perfusion-w
197 eloid leukemia, cutaneous melanoma, low- and high-grade gliomas of the brain, and adenocarcinomas of
202 ress has been made in the treatment of adult high-grade gliomas over the last two decades, thus neces
207 tion methods were used to collect data in 22 high-grade glioma patients, with informed written consen
208 und in a substantial proportion of pediatric high-grade gliomas (pHGG), often in association with TP5
209 d strongly upregulated in both low-grade and high-grade gliomas, reduces glioma cell growth by cell-c
214 evated protein levels of HDAC6 were found in high grade glioma samples, in contrast to the decreased
215 nchmark for comparison with future pediatric high-grade glioma studies, in addition to identifying at
218 e highest frequency of mutations detected in high-grade gliomas, T-lineage acute lymphoblastic leukae
219 rane localization, and its expression in all high-grade gliomas tested to date suggest that it may pl
220 noreactive score was significantly higher in high-grade glioma than low-grade glioma and normal brain
221 d (18)F-FDG PET were significantly higher in high-grade gliomas than in low-grade gliomas (2.15 +/- 0
222 axial kurtosis were significantly higher in high-grade gliomas than in low-grade gliomas (P = .02, P
224 f Ink4 and Arf tumor suppressors to generate high-grade gliomas that are commonly driven by Met ampli
225 peutic option in the subset of patients with high-grade gliomas that express both functional p53 and
226 d late toxicity, while in selected groups of high-grade gliomas the use of adjuvant or neo-adjuvant c
228 here has been progress in treating recurrent high-grade gliomas, the prognosis remains poor and much
230 in the management of patients with recurrent high-grade glioma treated with BEV/IR may be cost-effect
232 on of cultured cells originally derived from high grade gliomas (U87-MG and SK-MG1) with ASIC2 abolis
234 stigate the fresolimumab uptake in recurrent high-grade gliomas using (89)Zr-fresolimumab PET and to
235 (89)Zr-fresolimumab penetrated recurrent high-grade gliomas very well but did not result in clini
236 131I-TM-601 in adult patients with recurrent high-grade glioma was performed to determine the biodist
238 em/initiating cell (BTSC) lines derived from high-grade gliomas, we show that BTSCs are subject to im
239 e role of this pathway in the development of high-grade gliomas, we used the established RCAS/TVA gli
243 t EGR1-expressing cells are more frequent in high grade gliomas where the nuclear expression of EGR1
244 ocesses compared with nonbrainstem pediatric high-grade gliomas, whereas expression signatures of low
245 s were negative in 5 patients with recurrent high-grade glioma who subsequently suffered tumor progre
246 aterials and Methods Seventeen patients with high-grade gliomas who had received 10-44 administration
248 summarizes current treatments for recurrent high-grade gliomas with an emphasis on more novel approa
249 combination of activated Ras and Akt induces high-grade gliomas with the histological features of hum
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