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1 22 with glioblastoma multiforme and one with anaplastic astrocytoma).
2 glioblastoma multiforme, and 18 patients had anaplastic astrocytoma.
3 tomas, 1 anaplastic oligodendroglioma, and 1 anaplastic astrocytoma.
4 at patients with glioblastoma multiforme and anaplastic astrocytoma.
5 on tensor imaging (DTI) to two patients with anaplastic astrocytoma.
6 lioblastoma multiforme and two patients with anaplastic astrocytoma.
7 ocytoma (IMA) cell line from a WHO grade III anaplastic astrocytoma.
8 lioblastoma and one (8%) of 12 patients with anaplastic astrocytoma.
9 ioma, 1 had anaplastic ependymoma, and 1 had anaplastic astrocytoma.
10 pathways as key in the development of human anaplastic astrocytomas.
11 rase-positive, ras-activated human grade III anaplastic astrocytomas.
12 cent had glioblastoma multiforme and 12% had anaplastic astrocytomas.
13 expression was noted in 14 GBMs (33%) and 2 anaplastic astrocytomas.
14 gene were detected in 24 GBMs (57%) and in 2 anaplastic astrocytomas.
15 ian, 2 melanoma, 1 cholangiocarcinoma, and 1 anaplastic astrocytoma].
16 ses were as follows: low-grade gliomas, 19%; anaplastic astrocytomas, 11%; anaplastic oligodendroglio
17 erentiating normal tissue from low-grade and anaplastic astrocytomas, 13 showed statistical significa
18 involving 1p36 were frequently identified in anaplastic astrocytomas (22%) and glioblastomas (34%).
19 postradiation neoplasms presented as either anaplastic astrocytoma (3 cases) or glioblastoma multifo
20 ls) were included (5 diffuse astrocytomas, 2 anaplastic astrocytomas, 5 gliomatosis cerebri, and 1 gl
21 malignant astrocytoma (63% glioblastoma, 37% anaplastic astrocytoma), 64% had high (> 60,000 molecule
22 vious reports, 50% of gliomas tested (1 of 2 anaplastic astrocytomas, 7 of 12 glioblastoma multiforme
23 se 19 cases were 2 low-grade astrocytomas, 1 anaplastic astrocytoma, 8 glioblastomas, 6 meningiomas,
24 , 111 patients were confirmed to have had an anaplastic astrocytoma (AA) or anaplastic mixed oligoast
25 (GBM) and five patients with newly diagnosed anaplastic astrocytoma (AA) were treated with Temodal at
26 as VEGF is up-regulated in only a portion of anaplastic astrocytoma (AA), it is overexpressed in most
29 rocytic tumours (10 diffuse astrocytomas, 30 anaplastic astrocytomas (AA), 64 glioblastomas (GB)) wer
30 ioma (glioblastoma multiforme [GBM], n = 33; anaplastic astrocytoma [AA], n = 6; anaplastic oligodend
31 erms glioblastoma, glioma, malignant glioma, anaplastic astrocytoma, anaplastic oligodendroglioma, an
32 ma, pilocytic astrocytoma, oligoastrocytoma, anaplastic astrocytoma, anaplastic oligodendroglioma, gl
33 , however, showed frequent loss primarily in anaplastic astrocytomas and displayed deletion breakpoin
35 esults indicate that 1p deletions are common anaplastic astrocytomas and glioblastomas but are distin
38 ysis of ten primary malignant gliomas (three anaplastic astrocytomas and seven glioblastomas multifor
40 iate-grade (anaplastic oligodendroglioma and anaplastic astrocytoma), and high-grade (glioblastomas m
41 SWB61 (anaplastic oligodendroglioma), SWB40 (anaplastic astrocytoma), and SWB39 (glioblastoma multifo
43 d (15 with glioblastoma multiforme, two with anaplastic astrocytoma, and one with malignant glioma).
45 real-time quantitative RT-PCR in 41 GBMs, 43 anaplastic astrocytomas, and 7 adjacent normal tissues.
46 phorylated Shc is associated with FAK in the anaplastic astrocytoma biopsy samples and in astrocytoma
50 astomas and that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of h
51 astomas and that forced FoxM1B expression in anaplastic astrocytoma cells leads to the formation of h
52 igibility criteria included: age >=18 years, anaplastic astrocytoma, first recurrence >=6 months afte
53 identified in anaplastic oligodendrogliomas, anaplastic astrocytomas, glioblastoma multiforme, and me
54 of the molecular differences between primary anaplastic astrocytomas/glioblastomas and their subseque
55 (grade IV) tumor biopsy samples with that in anaplastic astrocytoma (grade III) tumors, nonneoplastic
57 4MG, D-65MG, U-251MG, U-373MG, and SK-MG-1), anaplastic astrocytoma (Hs-683), anaplastic glioma (U-87
58 both IDH-mt and 1p/19q co-deletion, whereas anaplastic astrocytoma is divided into IDH wild-type ( I
59 uman astrocytes genetically modified to form anaplastic astrocytoma-like tumors (Ras cells) on intrac
60 e gliomas [glioblastoma multiforme (GBM) and anaplastic astrocytoma], low-grade astrocytomas, or beni
62 ioma (glioblastoma multiforme [GBM], n = 27; anaplastic astrocytoma, n = 4; anaplastic oligodendrogli
63 ents; glioblastoma multiforme, two patients; anaplastic astrocytoma, one patient; pineal PNET, one pa
64 tumors with centrally reviewed diagnoses of anaplastic astrocytoma or glioblastoma multiforme had su
65 for institutional histologic diagnosis (eg, anaplastic astrocytoma or glioblastoma multiforme), as w
67 with glioblastoma multiforme, and those with anaplastic astrocytoma or oligodendroglioma were 54, 52,
68 ologic diagnosis of anaplastic mixed glioma, anaplastic astrocytoma, or glioblastoma multiforme who h
71 , gliomas that arose from FoxM1B-transfected anaplastic astrocytoma SW1783 cells displayed glioblasto
72 n levels were significantly higher in GB and anaplastic astrocytoma tissues than in grade II glioma a
73 om World Health Organization (WHO) grade III anaplastic astrocytomas to WHO grade IV glioblastomas.
74 is by histology (high v low MGMT levels) for anaplastic astrocytoma was 14 versus 62 months (n=24) an
75 47-0.82; P = 0.0007), and EGFR expression in anaplastic astrocytoma was associated with nearly 3-fold
76 ts with recurrent glioblastoma multiforme or anaplastic astrocytoma were seen for baseline evaluation
77 of 42 adult glioblastomas and 3 of 13 adult anaplastic astrocytomas, whereas none of the 21 low-grad
78 17 with glioblastoma multiforme and one with anaplastic astrocytoma) with histologically documented r