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1 fourth nerve palsy the presenting sign of an intracranial tumor.
2 oma (GBM) remains the most common and lethal intracranial tumor.
3 w and the cells have the ability of tracking intracranial tumor.
4 the CNS intravascularly, NSCs will target an intracranial tumor.
5 th cancer and represents the majority of all intracranial tumors.
6 tance-driving event in both subcutaneous and intracranial tumors.
7 Brain metastases encompass nearly 80% of all intracranial tumors.
8      Meningiomas are the most common primary intracranial tumors.
9    Meningiomas are the most frequent primary intracranial tumors.
10  P/L-selectins and accumulate selectively in intracranial tumors.
11 the brain or leaky vasculature of late-stage intracranial tumors.
12 g the host antitumor immune response against intracranial tumors.
13 A BPNPs in animals bearing either U87 or RG2 intracranial tumors.
14 immune disorders, systemic malignancies, and intracranial tumors.
15  are very rare, constituting less than 1% of intracranial tumors.
16 ting mice with either visceral metastases or intracranial tumors.
17 cells, and impaired growth and dispersion of intracranial tumors.
18 ival to highly immune resistant, established intracranial tumors.
19 he difficulty in delivering nanoparticles to intracranial tumors.
20 nhanced the survival of mice harboring LN229 intracranial tumors.
21  glioblastoma are the most common and lethal intracranial tumors.
22 m 2 to 6 h after injection, respectively, in intracranial tumors.
23 ion of growth and migration in GBM cells and intracranial tumors.
24 esulted in the regression of pre-established intracranial tumors.
25          Gliomas are the most common primary intracranial tumors.
26 activated ex vivo, can eliminate established intracranial tumors.
27  system lymphoma (PCNSL) represents 1% to 3% intracranial tumors.
28 imaging technique in patients irradiated for intracranial tumors.
29 wer and constricted blood vessels within the intracranial tumor after drug therapy.
30 stemic toxicity in mice with subcutaneous or intracranial tumors after daily intraperitoneal injectio
31             Previous studies have focused on intracranial tumors, although the skin receives much rad
32  multiforme (GBM) is the most common primary intracranial tumor and despite recent advances in treatm
33 cules for activating immune response against intracranial tumor and the identity of cellular and mole
34  Meningiomas constitute about 34% of primary intracranial tumors and are associated with increased mo
35        Malignant gliomas are the most common intracranial tumors and are considered incurable.
36      Meningiomas are the most common primary intracranial tumors and are resistant to all medical the
37 ts with neurofibromatosis, account for 8% of intracranial tumors and can only be treated by surgical
38           Pituitary adenomas comprise 10% of intracranial tumors and occur in about 20% of the popula
39 to subcutaneous tumors, lung metastases, and intracranial tumors and offers a solution to many of the
40 ell tolerated with adequate penetration into intracranial tumors and promising preliminary activity w
41 rowth was inhibited in both subcutaneous and intracranial tumors, and in the latter instance, treatme
42             Vestibular schwannoma (VS) is an intracranial tumor arising from neoplastic Schwann cells
43                                              Intracranial tumors arising from the subependymal layer
44 the suppressive immunological environment of intracranial tumor bearing mice both systemically and lo
45 )-23, the cells showed protective effects in intracranial tumor-bearing C57BL/6 mice.
46 ment for meningioma, the most common primary intracranial tumor, but improvements in meningioma risk
47      Meningiomas are the most common primary intracranial tumors, but the molecular drivers of mening
48 ds to increased survival of the mice bearing intracranial tumor by decreasing the number of regulator
49 so increased the survival of animals bearing intracranial tumors by 65%.
50 in addition to conventional outcomes such as intracranial tumor control and survival.
51                                     However, intracranial tumor control was improved with WBRT.
52                       For the present study, intracranial tumor control, cognitive deterioration, QOL
53                                              Intracranial tumor control, toxic effects, cognitive det
54     Advanced 10-day 3-methylcholanthrene 205 intracranial tumors could be cured by the transfer of 15
55 ich was predefined as an increase in maximum intracranial tumor diameter (ICTD) of 3 mm or greater wi
56 p. EL-4 tumors, but not MCA-205 pulmonary or intracranial tumors, displayed a significant requirement
57 eutic agents that can selectively target the intracranial tumor environment.
58                                 Experimental intracranial tumors from full-length transfectants showe
59 treatment paradigms for benign and malignant intracranial tumors, functional disorders, and vascular
60                         Our data reveal that intracranial tumor growth and angiogenesis is significan
61 n mice confirmed that ECs and IL-8 stimulate intracranial tumor growth and invasion in vivo.
62 ke kinase inhibition restricts migration and intracranial tumor growth in glioblastoma.
63        Last, BTIC-intrinsic PD-1 accelerated intracranial tumor growth, and this occurred in mice lac
64 tases but nevertheless appears to facilitate intracranial tumor growth.
65 IM59 activity that results in suppression of intracranial tumor growth.
66  the critical role of VLA-4 in the effective intracranial tumor homing of adoptive-transferred, antig
67 ioblastoma multiforme (GBM), the most common intracranial tumor in adults, is characterized by extens
68    Brain metastases (BM) are the most common intracranial tumor in adults.
69  astrocytic malignancies and the most common intracranial tumor in adults.
70   Upon gross inspection, we identified large intracranial tumors in 30% of aged SHRs.
71         Brain metastases are the most common intracranial tumors in adults and are associated with in
72 GBM cells led to reduced growth of resultant intracranial tumors in mice and significantly increased
73 nsfected dendritic cells (DC-IFN-alpha) into intracranial tumors in mice immunized previously with sy
74 more, the ST6Gal I transfectants produced no intracranial tumors in severe combined immunodeficient m
75 erred to eradicate established pulmonary and intracranial tumors in syngeneic mice, even without coad
76 th histologic evidence that R4009 eradicated intracranial tumors in this model.
77 ablished glioma tumor growth and invasion in intracranial tumors in vivo.
78                        Here, we investigated intracranial tumor incidence and origin in a cohort of s
79            The tumoristatic activity against intracranial tumors independent of the blood brain barri
80 ortem examination, FACS-based enumeration of intracranial tumor-infiltrating lymphocytes directly cor
81                                       Direct Intracranial tumor injection using this reagent resulted
82 astography (MRE) to predict the stiffness of intracranial tumors intraoperatively and assess the impa
83              The annual incidence of primary intracranial tumors is 7 to 19 cases per 100,000 people.
84 -based stereotactic radiosurgery (CK-SRS) of intracranial tumors is complicated by the unique charact
85                                      Primary intracranial tumors make up ~ 2% of all cancer cases but
86  longer than mock-transfected DCs within the intracranial tumor microenvironment, and DC-IFN-alpha-tr
87 0) value of 23 nM showed good efficacy in an intracranial tumor model and increased the median overal
88                    In a syngeneic scid mouse intracranial tumor model, recombinant herpes simplex vir
89  were detected from different regions of the intracranial tumor model.
90 SHH-MB tumors by 55%-80% in subcutaneous and intracranial tumor models in mice.
91               Prior to the experiments using intracranial tumor models in nude mice, we modified the
92                While spontaneous preclinical intracranial tumor models offer valuable insights into t
93 llular telephones in a case-control study of intracranial tumors of the nervous system conducted betw
94 t tumors tend to exhibit increased rigidity, intracranial tumors presented as remarkably softer than
95 overexpression promotes GSC self-renewal and intracranial tumor propagation.
96 transferred T cells is sufficient to mediate intracranial tumor regression.
97                      Definitive diagnosis of intracranial tumors relies on tissue specimens obtained
98 rmal human astrocytes into cells that formed intracranial tumors resembling human anaplastic astrocyt
99 -specific shRNA (shMMP-9) treatment of mouse intracranial tumors resulted in elevated expression of m
100 (BPNPs) have high potential for treatment of intracranial tumors since they offer the potential for c
101 al expression of IFN-alpha by DCs within the intracranial tumor site may enhance the clinical efficac
102  therapies and limited therapeutic access to intracranial tumor sites due to the presence of the bloo
103 as(V12)-transformed human astrocytes reduced intracranial tumor size, in association with reduced tum
104 or activation, to allow for the formation of intracranial tumors strongly resembling p53/pRb pathway-
105  derived from control animals formed smaller intracranial tumors than those derived from beta3 knocko
106             Vestibular schwannoma (VS) is an intracranial tumor that causes significant morbidity, in
107 t and accurately discriminate common primary intracranial tumors that share cell-of-origin lineages a
108 take and retention in primary and metastatic intracranial tumors treated by conventional radiotherapy
109 tcontrast T1-weighted MRI scans of different intracranial tumor types and discriminating images depic
110          Frequent chromosomal aberrations in intracranial tumors were gain of 1q and losses on 6q, 9,
111       Because we observed that s.c., but not intracranial, tumors were infiltrated with CD11c+ DCs, a
112  allowed time to passively accumulate in the intracranial tumors, which served as a proxy for an orth
113    The records of twelve patients with large intracranial tumors who underwent embolization were anal
114 in metastasis is the most commonly occurring intracranial tumor whose incidence seems to be increasin
115                             Meningioma is an intracranial tumor with few confirmed risk factors.
116 BM) is the most common and malignant type of intracranial tumors with poor prognosis.
117 sidered benign, meningiomas represent 32% of intracranial tumors with three grades of malignancy defi
118 eyes from 19 patients (63% with a history of intracranial tumor) with a mean follow-up of 40.1+/-20.3
119 lastoma (GBM) is the most aggressive primary intracranial tumor, with glioblastoma stem cells (GSCs)
120 minations were performed in 43 children with intracranial tumors within 24 hours of the completion of
121 4(+) T cells, both established pulmonary and intracranial tumors without coadministration of exogenou
122                                     Using an intracranial tumor xenograft model, we further demonstra
123 treatment also greatly reduced the volume of intracranial tumor xenografts and increased survival of
124 8 showed enhanced growth as tumorspheres and intracranial tumor xenografts, compared with mock-infect
125 ngly enhances the in vivo growth of s.c. and intracranial tumor xenografts.

 
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