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1 evelop low-grade brain tumors throughout the optic pathway.
2 ing to investigate the size of the uncrossed optic pathway.
3 nse guidance molecules distributed along the optic pathway.
4 ess navigated appropriately in the embryonic optic pathway.
5  receptors and N-cadherin into the embryonic optic pathway.
6 cur that result in the formation of multiple optic pathways.
7 dilection of these tumors to form within the optic pathway and brainstem (NF1-PA) and cerebellum (spo
8 risk for developing low-grade gliomas of the optic pathway and brainstem, individuals with NF2 typica
9  < .0001), supratentorial tumors (P = .008), optic pathway and diencephalic tumors (P = .012), and su
10 tivity for mGluR2/3 is found in cells in the optic pathway and thalamus.
11 n gerbils, but functional correlates of this optic pathway are unknown at present.
12 heir cognate receptors within the developing optic pathway as well as mechanisms underlying the plast
13     Addition of HS to the developing Xenopus optic pathway causes severe targeting errors yet it is n
14 ion, VEPs were a more sensitive indicator of optic pathway damage than visual acuity or optic nerve a
15                     Although many aspects of optic pathway development are beginning to be understood
16                       The molecular basis of optic pathway development is beginning to be elucidated
17 type 1 (NF1) occurs preferentially along the optic pathway during the first decade of life.
18  development of tuberculomas in the anterior optic pathway during treatment for tuberculosis and pres
19 ents (4 male, 5 female, aged 4-28 years) had optic pathway glioma (OPG) in addition to OFNF.
20                                              Optic pathway glioma (OPG), seen in 15% to 20% of indivi
21 f low-grade astrocytic optic pathway tumors (optic pathway glioma [OPG]).
22                   Forty-nine subjects had an optic pathway glioma and 10 subjects had NF1 without an
23  indicated magnetic resonance imaging for an optic pathway glioma and/or neurofibromatosis type 1 (NF
24 ic juvenile pilocytic astrocytoma and one in optic pathway glioma) at dose levels of 88 and 116 mg/m(
25 cluding cognitive problems and brain tumors (optic pathway glioma).
26 ay glioma and 10 subjects had NF1 without an optic pathway glioma.
27 ovement was observed in 20% of patients with optic pathway glioma.
28 of multiple nervous system tumors, including optic pathway gliomas (OPG).
29                                              Optic pathway gliomas (OPGs) and orbitofacial plexiform
30                  Nearly 50% of children with optic pathway gliomas (OPGs) experience visual impairmen
31               Monitoring young children with optic pathway gliomas (OPGs) for visual deterioration ca
32                                Children with optic pathway gliomas (OPGs) frequently experience visio
33                            The management of optic pathway gliomas (OPGs) remains controversial.
34 n with neurofibromatosis type 1 (NF1) and/or optic pathway gliomas (OPGs).
35                       Children with sporadic optic pathway gliomas and/or NF1 who had >/=2 volumes ac
36  individuals had symptomatic or asymptomatic optic pathway gliomas and/or skeletal abnormalities.
37                                              Optic pathway gliomas are an important neuro-ophthalmic
38    The growth patterns and histopathology of optic pathway gliomas are more consistent with those of
39                                              Optic pathway gliomas are not hamartomas but truly are n
40 Children experiencing vision loss from their optic pathway gliomas frequently demonstrate a >/=10% de
41 been shown to halt or improve vision loss in optic pathway gliomas in many cases.
42   New data for the prospective management of optic pathway gliomas is reviewed.
43                                Children with optic pathway gliomas or ocular causes of decreased visu
44 andheld OCT imaging in sedated children with optic pathway gliomas produces highly reproducible measu
45                            Neurofibromas and optic pathway gliomas result from NF1 inactivation in Sc
46 ofibromas, schwannomas, low grade, pilocytic optic pathway gliomas, as well as malignant peripheral n
47 ts may also show neurologic lesions, such as optic pathway gliomas, dural ectasia and aqueduct stenos
48 tumors frequently form in the optic pathway (optic pathway gliomas, OPGs), especially in children wit
49 c activated K-RAS expression in vivo develop optic pathway gliomas, similar to our previously reporte
50 en in neoplasms of other types as well as in optic pathway gliomas.
51  typical NF1 osseous lesions, or symptomatic optic pathway gliomas.
52 syndrome, neurofibromatosis 1 (NF1), develop optic pathway gliomas.
53 erplastic lesions, some of which progress to optic pathway gliomas.
54 making treatment decisions for children with optic pathway gliomas.
55               The diagnosis and treatment of optic-pathway gliomas has been aided greatly by a greate
56                Recently primary diagnoses of optic-pathway gliomas have been made in children aged si
57                   Important papers regarding optic-pathway gliomas have been published recently in th
58  history and disease progression patterns of optic-pathway gliomas in neurofibromatosis type 1 (NF1)
59 cumentation, current literature reveals that optic-pathway gliomas in NF1 can be diagnosed after the
60                                              Optic-pathway gliomas in NF1 can display a variety of ma
61  advances in the diagnosis and management of optic-pathway gliomas made within the past 5 years.
62  patients should be vigilantly evaluated for optic-pathway gliomas past the age of 12.
63  surrounding tissues are being used to treat optic-pathway gliomas, but chemotherapy has become the f
64                               The developing optic pathway has proven one of the most informative mod
65 he hindbrain; expression in the spinal cord, optic pathways, hindbrain commissures, midbrain, and per
66                                       In the optic pathway, however, netrin-1 is expressed in areas t
67      Dscam is expressed along the developing optic pathway in a pattern consistent with a role in reg
68 ss and neuronal size changes in the anterior optic pathway [including the optic nerve (ON), optic tra
69                           S3 labeling of the optic pathway is also complex, being initially strong in
70 e also show that CXCL12 expression along the optic pathway is higher in infant children and young mic
71 atial restriction of glioma formation to the optic pathway of young children.
72  low-grade brain tumors (gliomas) within the optic pathway (optic gliomas).
73          These tumors frequently form in the optic pathway (optic pathway gliomas, OPGs), especially
74 nificantly more abundant in the regenerating optic pathway, resulting from both transgene induction i
75                            In the developing optic pathways, retinal axons were misguided at the opti
76 tes clearly that, as in other regions of the optic pathway, Robo2 is the major receptor required for
77  added exogenously to the developing Xenopus optic pathway, severely disrupt target recognition causi
78 e to the development of low-grade astrocytic optic pathway tumors (optic pathway glioma [OPG]).
79 1c, 2/3 and 5) have been assessed in the rat optic pathway using specific antibodies.
80 re sacrificed and contiguous segments of the optic pathway were removed.
81                                Tumors in the optic pathways were associated with a shorter PFS (P =.0
82 ing filopodia, the axons navigated along the optic pathway without obvious guidance errors, indicatin

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