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1 ing to investigate the size of the uncrossed optic pathway.
2 evelop low-grade brain tumors throughout the 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 ent (VI) despite having a healthy retina and optic pathway.
7 cur that result in the formation of multiple optic pathways.
8 for diagnosing and following diseases in the optic pathways.
9  of various pathologies affecting either the optic pathway alone or multiple levels of the central ne
10 dilection of these tumors to form within the optic pathway and brainstem (NF1-PA) and cerebellum (spo
11 risk for developing low-grade gliomas of the optic pathway and brainstem, individuals with NF2 typica
12  < .0001), supratentorial tumors (P = .008), optic pathway and diencephalic tumors (P = .012), and su
13 tivity for mGluR2/3 is found in cells in the optic pathway and thalamus.
14 2 is expressed by the meninges bordering the optic pathway, and CXCR4 by both ipsilaterally and contr
15 n gerbils, but functional correlates of this optic pathway are unknown at present.
16 heir cognate receptors within the developing optic pathway as well as mechanisms underlying the plast
17 equent neurodegeneration occurring along the optic pathway broadens the plaque-centred view of these
18     Addition of HS to the developing Xenopus optic pathway causes severe targeting errors yet it is n
19 ion, VEPs were a more sensitive indicator of optic pathway damage than visual acuity or optic nerve a
20                     Although many aspects of optic pathway development are beginning to be understood
21                       The molecular basis of optic pathway development is beginning to be elucidated
22 olecular and cellular mechanisms controlling optic pathway development.
23 type 1 (NF1) occurs preferentially along the optic pathway during the first decade of life.
24  development of tuberculomas in the anterior optic pathway during treatment for tuberculosis and pres
25 exhibited bilateral thinning of the anterior optic pathway, especially the prechiasmatic optic nerves
26 ribution of these markers along the anterior optic pathway for each case in all compartments (i.e. pa
27 sis type 1 (NF1) and asthma, we leverage Nf1 optic pathway glioma (Nf1(OPG)) mice, human and mouse RN
28 ents (4 male, 5 female, aged 4-28 years) had optic pathway glioma (OPG) in addition to OFNF.
29                                              Optic Pathway Glioma (OPG) is a relatively common brain
30                                              Optic pathway glioma (OPG), seen in 15% to 20% of indivi
31 f low-grade astrocytic optic pathway tumors (optic pathway glioma [OPG]).
32                   Forty-nine subjects had an optic pathway glioma and 10 subjects had NF1 without an
33  indicated magnetic resonance imaging for an optic pathway glioma and/or neurofibromatosis type 1 (NF
34 ic juvenile pilocytic astrocytoma and one in optic pathway glioma) at dose levels of 88 and 116 mg/m(
35 cluding cognitive problems and brain tumors (optic pathway glioma).
36 ovement was observed in 20% of patients with optic pathway glioma.
37 ay glioma and 10 subjects had NF1 without an optic pathway glioma.
38 of multiple nervous system tumors, including optic pathway gliomas (OPG).
39 on neurofibromatosis type 1 (NF1)-associated optic pathway gliomas (OPGs) and a follow-up period of a
40                                              Optic pathway gliomas (OPGs) and orbitofacial plexiform
41                  Nearly 50% of children with optic pathway gliomas (OPGs) experience visual impairmen
42               Monitoring young children with optic pathway gliomas (OPGs) for visual deterioration ca
43                                Children with optic pathway gliomas (OPGs) frequently experience visio
44                            The management of optic pathway gliomas (OPGs) remains controversial.
45 ade neoplasms of the optic pathway (known as optic pathway gliomas (OPGs)) during early childhood(3,4
46 n with neurofibromatosis type 1 (NF1) and/or optic pathway gliomas (OPGs).
47                       Children with sporadic optic pathway gliomas and/or NF1 who had >/=2 volumes ac
48  individuals had symptomatic or asymptomatic optic pathway gliomas and/or skeletal abnormalities.
49                                              Optic pathway gliomas are an important neuro-ophthalmic
50    The growth patterns and histopathology of optic pathway gliomas are more consistent with those of
51                                              Optic pathway gliomas are not hamartomas but truly are n
52 Children experiencing vision loss from their optic pathway gliomas frequently demonstrate a >/=10% de
53 been shown to halt or improve vision loss in optic pathway gliomas in many cases.
54   New data for the prospective management of optic pathway gliomas is reviewed.
55                                Children with optic pathway gliomas or ocular causes of decreased visu
56 andheld OCT imaging in sedated children with optic pathway gliomas produces highly reproducible measu
57                            Neurofibromas and optic pathway gliomas result from NF1 inactivation in Sc
58 ofibromas, schwannomas, low grade, pilocytic optic pathway gliomas, as well as malignant peripheral n
59 ts may also show neurologic lesions, such as optic pathway gliomas, dural ectasia and aqueduct stenos
60 tumors frequently form in the optic pathway (optic pathway gliomas, OPGs), especially in children wit
61 c activated K-RAS expression in vivo develop optic pathway gliomas, similar to our previously reporte
62 making treatment decisions for children with optic pathway gliomas.
63 en in neoplasms of other types as well as in optic pathway gliomas.
64  typical NF1 osseous lesions, or symptomatic optic pathway gliomas.
65 syndrome, neurofibromatosis 1 (NF1), develop optic pathway gliomas.
66 erplastic lesions, some of which progress to optic pathway gliomas.
67               The diagnosis and treatment of optic-pathway gliomas has been aided greatly by a greate
68                Recently primary diagnoses of optic-pathway gliomas have been made in children aged si
69                   Important papers regarding optic-pathway gliomas have been published recently in th
70  history and disease progression patterns of optic-pathway gliomas in neurofibromatosis type 1 (NF1)
71 cumentation, current literature reveals that optic-pathway gliomas in NF1 can be diagnosed after the
72                                              Optic-pathway gliomas in NF1 can display a variety of ma
73  advances in the diagnosis and management of optic-pathway gliomas made within the past 5 years.
74  patients should be vigilantly evaluated for optic-pathway gliomas past the age of 12.
75  surrounding tissues are being used to treat optic-pathway gliomas, but chemotherapy has become the f
76                               The developing optic pathway has proven one of the most informative mod
77 he hindbrain; expression in the spinal cord, optic pathways, hindbrain commissures, midbrain, and per
78                                       In the optic pathway, however, netrin-1 is expressed in areas t
79      Dscam is expressed along the developing optic pathway in a pattern consistent with a role in reg
80 ss and neuronal size changes in the anterior optic pathway [including the optic nerve (ON), optic tra
81     An antero-posterior gradient of anterior optic pathway involvement was observed with optic nerves
82                           S3 labeling of the optic pathway is also complex, being initially strong in
83 e also show that CXCL12 expression along the optic pathway is higher in infant children and young mic
84                                 The anterior optic pathway is one of the preferential sites of involv
85 h nerves) develop low-grade neoplasms of the optic pathway (known as optic pathway gliomas (OPGs)) du
86 matosis type 1 (NF1)-associated pLGGs in the optic pathway (NF1-OPG), we demonstrate that NF1-OPG aro
87 atial restriction of glioma formation to the optic pathway of young children.
88  low-grade brain tumors (gliomas) within the optic pathway (optic gliomas).
89          These tumors frequently form in the optic pathway (optic pathway gliomas, OPGs), especially
90 nificantly more abundant in the regenerating optic pathway, resulting from both transgene induction i
91                            In the developing optic pathways, retinal axons were misguided at the opti
92 tes clearly that, as in other regions of the optic pathway, Robo2 is the major receptor required for
93  added exogenously to the developing Xenopus optic pathway, severely disrupt target recognition causi
94 e to the development of low-grade astrocytic optic pathway tumors (optic pathway glioma [OPG]).
95 mmune population in the TME, particularly in optic pathway tumors.
96  visual functional outcomes in patients with optic pathway tumours.
97 1c, 2/3 and 5) have been assessed in the rat optic pathway using specific antibodies.
98 re sacrificed and contiguous segments of the optic pathway were removed.
99                                Tumors in the optic pathways were associated with a shorter PFS (P =.0
100 ing filopodia, the axons navigated along the optic pathway without obvious guidance errors, indicatin