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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
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
18 development of tuberculomas in the anterior optic pathway during treatment for tuberculosis and pres
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(
38 The growth patterns and histopathology of optic pathway gliomas are more consistent with those of
40 Children experiencing vision loss from their optic pathway gliomas frequently demonstrate a >/=10% de
44 andheld OCT imaging in sedated children with optic pathway gliomas produces highly reproducible measu
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
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
63 surrounding tissues are being used to treat optic-pathway gliomas, but chemotherapy has become the f
65 he hindbrain; expression in the spinal cord, optic pathways, hindbrain commissures, midbrain, and per
68 ss and neuronal size changes in the anterior optic pathway [including the optic nerve (ON), optic tra
70 e also show that CXCL12 expression along the optic pathway is higher in infant children and young mic
74 nificantly more abundant in the regenerating optic pathway, resulting from both transgene induction i
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
82 ing filopodia, the axons navigated along the optic pathway without obvious guidance errors, indicatin
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