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1 n tumors (gliomas) within the optic pathway (optic gliomas).
2  compressive optic neuropathies such as from optic glioma.
3 ne whether NG2+ cells could give rise to Nf1 optic glioma.
4 ngineered Nf1 mouse and human NF1-associated optic glioma.
5 id from genetically engineered Nf1 mice with optic glioma.
6 ic model for NF1-associated astrogliosis and optic glioma.
7 netically-engineered mouse strains that form optic gliomas.
8 ntine glioma (DIPG), and pediatric low-grade optic gliomas.
9 with this disease suffer a high incidence of optic gliomas, a benign but potentially debilitating tum
10 1 neoplasms, which include myeloid leukemia, optic glioma, and plexiform neurofibroma.
11 + cells are not the cell of origin for mouse optic glioma, and support a model in which gliomagenesis
12                                              Optic gliomas are brain tumors characterized by slow gro
13           We found that although subtypes of optic gliomas are indistinguishable on imaging, the micr
14                                    Malignant optic gliomas are rare, but they rapidly become lethal v
15 only female Nf1 GEM exhibited a decrement in optic glioma-associated visual acuity, shorter RGC axons
16 e analyzed to determine the impact of sex on optic glioma-associated visual decline in children with
17 osis type I (NF1) and have increased risk of optic gliomas, astrocytomas and glioblastomas.
18          Moreover, SP600125 treatment of Nf1 optic glioma-bearing GEM results in reduced optic glioma
19                        After detection of an optic glioma by manganese-enhanced magnetic resonance im
20                    We propose that pediatric optic gliomas can maintain blood supply without endothel
21                                              Optic gliomas contain various amounts of myxoid matrix,
22  Nf1 gene mutation is a major determinant of optic glioma development and growth through by both tumo
23 und in NF1 patients lacking neurofibromas or optic gliomas, do not exhibit neuronal hyperexcitability
24 oss and Nf1 genetically engineered mice with optic glioma exhibit RGC neuronal apoptosis in vivo, we
25 1 expression in Nf1 optic glioma mice delays optic glioma formation.
26 act of the germline NF1 gene mutation on the optic gliomas frequently encountered in children with NF
27               Relative to neo(CKO) mice, the optic gliomas from R681X(CKO) mice had more microglia in
28 E4 inhibitor rolipram dramatically inhibited optic glioma growth and tumor size in Nf1 GEM in vivo.
29 roglia as a critical cellular determinant of optic glioma growth in Nf1 GEM.
30 cell type that promotes Nf1-/- astrocyte and optic glioma growth relevant to the pathogenesis of NF1-
31 timulation of optic nerve activity increases optic glioma growth, and that decreasing visual experien
32 ndings demonstrating that microglia maintain optic glioma growth, these new findings provide a strong
33  instructive role for CXCL12 in facilitating optic glioma growth, we also show that CXCL12 expression
34  prognosis of a case of unilateral malignant optic glioma in a young man with a history of brain glio
35 emonstrate that RGC apoptosis resulting from optic glioma in Nf1 genetically engineered mice is atten
36       Finally, we demonstrate that pediatric optic gliomas in Nf1 genetically engineered mice arise f
37 rlie the sexual dimorphic differences in Nf1 optic glioma-induced retinal dysfunction by operating at
38                                   Similar to optic glioma-induced RGC apoptosis, the increased RGC ne
39 ffected individuals develop glial neoplasms (optic gliomas, malignant astrocytomas) and neuronal dysf
40 ssor gene, individuals with NF1 are prone to optic gliomas, malignant gliomas, neurofibromas, and mal
41 enetic reduction of Cx3cr1 expression in Nf1 optic glioma mice delays optic glioma formation.
42 reduced expression of the microglia-produced optic glioma mitogen, Ccl5.
43 tively, these findings suggest that this Nf1 optic glioma model may be a potential preclinical benchm
44                   We first validated the Nf1 optic glioma model using conventional single-agent chemo
45                Previous studies in mouse Nf1 optic glioma models suggest that this patterning results
46 erence in clinical outcome, we leveraged Nf1 optic glioma (Nf1-OPG) mice.
47 d, can provide novel therapeutic avenues for optic gliomas of childhood.
48           Since children with NF1-associated optic gliomas often develop visual loss and Nf1 genetica
49                                 Using an Nf1 optic glioma (OPG) GEM model, we report novel defects in
50                         These differences in optic glioma phenotypes reflect both cell-autonomous and
51  optic glioma-bearing GEM results in reduced optic glioma proliferation in vivo.
52 ineered Nf1 mice significantly reduces mouse optic glioma proliferation in vivo.
53 a second metalloproteinase, MMP-9, in murine optic gliomas relative to normal non-neoplastic optic ne
54 nd protein structure of the myxoid matrix in optic gliomas to identify novel therapeutic targets.
55 of neurofibromatosis type 1 (NF1)-associated optic glioma, we now demonstrate that stromal microglia
56          Female patients with NF1-associated optic glioma were twice as likely to undergo brain magne
57 d liquid chromatography-mass spectrometry on optic gliomas, which varied in the amount of myxoid matr
58 work of pilomyxoid astrocytoma, a subtype of optic glioma with abundant myxoid matrix, is characteriz
59  R681X(CKO) but not G848R(CKO), mice develop optic gliomas with increased optic nerve volumes, glial