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1 land (seven with lymphadenopathy, one with a plexiform neurofibroma).
2 nalysis to measure the change in size of the plexiform neurofibroma.
3 include myeloid leukemia, optic glioma, and plexiform neurofibroma.
4 and to have NF1 and a clinically significant plexiform neurofibroma.
5 ically treated a patient with a debilitating plexiform neurofibroma.
6 l databases for children with orbitotemporal plexiform neurofibromas.
7 utaneous neurofibromas or clinically obvious plexiform neurofibromas.
8 and neurofibromatosis type 1 (NF1) -related plexiform neurofibromas.
9 firmed RUNX1 protein overexpression in human plexiform neurofibromas.
10 ues define the cell of origin for murine Nf1 plexiform neurofibroma and leverage this finding to deve
11 life, whereas loss in adulthood caused large plexiform neurofibromas and morbidity beginning 4 months
13 n S-100 positive Schwann cells of dermal and plexiform neurofibromas, and in endothelial cells of tum
21 ptic pathway gliomas (OPGs) and orbitofacial plexiform neurofibromas are two of the more common ophth
23 with neurofibromatosis type 1 and inoperable plexiform neurofibromas benefited from long-term dose-ad
25 es were established from 10 dermal and eight plexiform neurofibromas by selective subculture using gl
26 (NF-1), malignant transformation of internal plexiform neurofibromas carries a poor prognosis, in par
28 urine models that closely recapitulate human plexiform neurofibroma formation indicate that tumorigen
30 dies implicating the hematopoietic system in plexiform neurofibroma genesis, delineate the physiology
36 val overgrowth is caused by the formation of plexiform neurofibromas in the connective tissue of the
39 of Nf1 resulted in the development of small plexiform neurofibromas late in life, whereas loss in ad
42 that mast cells underpin inflammation in the plexiform neurofibroma microenvironment of neurofibromat
43 delineate hematopoietic contributions to the plexiform neurofibroma microenvironment, and highlight a
44 han half of NF1 children with orbitotemporal plexiform neurofibromas, most commonly because of ptosis
45 ngineered mouse model that accurately models plexiform neurofibroma-MPNST progression in humans would
47 , and facial structures (orbital-periorbital plexiform neurofibroma [OPPN]) can result in significant
49 irtually pathognomonic finding of NF1 is the plexiform neurofibroma (PN), a benign, likely congenital
51 for sensitive measurement of orbitotemporal plexiform neurofibroma size, and larger volumes were ass
52 viable therapeutic options for patients with plexiform neurofibromas that cannot be surgically remove
53 eurofibromatosis type 1 (NF1) develop benign plexiform neurofibromas that frequently progress to beco
54 had neurofibromatosis type 1 and inoperable plexiform neurofibromas to determine the maximum tolerat
57 tients with NF1 have cutaneous, diffuse, and plexiform neurofibromas, tumors comprised primarily of S
58 0%; 95% CI, 0%-7%) had discrete cutaneous or plexiform neurofibromas, typical NF1 osseous lesions, or
60 Amblyopia secondary to the orbitotemporal plexiform neurofibroma was present in 13 subjects (62%)
61 e or decrease from baseline in the volume of plexiform neurofibromas) was monitored by using volumetr
62 reatment of neurofibromatosis type 1-related plexiform neurofibromas, which are characterized by elev
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