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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
12                            Major superficial plexiform neurofibromas and symptomatic spinal neurofibr
13 n S-100 positive Schwann cells of dermal and plexiform neurofibromas, and in endothelial cells of tum
14                                              Plexiform neurofibromas are common NF1 tumors carrying a
15                                              Plexiform neurofibromas are one of the most common tumor
16                                              Plexiform neurofibromas are pathognomonic of the disease
17                                              Plexiform neurofibromas are peripheral nerve sheath tumo
18                                   Dermal and plexiform neurofibromas are peripheral nerve sheath tumo
19                                              Plexiform neurofibromas are slow growing benign tumors t
20                                              Plexiform neurofibromas are slow-growing chemoradiothera
21 ptic pathway gliomas (OPGs) and orbitofacial plexiform neurofibromas are two of the more common ophth
22                                   Dermal and plexiform neurofibromas as well as malignant peripheral
23 with neurofibromatosis type 1 and inoperable plexiform neurofibromas benefited from long-term dose-ad
24               Patients commonly present with plexiform neurofibromas, benign but debilitating growths
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
27                  Previous studies found that plexiform neurofibroma formation in a mouse model requir
28 urine models that closely recapitulate human plexiform neurofibroma formation indicate that tumorigen
29                           In mouse models of plexiform neurofibroma formation, Nf1 haploinsufficient
30 dies implicating the hematopoietic system in plexiform neurofibroma genesis, delineate the physiology
31 indicated a role for the microenvironment in plexiform neurofibroma genesis.
32                                              Plexiform neurofibromas have an intermediate range of le
33                                       Benign plexiform neurofibromas in NF1 patients can transform sp
34     Imatinib mesylate could be used to treat plexiform neurofibromas in patients with NF1.
35  the volume burden of clinically significant plexiform neurofibromas in patients with NF1.
36 val overgrowth is caused by the formation of plexiform neurofibromas in the connective tissue of the
37 cursors (SCP), which have been implicated in plexiform neurofibroma initiation.
38                     Extent of orbitotemporal plexiform neurofibroma involvement was assessed clinical
39  of Nf1 resulted in the development of small plexiform neurofibromas late in life, whereas loss in ad
40                               Orbitotemporal plexiform neurofibroma location was classified as isolat
41                                    Thus, the plexiform neurofibroma microenvironment involves a tumor
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
46 pe with neither externally visible cutaneous/plexiform neurofibromas nor other tumors.
47 , and facial structures (orbital-periorbital plexiform neurofibroma [OPPN]) can result in significant
48                                     Although plexiform neurofibroma (PN) is thought to represent a be
49 irtually pathognomonic finding of NF1 is the plexiform neurofibroma (PN), a benign, likely congenital
50                                              Plexiform neurofibromas (PNs) involving the eyelid, orbi
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
55        In addition, malignant progression of plexiform neurofibromas to malignant peripheral nerve sh
56 nt coincides with enhanced susceptibility to plexiform neurofibroma tumorigenesis.
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
59 l subjects with amblyopia had orbitotemporal plexiform neurofibroma volumes greater than 10 mL.
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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