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1 to the impairment of QOL in individuals with neurofibromatosis 1.
4 was to determine the diagnostic criteria for neurofibromatosis 1 and neurofibromatosis 2, recommendat
8 ysfunction is among the hallmark symptoms of Neurofibromatosis 1, and accordingly, loss of the Drosop
10 expression profiles of six sporadic and two neurofibromatosis 1-associated PAs with other tissues an
11 ession was also determined in KIT mutant and neurofibromatosis-1-associated GIST, and complex II acti
13 ated with neurofibromatosis 1 show a loss of neurofibromatosis 1 expression and high levels of Ras, b
14 n EVH [Ena/Vasp homology] domain 1) and NF1 (neurofibromatosis 1) genes underlie clinically related h
17 in SDHB (n = 2), SDHD (n = 3), RET (n = 5), neurofibromatosis 1 (n = 1), and myc-associated factor X
20 negative Ras-MAPK-ERK regulator linked to a neurofibromatosis 1 (NF-1)-like human syndrome; however,
21 viduals with two inherited cancer syndromes, neurofibromatosis 1 (NF1) and neurofibromatosis 2 (NF2),
23 Fifteen per cent of individuals with the neurofibromatosis 1 (NF1) cancer predisposition syndrome
25 We have identified a protein isoform of the neurofibromatosis 1 (NF1) gene (neurofibromin) containin
29 he phosphatase and tensin homolog (Pten) and neurofibromatosis 1 (Nf1) genes recently were found to b
32 arning to rut mutants, whereas expression of Neurofibromatosis 1 (NF1) in alpha/beta neurons is suffi
34 of children develop PA in the context of the neurofibromatosis 1 (NF1) inherited tumor predisposition
41 aches to mutation detection in mRNA from the neurofibromatosis 1 (NF1) locus have required the PCR am
46 c nerve gliomas) are closely associated with neurofibromatosis 1 (NF1), and allelic losses of the NF1
47 uals with the tumor predisposition syndrome, neurofibromatosis 1 (NF1), are prone to development of n
48 the inherited tumor predisposition syndrome, neurofibromatosis 1 (NF1), are prone to the development
49 dren with the tumor predisposition syndrome, neurofibromatosis 1 (NF1), develop optic pathway gliomas
50 s using cells derived from a murine model of neurofibromatosis 1 (NF1), Yang et al. dissect the molec
57 aracterized by inactivating mutations of the Neurofibromatosis-1 (NF1) gene that predisposes these pa
58 ious studies from our laboratories have used neurofibromatosis-1 (NF1) genetically engineered mouse (
60 ommon clinical problems in children with the neurofibromatosis-1 (NF1) inherited cancer syndrome.
62 s, T cells, and microglia interact to govern Neurofibromatosis-1 (NF1) low-grade glioma (LGG) growth.
63 ma resulting from either inactivation of the neurofibromatosis-1 (Nf1) tumor suppressor gene or const
64 In this regard, mutational inactivation of neurofibromatosis-1 (NF1), tuberous sclerosis complex (T
65 models of the tumor predisposition syndrome Neurofibromatosis-1 (NF1), with different propensities t
67 ients and are a major contributing factor to neurofibromatosis-1 patient mortality and morbidity.
68 yndrome, tuberous sclerosis complex 1 and 2, neurofibromatosis 1, phosphatase and tensin homolog, and
70 ouse model of OPG driven by mutations in the neurofibromatosis 1 tumour suppressor gene (Nf1)(5) to d