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3 was to determine the diagnostic criteria for neurofibromatosis 1 and neurofibromatosis 2, recommendat
8 expression profiles of six sporadic and two neurofibromatosis 1-associated PAs with other tissues an
9 ession was also determined in KIT mutant and neurofibromatosis-1-associated GIST, and complex II acti
11 ated with neurofibromatosis 1 show a loss of neurofibromatosis 1 expression and high levels of Ras, b
12 n EVH [Ena/Vasp homology] domain 1) and NF1 (neurofibromatosis 1) genes underlie clinically related h
15 in SDHB (n = 2), SDHD (n = 3), RET (n = 5), neurofibromatosis 1 (n = 1), and myc-associated factor X
18 negative Ras-MAPK-ERK regulator linked to a neurofibromatosis 1 (NF-1)-like human syndrome; however,
19 viduals with two inherited cancer syndromes, neurofibromatosis 1 (NF1) and neurofibromatosis 2 (NF2),
22 We have identified a protein isoform of the neurofibromatosis 1 (NF1) gene (neurofibromin) containin
26 he phosphatase and tensin homolog (Pten) and neurofibromatosis 1 (Nf1) genes recently were found to b
29 arning to rut mutants, whereas expression of Neurofibromatosis 1 (NF1) in alpha/beta neurons is suffi
31 of children develop PA in the context of the neurofibromatosis 1 (NF1) inherited tumor predisposition
36 aches to mutation detection in mRNA from the neurofibromatosis 1 (NF1) locus have required the PCR am
41 c nerve gliomas) are closely associated with neurofibromatosis 1 (NF1), and allelic losses of the NF1
42 uals with the tumor predisposition syndrome, neurofibromatosis 1 (NF1), are prone to development of n
43 the inherited tumor predisposition syndrome, neurofibromatosis 1 (NF1), are prone to the development
44 dren with the tumor predisposition syndrome, neurofibromatosis 1 (NF1), develop optic pathway gliomas
45 s using cells derived from a murine model of neurofibromatosis 1 (NF1), Yang et al. dissect the molec
52 aracterized by inactivating mutations of the Neurofibromatosis-1 (NF1) gene that predisposes these pa
53 ious studies from our laboratories have used neurofibromatosis-1 (NF1) genetically engineered mouse (
55 ommon clinical problems in children with the neurofibromatosis-1 (NF1) inherited cancer syndrome.
57 ma resulting from either inactivation of the neurofibromatosis-1 (Nf1) tumor suppressor gene or const
58 In this regard, mutational inactivation of neurofibromatosis-1 (NF1), tuberous sclerosis complex (T
60 ients and are a major contributing factor to neurofibromatosis-1 patient mortality and morbidity.
61 yndrome, tuberous sclerosis complex 1 and 2, neurofibromatosis 1, phosphatase and tensin homolog, and
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