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1 help guide molecular interventions in ocular von Hippel-Lindau disease.
2 of these mutants may rescue pVHL function in von Hippel-Lindau disease.
3 cal characterization and treatment of ocular von Hippel-Lindau disease.
4 ogenesis, which can occur sporadically or in von Hippel-Lindau disease.
5 role in the pathogenesis of renal cancer and von Hippel-Lindau disease.
6 pects, management, and treatment options for von Hippel-Lindau disease.
7 familial disposition to pheochromocytoma in von Hippel-Lindau disease.
8 hromocytoma should be screened for MEN-2 and Von Hippel-Lindau disease.
9 the familial cancer predisposition syndrome von Hippel-Lindau disease.
10 hemangioma with or without association with von Hippel-Lindau disease.
11 rmline mutation in the VHL gene leads to the von Hippel-Lindau disease, a familial syndrome character
12 suppressor protein (pVHL) is associated with von Hippel-Lindau disease, an inherited cancer syndrome,
14 hereditary renal cancers in adults included von Hippel-Lindau disease and a rare form of chromosomal
15 hatic sac tumors (ELSTs) are associated with von Hippel-Lindau disease and cause irreversible sensori
16 ctive and serial evaluation of patients with von Hippel-Lindau disease and ELSTs at the National Inst
18 pressor gene is inactivated in patients with von Hippel-Lindau disease and in most sporadic clear cel
21 t knowledge of the molecular pathogenesis of von Hippel-Lindau disease and the role of the VHL gene p
22 Two had prior clinical manifestations of von Hippel-Lindau disease and, as expected, had germline
24 pressor gene predisposes patients to develop von Hippel-Lindau disease, and somatic VHL inactivation
26 f eye disease may inform us as to how ocular von Hippel-Lindau disease arises, and help guide molecul
27 C), as VHL mutations have been found in both von Hippel-Lindau disease-associated and sporadic RCCs.
29 erization of renal cancer syndromes includes von Hippel-Lindau disease, Birt-Hogg-Dube syndrome, here
32 s of metanephrine, whereas the patients with von Hippel-Lindau disease had almost exclusively high pl
33 titative clinical characterization of ocular von Hippel-Lindau disease has been limited by small pati
37 ble a full characterization of the impact of von Hippel-Lindau disease on eye health and visual funct
39 ified pheochromocytomas and 50 patients with von Hippel-Lindau disease or MEN-2 who had no radiologic
41 risk for these tumors, such as patients with von Hippel-Lindau disease or multiple endocrine neoplasi
43 s performed on postmortem tissues from three von Hippel-Lindau disease patients (not in the clinical
44 correlated with the clinical findings in 16 von Hippel-Lindau disease patients with 22 CNS hemangiob
45 netic resonance imaging (MRI) is obtained in von Hippel-Lindau disease patients, hemangioblastomas pr
46 ularly US screening studies in patients with von Hippel-Lindau disease should be interpreted cautious
47 therapies targeting the molecular biology of von Hippel-Lindau disease, some of which are presently b
49 o other causes of inherited renal carcinoma, von Hippel-Lindau disease (VHL) and the chromosome trans
53 euroendocrine tumors (PNETs) associated with von Hippel-Lindau disease (VHL) is challenging because o
56 dromes, multiple endocrine neoplasia type 2, von Hippel-Lindau disease (VHL), and, very rarely, type
57 uses of phaeochromocytoma susceptibility are von Hippel-Lindau disease (VHL), multiple endocrine neop
58 examined the promoter methylation status of von Hippel-Lindau disease (VHL), retinoic acid receptor
60 ents with clinically and genetically defined von Hippel-Lindau disease was systemically characterized
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