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1 molecular interventions in ocular von Hippel-Lindau disease.
2 tants may rescue pVHL function in von Hippel-Lindau disease.
3 erization and treatment of ocular von Hippel-Lindau disease.
4 hich can occur sporadically or in von Hippel-Lindau disease.
5 pathogenesis of renal cancer and von Hippel-Lindau disease.
6 gement, and treatment options for von Hippel-Lindau disease.
7 isposition to pheochromocytoma in von Hippel-Lindau disease.
8 should be screened for MEN-2 and Von Hippel-Lindau disease.
9 al cancer predisposition syndrome von Hippel-Lindau disease.
10 with or without association with von Hippel-Lindau disease.
11 tion in the VHL gene leads to the von Hippel-Lindau disease, a familial syndrome characterized by ben
12 protein (pVHL) is associated with von Hippel-Lindau disease, an inherited cancer syndrome, as well as
14 renal cancers in adults included von Hippel-Lindau disease and a rare form of chromosomal translocat
15 umors (ELSTs) are associated with von Hippel-Lindau disease and cause irreversible sensorineural hear
16 erial evaluation of patients with von Hippel-Lindau disease and ELSTs at the National Institutes of H
18 e is inactivated in patients with von Hippel-Lindau disease and in most sporadic clear cell renal car
21 of the molecular pathogenesis of von Hippel-Lindau disease and the role of the VHL gene product (pVH
22 prior clinical manifestations of von Hippel-Lindau disease and, as expected, had germline von Hippel
24 tiple endocrine neoplasia type 2, von Hippel-Lindau disease, and familial adenomatous polyposis are e
25 e predisposes patients to develop von Hippel-Lindau disease, and somatic VHL inactivation is an early
27 se may inform us as to how ocular von Hippel-Lindau disease arises, and help guide molecular interven
30 nts with an objective response in von Hippel-Lindau disease-associated renal cell carcinoma per Respo
31 ibitor belzutifan is approved for von Hippel-Lindau disease-associated renal cell carcinoma, CNS haem
35 ears or older with a diagnosis of von Hippel-Lindau disease (based on germline VHL alterations), at l
36 f renal cancer syndromes includes von Hippel-Lindau disease, Birt-Hogg-Dube syndrome, hereditary papi
39 phrine, whereas the patients with von Hippel-Lindau disease had almost exclusively high plasma concen
40 inical characterization of ocular von Hippel-Lindau disease has been limited by small patient numbers
42 promising activity against ocular von Hippel-Lindau disease, including capacity to control retinal he
48 hromocytomas and 50 patients with von Hippel-Lindau disease or MEN-2 who had no radiologic evidence o
50 ese tumors, such as patients with von Hippel-Lindau disease or multiple endocrine neoplasia type 2 (M
52 on postmortem tissues from three von Hippel-Lindau disease patients (not in the clinical series).
53 with the clinical findings in 16 von Hippel-Lindau disease patients with 22 CNS hemangioblastomas (1
54 ance imaging (MRI) is obtained in von Hippel-Lindau disease patients, hemangioblastomas provide an op
55 creening studies in patients with von Hippel-Lindau disease should be interpreted cautiously because
56 argeting the molecular biology of von Hippel-Lindau disease, some of which are presently being invest
58 ses of inherited renal carcinoma, von Hippel-Lindau disease (VHL) and the chromosome translocation (3
60 meet the diagnostic criteria for von Hippel-Lindau disease (VHL) have a detectable inactivating germ
63 ne tumors (PNETs) associated with von Hippel-Lindau disease (VHL) is challenging because of the malig
66 tiple endocrine neoplasia type 2, von Hippel-Lindau disease (VHL), and, very rarely, type 1 neurofibr
67 eochromocytoma susceptibility are von Hippel-Lindau disease (VHL), multiple endocrine neoplasia type
68 he promoter methylation status of von Hippel-Lindau disease (VHL), retinoic acid receptor beta (RAR-b
70 linically and genetically defined von Hippel-Lindau disease was systemically characterized in a singl
71 e VHL tumor suppressor gene cause von Hippel-Lindau disease, which is associated with an increased ri