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1 ts with multiple endocrine neoplasia type 2 (MEN 2).
2 ndromes multiple endocrine neoplasia type 2 (MEN 2).
3 HD 2 to 63 years before being diagnosed with MEN 2.
4 mptoms 1 to 24 years before the diagnosis of MEN 2.
5 ochromocytoma tumorigenesis in patients with MEN 2.
6 d treatment they had before the diagnosis of MEN 2.
7 n patients with von Hippel-Lindau disease or MEN-2.
8 d randomisation (via minimisation) allocated men 2:1:1:1 to standard of care only (SOC-only; control)
9 ire population was 2.88% (women 4.24% versus men 2.23%, P<0.0001).
10 x effect for bladder cancer (OR for women vs men 2.31, 95% CI 1.98-2.69) and no apparent ethnic group
11 chromocytoma developed in four patients with MEN 2 (33%); three of them underwent adrenalectomy.
12 azard ratio in women 2.9 [1.7 to 5.0] and in men 2.4 [1.5 to 4.0]).
13  right ventricular muscle mass (women, 1.58; men 2.45; P=0.001), poorer peak oxygen uptake (women, -1
14 icant (women 3.83, 95% CI 1.09 to 13.47, and men 2.70, 95% CI 1.11 to 6.55).
15 sion of multiple endocrine neoplasia type 2 (MEN 2), a dominantly inherited cancer predisposition.
16 T cause multiple endocrine neoplasia type 2 (MEN 2), an inherited cancer syndrome characterized by me
17                      Rare families with both MEN 2 and Hirschsprung disease were found to have MEN 2-
18  and in the VHL tumour suppressor gene cause MEN 2 and VHL disease, respectively.
19 dic" pheochromocytoma should be screened for MEN-2 and Von Hippel-Lindau disease.
20 jority of cases of inherited cancer syndrome MEN 2, and inactivating mutations in some cases of domin
21 ermline mutations in RET are responsible for MEN 2 but the precise pathogenetic mechanisms of tumorig
22 to treat human papillary thyroid carcinomas, MEN 2 disease, as well as the sporadic cancers relevant
23  as well as the sporadic cancers relevant to MEN 2 disease.
24  The identification of RET mutations in most MEN 2 families (95%) has translated into improved care f
25 esting is considered the standard of care in MEN 2 families because clinical decisions are made based
26                            All patients with MEN-2 had high plasma concentrations of metanephrine, wh
27         Multiple endocrine neoplasia type 2 (MEN 2) is an autosomal dominant disorder.
28         Multiple endocrine neoplasia type 2 (MEN 2) is an inherited cancer syndrome that includes phe
29 ease or multiple endocrine neoplasia type 2 (MEN-2), is hindered by the inadequate sensitivity of com
30 RET lead to tumor formation in patients with MEN 2, it is not understood why only selected cells deve
31                     The clinical subtypes of MEN 2 (MEN 2A, MEN 2B and familial MTC) all have medulla
32 curs in multiple endocrine neoplasia type 2 (MEN 2) (MIM No 171400), von Hippel-Lindau (VHL) disease
33                     Using RET activated by a MEN 2 mutation, we show that both the SH2 and PTB domain
34 of patients with no evidence of VHL disease, MEN 2 or NF1: Group A, eight kindreds with familial phae
35  (95%) has translated into improved care for MEN 2 patients.
36 n GDNF in 28 sporadic phaeochromocytomas, 12 MEN 2 phaeochromocytomas and five VHL phaeochromocytomas
37 associated with tumorigenesis in hereditary, MEN 2-related pheochromocytoma.
38 omocytomas from five unrelated patients with MEN 2 showed either duplication of the mutant RET allele
39  and Hirschsprung disease were found to have MEN 2-specific codon mutations.
40                     The familial MTC type of MEN 2 syndrome was included within the spectrum of MEN 2
41         Multiple endocrine neoplasia type 2 (MEN 2) syndrome is an autosomal dominant, hereditary can
42                                          The MEN 2 syndromes are characterized by medullary thyroid c
43  called multiple endocrine neoplasia type 2 (MEN 2) that includes medullary thyroid carcinoma (MTC).
44  (VHL), multiple endocrine neoplasia type 2 (MEN 2), the newly delineated phaeochromocytoma-paragangl
45 be monitored for the possible development of MEN 2 tumors.
46                Von Hippel-Lindau disease and MEN-2 were diagnosed on the basis of germ-line mutations
47  the presence of certain disease features in MEN 2 which could help in clinical decision making.
48 on Hippel-Lindau disease and 9 patients with MEN-2 who had histologically verified pheochromocytomas
49 0 patients with von Hippel-Lindau disease or MEN-2 who had no radiologic evidence of pheochromocytoma

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