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1 ullary thyroid carcinoma not associated with multiple endocrine neoplasia.
2 rectal, ovarian and endometrial cancers, and multiple endocrine neoplasia.
3 ine tumors (NETs), with special reference to multiple endocrine neoplasia 1 (MEN1) syndrome, using a
4 or protein whose loss or inactivation causes multiple endocrine neoplasia 1 (MEN1), a hereditary auto
5 pressor protein that is encoded by the MEN1 (multiple endocrine neoplasia 1) gene and controls cell g
6 or spectrum that overlaps with the inherited multiple endocrine neoplasia-1 (MEN1) and MEN2 syndromes
12 were not associated with pituitary tumors or multiple endocrine neoplasia but were due to a heterozyg
14 riers for highly penetrant syndromes such as multiple endocrine neoplasias, familial adenomatous poly
16 and astrocytic brain tumors, paraganglioma, multiple endocrine neoplasia IIB, and neuroendocrine tum
18 lasia types 2A and 2B and with familial, non-multiple endocrine neoplasia medullary thyroid carcinoma
19 in the ret oncogene are the direct cause of multiple endocrine neoplasia (MEN) 2A and 2B, familial m
24 most common cause of death in patients with multiple endocrine neoplasia (MEN) type 2A (MEN-2A) or t
25 carcinomas, MTCs) tumors from patients with multiple endocrine neoplasia (MEN) type 2A or 2B, relate
26 cancer may occur in isolation or as part of multiple endocrine neoplasia (MEN) type II syndromes.
28 lary thyroid carcinoma (MTC) associated with multiple endocrine neoplasia (MEN) types 2A and 2B and f
29 nts with familial pheochromocytomas (15 with multiple endocrine neoplasia [MEN] 2A, 4 with MEN 2B, 1
30 edullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cyste
32 Their presence should raise concern about a multiple endocrine neoplasia syndrome and appropriate di
33 Here, we report that rats affected by the multiple endocrine neoplasia syndrome MENX, caused by a
34 ons in the MEN1 gene are associated with the multiple endocrine neoplasia syndrome type 1 (MEN1), whi
35 years (range, <0.5-21); 13 were male, 7 had multiple endocrine neoplasia syndrome type I, 4 had unde
45 g in a large group of extended families with multiple endocrine neoplasia type 1 (MEN 1), with the ul
46 nts with sporadic ZES, but not in those with multiple endocrine neoplasia type 1 (MEN-1) and ZES, the
47 of heterozygosity (LOH) at the locus of the multiple endocrine neoplasia type 1 (MEN-1) gene was stu
49 previously identified at the locus linked to multiple endocrine neoplasia type 1 (MEN1) and as prespl
66 s occur both sporadically and as part of the multiple endocrine neoplasia type 1 (MEN1) syndrome.
68 nscriptionally active chromatin, whereas the multiple endocrine neoplasia type 1 (MEN1) tumor suppres
71 they are especially common in patients with multiple endocrine neoplasia type 1 (MEN1), and most stu
72 gene, mutations in which are responsible for multiple endocrine neoplasia type 1 (MEN1), encodes a 61
74 crine tumor susceptibility syndromes such as multiple endocrine neoplasia type 1 (MEN1), von Hippel L
84 ith lymph node involvement and patients with multiple endocrine neoplasia type 1 did not demonstrate
85 ar, the areas of gastrinoma, insulinoma, and multiple endocrine neoplasia type 1 have received carefu
86 from pituitary adenomas in two patients with multiple endocrine neoplasia type 1 in which cells with
90 ncing analysis, and deletion analysis of the multiple endocrine neoplasia type 1 locus succeeded in t
91 sm (FIHP), or as part of a syndrome, such as multiple endocrine neoplasia type 1 or hyperparathyroidi
92 e Zollinger-Ellison syndrome who do not have multiple endocrine neoplasia type 1 or metastatic diseas
97 nts, 123 had sporadic gastrinomas and 28 had multiple endocrine neoplasia type 1 with an imaged tumor
98 missense mutations found in individuals with multiple endocrine neoplasia type 1, and the interacting
99 in patients with ZES, especially those with multiple endocrine neoplasia type 1, and the precise ord
100 uitary neoplasias: McCune-Albright syndrome, multiple endocrine neoplasia type 1, Carney complex and,
101 product of the MEN1 gene mutated in familial multiple endocrine neoplasia type 1, has not been define
102 ect genetic evidence that MEN1, the gene for multiple endocrine neoplasia type 1, is a tumor suppress
106 phaeochromocytoma (MIM No 171300) occurs in multiple endocrine neoplasia type 2 (MEN 2) (MIM No 1714
110 sible for the familial tumor syndrome called multiple endocrine neoplasia type 2 (MEN 2) that include
111 ase underlies the genesis and progression of multiple endocrine neoplasia type 2 (MEN 2), a dominantl
112 ery cell of the body) mutations in RET cause multiple endocrine neoplasia type 2 (MEN 2), an inherite
113 ibility are von Hippel-Lindau disease (VHL), multiple endocrine neoplasia type 2 (MEN 2), the newly d
116 s patients with von Hippel-Lindau disease or multiple endocrine neoplasia type 2 (MEN-2), is hindered
118 and nonmedullary thyroid cancers related to multiple endocrine neoplasia type 2 (MEN2), Cowden syndr
122 sing a Ret-kinase-driven Drosophila model of multiple endocrine neoplasia type 2 and kinome-wide drug
123 n-based study compiled data on patients with multiple endocrine neoplasia type 2 from 30 academic med
124 ast year addressing the surgical approach to multiple endocrine neoplasia type 2 in the pediatric pop
126 of medullary thyroid cancer in patients with multiple endocrine neoplasia type 2 syndrome has demonst
128 tential therapeutic agents for patients with multiple endocrine neoplasia type 2 tumors because both,
130 gical intervention in children affected with multiple endocrine neoplasia type 2 will lead to better
131 ly active oncogenic RET, were found to cause multiple endocrine neoplasia type 2, a dominant inherite
132 r, the other major neoplasia associated with multiple endocrine neoplasia type 2, phaeochromocytoma,
134 somal dominantly inherited cancer syndromes, multiple endocrine neoplasia type 2, von Hippel-Lindau d
135 d for 84% of the patients; the other 16% had multiple endocrine neoplasia type 2, von Recklinghausen'
144 been described as the following phenotypes: multiple endocrine neoplasia type 2A (MEN 2A) and multip
149 l as RET oncoproteins found in patients with multiple endocrine neoplasia type 2A and 2B (2A/RET and
152 ple endocrine neoplasia type 2A (MEN 2A) and multiple endocrine neoplasia type 2B (MEN 2B) syndromes.
156 taining the Ret mutation responsible for the multiple endocrine neoplasia type 2B syndrome (MEN 2B).
157 ases, and homologous to the codon mutated in multiple endocrine neoplasia type 2B, and many cases of
165 suppressor that is mutated in patients with multiple endocrine neoplasia type I (MEN1), an inherited
166 markers is still required for patients with multiple endocrine neoplasia type I because the responsi
168 hese include menin, which is responsible for multiple endocrine neoplasia type I, and the hybrid gene
169 milial predisposition to pheochromocytoma in multiple endocrine neoplasia type II, and mutations in t
170 beta), T-type calcium channel (CACNA1G), and multiple endocrine neoplasia type-1 (MEN1) genes, and of
171 have shown that the gene responsible for the multiple endocrine neoplasia type-1 (MEN1) syndrome loca
174 S were studied prospectively, with 39 having multiple endocrine neoplasia, type 1 (MEN-1) (high incre
176 d with cystic fibrosis, hemochromatosis, and multiple endocrine neoplasia, type 2, respectively.
181 gical cure rate in patients with and without Multiple Endocrine Neoplasia-type1 (MEN1), the biologica
183 de the dominantly inherited cancer syndromes multiple endocrine neoplasia types 2A and 2B (MEN 2A and
184 Experience with management of patients with multiple endocrine neoplasia types 2A and 2B and with fa
185 , breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and famili
186 gene have been demonstrated in patients with multiple endocrine neoplasia types IIA, IIB, and familia
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