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1                                              MEN1 and its coactivator, the mixed-lineage leukemia his
2                                              MEN1 is a likely tumor suppressor gene that encodes a no
3                                              MEN1 is a tumor suppressor gene that encodes a 610 amino
4                                              MEN1 is an autosomal dominant disease characterized by p
5                                              MEN1 knockdown decreased nAChR alpha5 subunit expression
6                                              MEN1 mutations frequently cause neuroendocrine tumors su
7                                              MEN1 RNA and corresponding protein levels were all reduc
8                                              MEN1-associated gastrinomas, which develop in the submuc
9                                              MEN1-associated neuroendocrine and some mesenchymal tumo
10 reference to multiple endocrine neoplasia 1 (MEN1) syndrome, using a Men1 mouse model.
11 ation causes multiple endocrine neoplasia 1 (MEN1), a hereditary autosomal dominant tumour syndrome t
12 he inherited multiple endocrine neoplasia-1 (MEN1) and MEN2 syndromes in humans, including medullary
13 nked to multiple endocrine neoplasia type 1 (MEN1) and as presplicing factor SF1.
14 nes for multiple endocrine neoplasia type 1 (MEN1) at 11q13, we cloned the human homologue of Sipa-1.
15         Multiple endocrine neoplasia type 1 (MEN1) consists of benign, and sometimes malignant, tumor
16 ts with multiple endocrine neoplasia type 1 (MEN1) develop multiple endocrine tumors, primarily affec
17         Multiple endocrine neoplasia type 1 (MEN1) is a dominantly inherited tumor syndrome that resu
18         Multiple endocrine neoplasia type 1 (MEN1) is a familial cancer syndrome characterized by tum
19         Multiple endocrine neoplasia type 1 (MEN1) is a familial tumor syndrome linked to mutation of
20         Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant cancer syndrome, characte
21         Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder associated mainl
22         Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder that results in
23         Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant hereditary disorder chara
24         Multiple endocrine neoplasia type 1 (MEN1) is an autosomal syndrome caused by mutations in th
25         Multiple endocrine neoplasia type 1 (MEN1) is an inherited syndrome characterized by developm
26         Multiple endocrine neoplasia type 1 (MEN1) is an inherited tumor syndrome that includes susce
27         Multiple endocrine neoplasia type 1 (MEN1) is characterized by the combined occurrence of pit
28         Multiple endocrine neoplasia type 1 (MEN1) is characterized by tumors of the parathyroid, ent
29 S: The multiple endocrine neoplasia, type 1 (MEN1) locus encodes the nuclear protein and tumor suppre
30 HPT) in multiple endocrine neoplasia type 1 (MEN1) patients with Zollinger-Ellison syndrome (ZES) is
31  of the multiple endocrine neoplasia type 1 (MEN1) syndrome.
32 eas the multiple endocrine neoplasia type 1 (MEN1) tumor suppressor promotes H3K4 methylation.
33         Multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant disorder, is characterised
34         Multiple endocrine neoplasia type 1 (MEN1), an inherited tumor syndrome affecting endocrine o
35 ts with multiple endocrine neoplasia type 1 (MEN1), and most studies of these tumors have focused on
36 ble for multiple endocrine neoplasia type 1 (MEN1), encodes a 610-amino acid protein, denoted menin.
37         Multiple endocrine neoplasia type 1 (MEN1), the heritable tendency to develop tumors of the p
38 such as multiple endocrine neoplasia type 1 (MEN1), von Hippel Lindau (VHL) syndrome, neurofibromatos
39 ultiple endocrine neoplasia syndrome type 1 (MEN1), which is characterized by parathyroid hyperplasia
40 yndrome multiple endocrine neoplasia type 1 (MEN1).
41 ndrome, multiple endocrine neoplasia type 1 (MEN1).
42 ts with multiple endocrine neoplasia type 1 (MEN1).
43 on with multiple endocrine neoplasia type 1 (MEN1).
44 part of multiple endocrine neoplasia type 1 (MEN1).
45 uent in multiple endocrine neoplasia type 1 (MEN1).
46 ns with multiple endocrine neoplasia type 1 (MEN1).
47 G), and multiple endocrine neoplasia type-1 (MEN1) genes, and of MINT1, MINT2, MINT25, MINT27 and MIN
48 rome of multiple endocrine neoplasia type-1 (MEN1).
49 es located on chromosomes 9p21 (p16), 11q13 (MEN1), 11q23 (SDHD), 16q21, 18q21, and 18q22-23.
50 creatic ETs (nongastrinomas), 14 of 34 (41%) MEN1-associated gastrinomas, 3 of 16 (19%) sporadic insu
51     11q13 LOH was detected in 10 of 12 (83%) MEN1-associated esophageal and uterine smooth muscle tum
52 ome 11q13 LOH was detected in 23 of 27 (85%) MEN1-associated pancreatic ETs (nongastrinomas), 14 of 3
53        Additionally, a lung carcinoid from a MEN1 patient was studied.
54     All four tumors showed the presence of a MEN1 gene mutation and loss of the other allele.
55 even tumors showed neither the presence of a MEN1 gene mutation nor 11q13 LOH.
56       We report here the identification of a MEN1 ortholog in Drosophila melanogaster, Menin1, that e
57                    Most germline or acquired MEN1 mutations predicted truncation (and thus likely ina
58 tic testing identifies patients harboring an MEN1 mutation before the development of clinical signs o
59                     Twenty-nine sporadic and MEN1 pancreatic endocrine tumors were studied for loss o
60 with sporadic ZES and 0% (0/38) with ZES and MEN1 remained cured with only a LN tumor removed.
61 ions in ubiquitously expressed genes such as MEN1 could occur because of functional consequences on t
62 ect genetic testing for a disease-associated MEN1 mutation is now possible in selected families.
63 rminus of menin mediates binding to DNA, but MEN1 disease-derived mutations in the COOH terminus abol
64  as a downstream target of menin (encoded by MEN1).
65 he 610-amino acid nuclear protein encoded by MEN1, binds to the transcription factor JunD and can rep
66         Menin is a 70-kDa protein encoded by MEN1, the tumor suppressor gene disrupted in multiple en
67  activity is related to tumor suppression by MEN1.
68  of glutamatergic synapses was unaffected by MEN1 knockdown, indicating that the synaptogenic actions
69 enes have already been excluded as candidate MEN1 genes.
70 gressively narrows the size of the candidate MEN1 gene interval on the chromosome and then finds and
71                        The MEN1 gene causing MEN1 is a tumor suppressor gene and seems to act as a re
72    Several naturally occurring and clustered MEN1 missense mutations disrupted menin interaction with
73 s and outcomes of 27 prospectively collected MEN1 patients with biochemically proven gastrinoma, who
74                        Following DNA damage, MEN1 levels increase as a result of phosphorylation by t
75  and some mesenchymal tumors have documented MEN1 gene alterations on chromosome 11q13.
76        Patients were selected from the Dutch MEN1 database, including all patients 16 years or older
77 ents and 1 pituitary adenoma from a familial MEN1 patient were examined for MEN1 gene mutations and a
78 he tumor suppressor gene mutated in familial MEN1, we characterized p18-Men1 and p27-Men1 double muta
79 he tumor suppressor gene mutated in familial MEN1, we characterized p18-Men1 and p27-Men1 double muta
80 ing germ-line DNA in a patient with familial MEN1.
81                          However, only a few MEN1-associated duodenal gastrinomas and sporadic pancre
82 ponderance of cancer genes, including FGFR2, MEN1, HOOK3, EZH2, MLF1, CARD11, VHL, NONO, and SMAD1.
83                               Candidates for MEN1 mutation testing include patients with MEN1 or its
84 bilateral TCT is the procedure of choice for MEN1-related pHPT.
85 n and a permissive endocrine environment for MEN1 tumorigenesis in endocrine pancreas.
86 om a familial MEN1 patient were examined for MEN1 gene mutations and allelic deletions.
87 mas and 12 insulinomas) from 40 patients for MEN1 gene mutations and allelic deletions.
88           Recently, the gene responsible for MEN1 was cloned.
89 A alterations, including disparate roles for MEN1 gene inactivation, indicate that markedly different
90                                  Testing for MEN1 germline mutation is possible in a research setting
91 g all patients 16 years or older treated for MEN1 from 1990 to 2009.
92 enin is encoded by the tumor suppressor gene MEN1 that is mutated in patients with an inherited tumor
93 gosity in the putative tumor suppressor gene MEN1.
94 onstrated that members of a three-generation MEN1 kindred are heterozygous for a donor splice site mu
95 racterization of the tumor suppressor genes, MEN1, VHL, NF-1, TSC1, and TSC2.
96                                     Germline MEN1 mutations were found in most families with MEN1 and
97 H at chromosome 11q13 and a complex germline MEN1 gene mutation.
98 ein are the predominant cause for hereditary MEN1 syndrome.
99                                          HPT/MEN1/ZES is a severe form of parathyroid hyperplasia wit
100 al procedure of choice for patients with HPT/MEN1/ZES is 3.5-gland parathyroidectomy.
101         Multiple endocrine neoplasia type I (MEN1) is a hereditary tumor syndrome characterized by mu
102         Multiple endocrine neoplasia type I (MEN1) is an autosomal dominant cancer predisposition syn
103        Multiple endocrine neoplasia, type I (MEN1) is an inherited cancer syndrome characterized by t
104         Multiple endocrine neoplasia type I (MEN1) is an inherited syndrome that includes susceptibil
105         Multiple endocrine neoplasia type I (MEN1) is an inherited tumor syndrome characterized by tu
106         Multiple endocrine neoplasia type I (MEN1), a hereditary tumor syndrome, is characterized by
107 ts with multiple endocrine neoplasia type I (MEN1), an inherited tumor-prone syndrome.
108                                           In MEN1, multiple gastrinomas have been shown to arise by i
109 Twenty-two (81%) patients with gastrinoma in MEN1 had duodenal gastrinomas and 5 patients (19%) had p
110                                Gastrinoma in MEN1 is considered a rarely curable disease and its mana
111                       Duodenal gastrinoma in MEN1 should be considered a surgically curable disease.
112 vated in beta cells with menin knockdown, in MEN1-associated beta cell tumors (insulinomas), and also
113               The lower rate of 11q13 LOH in MEN1-associated and sporadic gastrinomas and sporadic in
114 or gene Men1, which is frequently mutated in MEN1 patients, encodes the nuclear protein menin.
115                          The gene mutated in MEN1 patients, Men1, encodes a protein of 610 amino acid
116                          The gene mutated in MEN1 patients, Men1, encodes a tumor suppressor, menin.
117                   Together with mutations in MEN1 and VHL, these mutations occur in 17% of patients.
118 tumors had somatic inactivating mutations in MEN1, which encodes menin, a component of a histone meth
119 ome that is caused by germ line mutations in MEN1.
120 methods for detecting and treating P-NETs in MEN1 patients, and extrapolations from approaches used i
121 mponent to development of pancreatic NETs in MEN1 syndrome.
122 r more should not be considered permanent in MEN1.
123 dgehog signaling targets including Ptch1, in MEN1 tumors of mice.
124 mutations and in-frame deletions reported in MEN1 patients appear in amino acid residues that are ide
125        Surgery is the preferred treatment in MEN1-related pHPT, but the surgical procedure of choice
126 and concomitant presence of other tumours in MEN1 patients.
127 t leiomyomata of the esophagus and uterus in MEN1 patients arise as independent clones, develop throu
128 hods was used to assess clonality, including MEN1 gene mutation analysis, loss of heterozygosity anal
129 tive and intraoperative localization of many MEN1-associated tumors.
130                                       Menin (MEN1) is a tumor-suppressor protein in neuroendocrine ti
131 th factor expression in both human and mouse MEN1 pancreatic endocrine tumors.
132 ors in these patients result when the mutant MEN1 allele is accompanied by loss of the normal MEN1 al
133    Three different regions of loss, one near MEN1, the second near D11S913, and the third near INT2 l
134                                           No MEN1 germline mutation was found in five probands with f
135          All patients with sporadic ZES (non-MEN1) undergoing surgery for possible cure without a pri
136  allele is accompanied by loss of the normal MEN1 allele.
137                                     Notably, MEN1 disease-related menin mutants have reduced binding
138 nctioning tumours, occur in more than 80% of MEN1 patients and account for 50% of disease-specific de
139  cell hyperplasia precedes the appearance of MEN1 gastrinomas, which develop within submucosal Brunne
140  a useful resource for positional cloning of MEN1 and other disease genes whose loci fall within this
141         We find that melanocytes depleted of MEN1 are deficient in homologous recombination (HR)-dire
142  important in suppressing the development of MEN1.
143 n control contributing to the development of MEN1.
144 dy, we conducted a preclinical evaluation of MEN1 gene therapy in pituitary tumors of Men1(+/-) mice,
145 n order to further elucidate the function of MEN1, we generated a null allele of this gene in Drosoph
146                    The Drosophila homolog of MEN1, Mnn1, encodes a protein 50% identical to human men
147                        The identification of MEN1 will enable improved understanding of the mechanism
148 to lead to tumorigenesis in a mouse model of MEN1 must be unusually subtle, occurring at either the n
149                     Stable overexpression of MEN1 has been shown to partially suppress the Ras-mediat
150      In conclusion, stable overexpression of MEN1 suppressed partially the RAS-mediated tumor phenoty
151  mutations in most DNAs from a test panel of MEN1 cases.
152 ene alterations, and are an integral part of MEN1.
153               Whereas the protein product of MEN1, menin, is ubiquitously expressed, somatic loss of
154                       To examine the role of MEN1 in tumor formation, a mouse model was generated thr
155 that CDK4 is a critical downstream target of MEN1-dependent tumor suppression and is required for tum
156 mice lacking the tumor suppressor gene RB or MEN1, genetic ablation of RBP2 can suppress tumor initia
157  [TBL1XR1, CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent
158 ic markers spanning the area of the putative MEN1 gene.
159 ontained a somatic mutation of the remaining MEN1 allele (221del18).
160 pase 8 expression plays a role in repressing MEN1 development.
161                                      Several MEN1 missense mutations disrupt the menin-JUND interacti
162                In three patients, a somantic MEN1 gene mutation was detected in the tumor.
163                                      Somatic MEN1 gene mutations and deletions play a critical role i
164                The data suggest that somatic MEN1 gene mutations and deletions play a causative role
165                                Thus, somatic MEN1 gene mutation contributes to tumorigenesis in a sub
166                                Thus, somatic MEN1 gene mutation for the mutant allele.
167 of one copy of the MEN1 gene, and a specific MEN1 gene mutation in the remaining gene copy was detect
168                                   A specific MEN1 mutation was detected in a pituitary adenoma and co
169 erent mutations (32 FMEN1 and eight sporadic MEN1) were distributed across the MEN1 gene.
170 lies with MEN1 and in most cases of sporadic MEN1.
171 on studies in enteropancreatic ETs suggested MEN1 gene involvement in tumorigenesis of familial pancr
172  had biological effects, directly supporting MEN1 gene function as a tumor suppressor.
173 molecular mechanism whereby menin suppresses MEN1 tumorigenesis at least partly through repression of
174 e 8 locus, and suggest that menin suppresses MEN1 tumorigenesis, at least in part, by up-regulating c
175 e previously identified the tumor suppressor MEN1 as a gene required for oncogene-induced senescence
176 as at multiple sites are monoclonal and that MEN1 gene alterations in gastrinomas occur before the de
177                  Our findings establish that MEN1 gene replacement therapy can generate menin express
178 ough there is indirect genetic evidence that MEN1, the gene for multiple endocrine neoplasia type 1,
179      Collectively, our results indicate that MEN1 is a melanoma tumor suppressor that functions by st
180 in melanocytes, raising the possibility that MEN1 is a melanoma tumor suppressor.
181                Recently it was reported that MEN1 patients also exhibit several cutaneous tumors, inc
182                            Here we show that MEN1 expression is lost in a high percentage of human me
183               Most importantly, we show that MEN1 functions by directly stimulating the transcription
184                   It has been suggested that MEN1, like many hereditary cancer syndromes, is caused b
185                                          The MEN1 gene called MENIN maps to chromosome 11q13 and is t
186                                          The MEN1 gene causing MEN1 is a tumor suppressor gene and se
187                                          The MEN1 gene encodes the tumor suppressor menin of 610 amin
188                                          The MEN1 gene was finally identified because it was the one
189                                          The MEN1 gene was recently isolated by positional cloning.
190                                          The MEN1 gene, mutations in which are responsible for multip
191                                          The MEN1 tumor suppressor gene encodes menin, a 610 amino ac
192                                          The MEN1 tumor suppressor gene has been localized to chromos
193                                          The MEN1 tumor suppressor gene was recently identified.
194                                          The MEN1 tumor suppressor gene, which encodes the protein me
195     During the course of cloning SIPA-1, the MEN1 gene was identified, thus excluding human SIPA-1 as
196 r suppressor gene, little is known about the MEN1-encoded protein, menin.
197 t sporadic MEN1) were distributed across the MEN1 gene.
198                             In addition, the MEN1 gene was the gene most likely to show acquired muta
199 or suppressor gene loci, one on 3p25 and the MEN1 gene on 11q13, have thus far been implicated in the
200                      In contrast, LOH at the MEN1 gene locus was demonstrated only in 2 of 40 (5%) sp
201 ed using four polymorphic DNA markers at the MEN1 gene locus; D11S480, PYGM, D11S449, and INT-2.
202 or suppressor protein that is encoded by the MEN1 (multiple endocrine neoplasia 1) gene and controls
203           Whereas deletions encompassing the MEN1 gene were seen in two tumors, the most striking res
204 ion map of a 1200-kb region encompassing the MEN1 locus was constructed by direct cDNA selection and
205 NP36 gene was studied as a candidate for the MEN1 gene.
206                           The tumor from the MEN1 patient showed LOH at chromosome 11q13 and a comple
207 ility in the peripheral lymphocytes from the MEN1 patients has been reported previously, it is not cl
208                                 However, the MEN1 gene is not a significant contributor to the tumori
209                       The data implicate the MEN1 gene in the pathogenesis of sporadic lung carcinoid
210                 Clinically, mutations in the MEN1 and DAXX/ATRX genes were associated with better pro
211                             Mutations in the MEN1 gene are associated with the multiple endocrine neo
212 o determine whether somatic mutations in the MEN1 gene are present.
213 lways have loss-of-function mutations in the MEN1 gene on chromosome 11, and endocrine tumors arising
214                             Mutations in the MEN1 gene that encodes for the menin protein are the pre
215  This syndrome results from mutations in the MEN1 gene, encoding menin.
216  This syndrome results from mutations in the MEN1 gene, which encodes menin protein.
217  and caused by inactivating mutations in the MEN1 gene.
218 he consequence of a germline mutation in the MEN1 gene.
219 lting from loss-of-function mutations in the MEN1 gene.
220 ation, recapitulating phenotypes seen in the MEN1 patients.
221                    Germline mutations in the MEN1 tumor suppressor gene are responsible for the MEN 1
222 utosomal syndrome caused by mutations in the MEN1 tumor suppressor gene.
223                The present data indicate the MEN1 gene is located between markers D11S1883 and D11S49
224 ures of gastrinomas; deletions involving the MEN1 gene were con firmed, but the rest of the genome wa
225    Pancreatic islet beta-cells that lack the MEN1-encoded protein menin develop into tumors.
226       We have recently shown that menin, the MEN1 protein product, interacts with mixed lineage leuke
227                                 Notably, the MEN1-derived menin point mutants lose their ability to b
228 cidate the potential etiological role of the MEN1 gene in pituitary tumorigenesis, 39 sporadic pituit
229     To elucidate the etiological role of the MEN1 gene in sporadic enteropancreatic endocrine tumorig
230 lopment of these tumors or mechanisms of the MEN1 gene inactivation that do not involve large deletio
231                         The isolation of the MEN1 gene is necessary to further define its role in pat
232 nin tumor suppressor protein, product of the MEN1 gene mutated in familial multiple endocrine neoplas
233  of heterozygosity (LOH) at the locus of the MEN1 gene on chromosome 11q13, and for mutations of the
234 sporadic endocrine tumors independent of the MEN1 gene or in other tumors, such as breast cancer, tha
235                   Genetic alterations of the MEN1 gene represent a candidate pathogenetic mechanism o
236 ndrome that results from the mutation of the MEN1 gene that encodes protein menin.
237 n chromosome 11q13, and for mutations of the MEN1 gene using dideoxy fingerprinting.
238 llelic deletion of the remaining copy of the MEN1 gene was also found in the patient's tumor.
239 11 (36%) sporadic tumors, both copies of the MEN1 gene were inactivated.
240 denomas showed a deletion of one copy of the MEN1 gene, and a specific MEN1 gene mutation in the rema
241 ological consequences of the deletion of the MEN1 gene, we set out to create a mouse model of hyperpa
242 ial tumor syndrome linked to mutation of the MEN1 gene, which encodes a tumor suppressor, menin.
243 ine pancreas, due to the inactivation of the MEN1 gene.
244 these tumors have focused on the role of the MEN1 gene.
245 m patients with MEN1 for allelic loss of the MEN1 gene.
246 nd one lipoma showed allelic deletion of the MEN1 gene.
247 quential inactivation of both alleles of the MEN1 gene.
248 ysis, loss of heterozygosity analysis of the MEN1 locus, and analysis of X-chromosome inactivation at
249                    The identification of the MEN1 ortholog from Drosophila melanogaster will provide
250  that occur sporadically or as a part of the MEN1 syndrome that is caused by germ line mutations in M
251  understand the endocrine specificity of the MEN1 syndrome, we evaluated biallelic loss of Men1 by in
252 ain the endocrine- restrictive nature of the MEN1 syndrome.
253                      The inactivation of the MEN1 tumor suppressor gene in patients leads to a conste
254 dies, JunD alone bound menin, product of the MEN1 tumor suppressor gene, and JunD's transcriptional a
255                    Menin, the product of the MEN1 tumor suppressor gene, binds to the AP1 transcripti
256 lytic fragments of menin, the product of the MEN1 tumor suppressor gene, in coordinating the transcri
257                      Menin, a product of the MEN1 tumor suppressor gene, is also a component of the 1
258 omplex that includes menin, a product of the MEN1 tumor suppressor gene, which is mutated in heritabl
259 Although both of these genes map outside the MEN1 consensus region they may play a role in sporadic e
260 d tumor) showed allelic loss that placed the MEN1 gene distal to marker PYGM.
261  together, the present data suggest that the MEN1 gene lies between PYGM and D11S4936, a region of ap
262  of 10 different siRNAs corresponding to the MEN1 gene by examining the expression of two additional
263 b of D11S913, a marker tightly linked to the MEN1 gene.
264 , and mutations in the Men1 gene lead to the MEN1 syndrome.
265                          To test whether the MEN1 gene is involved in the pathogenesis of multiple sm
266  parathyroid tumours not associated with the MEN1 syndrome.
267                           Importantly, these MEN1 disease-related menin mutants also fail to repress
268                            Six tumors (three MEN1 and three sporadic tumors) were identified that pro
269 arise as independent clones, develop through MEN1 gene alterations, and are an integral part of MEN1.
270 omas and sporadic insulinomas as compared to MEN1 nongastrinomas may reflect alternative genetic path
271 omal location at 11q13 in close proximity to MEN1, a tumor suppressor gene frequently mutated in fami
272 aling, revealing it as a target for treating MEN1 tumors.
273 sed, somatic loss of the remaining wild-type MEN1 allele results in tumors primarily in parathyroid,
274 ggest that loss of function of the wild-type MEN1 gene product plays a role in the development of ang
275  without Multiple Endocrine Neoplasia-type1 (MEN1), the biological behavior of duodenal and pancreati
276                                   Typically, MEN1 tumors begin two decades earlier than sporadic tumo
277                       The mechanism by which MEN1 acts as a tumor suppressor is unclear.
278                       The mechanism by which MEN1 mutations cause tumorigenesis is unknown.
279 died parathyroid tumours not associated with MEN1 to determine whether somatic mutations in the MEN1
280 1 mutations were found in most families with MEN1 and in most cases of sporadic MEN1.
281 e tissues, which is analogous to humans with MEN1 mutations.
282                             Individuals with MEN1 almost always have loss-of-function mutations in th
283 oth muscle tumors from a single patient with MEN1.
284 , diagnosis, and management of patients with MEN1 and MEN2 are reviewed.
285                  Almost 40% of patients with MEN1 and ZES have advanced disease without diffuse dista
286         The role of surgery in patients with MEN1 and ZES is controversial.
287         Eighty-one consecutive patients with MEN1 and ZES were assigned to one of four groups dependi
288 s to examine skin lesions from patients with MEN1 for allelic loss of the MEN1 gene.
289          The large majority of patients with MEN1 have mutations in the menin gene.
290  MEN1 mutation testing include patients with MEN1 or its phenocopies and first-degree relatives of pe
291         Skin lesions from five patients with MEN1 were examined using fluorescence in situ hybridizat
292 section should be performed in patients with MEN1 who have ZES and advanced localized PET.
293 trasound (EUS), surgery in ZES patients with MEN1, pancreaticoduodenectomy (Whipple procedure), lymph
294 us, lung, and uterus from five patients with MEN1.
295 , collagenomas, and lipomas in patients with MEN1.
296 ytic nevus or acrochordon from patients with MEN1.
297 s and first-degree relatives of persons with MEN1.
298 0 and 22.2% of the cases, respectively, with MEN1, PSIP1 and ARID1A being recurrently affected.
299                             All tumours with MEN1 gene mutation showed LOH on 11q13, making the tumou
300                     Long-term outcome in ZES/MEN1/HPT is not well known.
301 ur consecutive patients (49 F/35 M) with ZES/MEN1/HPT underwent initial parathyroidectomy (PTX) and w

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