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