ライフサイエンスコーパス: MEN

1 MEN 2B patients, running a high risk of metastatic MTC,

2 MEN activation must be reversed after mitotic exit to re

3 MEN promotes the release of the protein phosphatase Cdc1

4 MEN was consumed for a mean of 10.8 months (range 4-14 m

5 MENs and control ferromagnetic and polymer nanoparticles

6 MENs distinguish cancer cells from normal cells through

7 es with multiple endocrine neoplasia type 1 (MEN 1), with the ultimate aim of early tumor detection a

8 osis of multiple endocrine neoplasia-type 1 (MEN-1).

9 Multiple endocrine neoplasia type 2 (MEN 2) is an inherited cancer syndrome that includes phe

10 Multiple endocrine neoplasia type 2 (MEN 2) syndrome is an autosomal dominant, hereditary can

11 called multiple endocrine neoplasia type 2 (MEN 2) that includes medullary thyroid carcinoma (MTC).

12 sion of multiple endocrine neoplasia type 2 (MEN 2), a dominantly inherited cancer predisposition.

13 (VHL), multiple endocrine neoplasia type 2 (MEN 2), the newly delineated phaeochromocytoma-paragangl

14 types: multiple endocrine neoplasia type 2A (MEN 2A) and multiple endocrine neoplasia type 2B (MEN 2B

15 multiple endocrine neoplasia (MEN) type 2A (MEN-2A) or type 2B or familial medullary thyroid carcino

16 In multiple endocrine neoplasia 2B (MEN-2B) patients expressing RET(M918T), nuclear enrichme

17 A) and multiple endocrine neoplasia type 2B (MEN 2B) syndromes.

18 sis of multiple endocrine neoplasia type 2B (MEN 2B).

19 the 61 patients (59%) responded (MEN 2A = 8, MEN 2B = 28) to the questionnaires.

20 In this study, we show that a MEN component, protein kinase Dbf2-Mob1, promotes transf

21 Thus, only when a MEN bearing SPB leaves the mother cell and the spindle i

22 zone model', exit from mitosis occurs when a MEN-bearing SPB enters the bud.

23 We aimed to assess how achievable MEN is and whether it helps to prolong remission.

24 An additional MEN-activating function of Lte1 is mediated by its N- an

25 We find that hypertonic stress allows MEN mutants to exit from mitosis in a manner dependent o

26 ciated lung adenocarcinoma transcript 1) and MEN beta, are formed by cleavage by RNase P and are capp

27 Comparisons of MEN 2B and MEN 2A MTCs revealed that genes involved in the process

28 ter consisting mainly of primary adenoma and MEN 1 tumors.

29 se from Cfi1/Net1 during early anaphase, and MEN maintains Cdc14 in the released state during late an

30 before age 6 in medullary thyroid cancer and MEN type IIA, and as soon as the diagnosis is made in ME

31 We propose that these CPC- and MEN-dependent mechanisms are important for coordinating

32 nd late anaphase, controlled by the FEAR and MEN pathways, respectively.

33 ast, FEAR (Cdc14 early anaphase release) and MEN (mitotic exit network) activate phosphatase Cdc14 by

34 1 negatively regulate the homologous SIN and MEN pathways.

35 ated phosphorylation of the Cbk1 HM site and MEN-activated reversal of mitotic CDK phosphorylations t

36 An NKII antagonist (MEN 10,376, 500 nM) had no effect on the evoked response

37 suggesting compensatory interactions between MEN, IDH, and G6PD.

38 e to electric-field interactions (i) between MENs and a drug and (ii) between drug-loaded MENs and ce

39 d two bacterial datasets, and show that both MEN and BBSR infer accurate GRNs even when the structure

40 ely positioned along the mother-bud axis can MEN signaling occur and cell division proceed.

41 tion of Mob1p to the bud neck required CDC3, MEN genes CDC5, CDC14, CDC15, and DBF2, and spindle pole

42 , in addition to mitotic exit, S. cerevisiae MEN gene MOB1 is required for cytokinesis and cell separ

43 ction distinct from that known for classical MEN 2B mutations.

44 We showed that the constructed MENs under both warming and unwarming conditions exhibit

45 A sub group of patients can continue MEN as a maintenance treatment and this seems a useful s

46 15/48 (31%) patients were able to continue MEN post EEN completion.

47 nts who took EEN were encouraged to continue MEN post EEN.

48 ssion rates at 1 year in patients continuing MEN were 60% (9/15) compared to 15% (2/13) in patients t

49 However, p27(-/-) mice develop MEN-like tumors only in combination with loss of another

50 properties of cells which result in distinct MEN organization and the minimization of electrical ener

51 14/15 patients drank MEN and 1/15 had MEN via NGT.

52 ughter cell asymmetry determinants establish MEN signaling asymmetry through microtubule-bud cortex i

53 lasmic microtubules collaborate to establish MEN asymmetry.

54 To examine MEN proteins during mitotic exit, we imaged the MEN acti

55 There are two competing models that explain MEN regulation by spindle position.

56 spindle pole bodies (SPBs) is necessary for MEN signaling during mitosis, during meiosis MEN signali

57 ermline mutations in RET are responsible for MEN 2 but the precise pathogenetic mechanisms of tumorig

58 c thyroidectomy and diagnostic screening for MEN-associated endocrine diseases should occur.

59 se findings reveal kinetochores as sites for MEN signaling and implicate MEN in coordinating chromoso

60 ce for somatic VHL gene deletion in all four MEN 2A-related pheochromocytomas.

61 Forty-four MEN 2B patients carrying inherited (3 patients) and de n

62 ized activating signal is necessary for full MEN activation.

63 14/15 patients drank MEN and 1/15 had MEN via NGT.

64 associated with tumorigenesis in hereditary, MEN 2-related pheochromocytoma.

65 2A, eight patients with HD were identified (MEN 2A-HD).

66 res as sites for MEN signaling and implicate MEN in coordinating chromosome segregation and/or spindl

67 th the presence of skeletal abnormalities in MEN 2B patients.

68 noted in 8% of cases and were more common in MEN-1 patients.

69 7 or cdc14-1 mutants, which are defective in MEN signaling, even when cell cycle arrest is bypassed.

70 , cutaneous lesions classically described in MEN 2B syndrome, and 1 relative also showing multiple sc

71 IIA, and as soon as the diagnosis is made in MEN type IIB after the first year of life.

72 may explain the early onset of malignancy in MEN 2B compared with MEN 2A patients.

73 eletal abnormalities and early malignancy in MEN 2B compared with MEN 2A syndrome.

74 The HOG pathway drives exit from mitosis in MEN mutants by promoting the activation of the MEN effec

75 thoracic neuroendocrine tumors that occur in MEN 1 carry a malignant potential.

76 y nuclear localized Cdc14, the key player in MEN pathway, indicative of MEN activation.

77 th factor beta pathway, were up-regulated in MEN 2B MTCs.

78 tex has an important but ill-defined role in MEN regulation.

79 was expressed at high levels specifically in MEN 2B MTCs.

80 but also of p18 expression is a key step in MEN tumorigenesis.

81 hibition by DRB treatment, was suppressed in MEN epsilon/beta-depleted cells.

82 has been assumed to be the central switch in MEN regulation.

83 h is both necessary and sufficient to induce MEN signaling.

84 lls, where it is ideally situated to inhibit MEN signaling at spindle pole bodies (SPBs) when anaphas

85 (SPBs) located in the mother cell to inhibit MEN signaling.

86 his domain within Cdc15 functions to inhibit MEN signaling.

87 MENs and a drug and (ii) between drug-loaded MENs and cells.

88 void its premature release, (ii) drug-loaded MENs could be delivered into cancer cells via applicatio

89 Only the mice treated with PTX-loaded MENs (15/200 mug) in a field for three months were compl

90 The bud-localized MEN regulator Lte1, whose molecular function has long be

91 patterns of MEN and SPoC components mediate MEN inhibition.

92 MEN signaling during mitosis, during meiosis MEN signaling occurs off SPBs and does not require the S

93 However, in metazoans, MEN and Cdc14 function is not conserved.

94 Furthermore, unlike during mitosis, MEN signaling is controlled through the regulated intera

95 To ensure the accurate execution of mitosis, MEN activity is coordinated with other cellular events a

96 hways distinct from those involved in mutant MEN 1-related parathyroid tumors.

97 Among 41 patients with de novo mutations, MEN 2B was diagnosed in 12 patients after recognition of

98 We used magnetoelectric nanoparticles (MENs) to control drug delivery and release.

99 Magnetoelectric (ME) nanoparticles (MENs) intrinsically couple magnetic and electric fields.

100 The multiple endocrine neoplasia (MEN) syndromes present a diverse array of challenges to

101 scent of human multiple endocrine neoplasia (MEN) syndromes.

102 scent of human multiple endocrine neoplasia (MEN) syndromes.

103 Multiple endocrine neoplasia (MEN) type 1 and type 2 exhibit an autosomal dominant pat

104 patients with multiple endocrine neoplasia (MEN) type 2A (MEN-2A) or type 2B or familial medullary t

105 patients with multiple endocrine neoplasia (MEN) type 2A or 2B, related syndromes that result from d

106 or as part of multiple endocrine neoplasia (MEN) type II syndromes.

107 Multiple endocrine neoplasia (MEN) types 1 and 2 are rare hereditary cancer syndromes

108 ssociated with multiple endocrine neoplasia (MEN) types 2A and 2B and familial MTC (FMTC) have mutati

109 tomas (15 with multiple endocrine neoplasia [MEN] 2A, 4 with MEN 2B, 1 each with von Hippel-Lindau an

110 Both methods [Modified Elastic Net (MEN) and Bayesian Best Subset Regression (BBSR)] extend

111 anaphase, whereas the mitotic exit network (MEN) activates Cdc14 during late stages of anaphase.

112 bf4 also regulates the mitotic exit network (MEN) and monopolar homolog orientation in meiosis I.

113 ng pathways termed the mitotic exit network (MEN) and the septation initiation network (SIN) keeps Cd

114 Release of the mitotic exit network (MEN) component, Cdc14p, from the nucleolus during anapha

115 parase (Esp1); and the mitotic exit network (MEN) driven by interaction between the spindle pole body

116 romyces cerevisiae the mitotic-exit network (MEN) functions in anaphase to promote the release of the

117 ion pathway called the mitotic exit network (MEN) governs the transition from mitosis to the G1 phase

118 d axis to activate the mitotic exit network (MEN) in anaphase.

119 proteins comprise the Mitotic Exit Network (MEN) in budding yeast.

120 The mitotic exit network (MEN) in S. cerevisiae and its homologous network, the se

121 ccharomyces cerevisiae mitotic exit network (MEN) is a conserved signaling network that coordinates C

122 ccharomyces cerevisiae mitotic exit network (MEN) is a conserved signaling network that coordinates e

123 The budding yeast mitotic exit network (MEN) is a GTPase-driven signal transduction cascade that

124 The budding yeast mitotic exit network (MEN) is a signal transduction cascade that controls exit

125 The mitotic exit network (MEN) is an essential GTPase signaling pathway that trigg

126 anaphase release") and mitotic exit network (MEN) pathways.

127 Components in the mitotic exit network (MEN) play important roles in normal cytokinesis.

128 arly anaphase, and the Mitotic Exit Network (MEN) promotes Cdc14 release during late anaphase.

129 g cascade known as the mitotic exit network (MEN) promotes exit from mitosis.

130 In budding yeast, the Mitotic Exit Network (MEN) releases Cdc14 phosphatase from the nucleolus durin

131 tion network (SIN) and mitotic exit network (MEN) signaling pathways regulate cytokinesis and mitotic

132 g network known as the mitotic exit network (MEN) triggers exit from mitosis.

133 clei by inhibiting the mitotic exit network (MEN), a GTPase signaling cascade that promotes exit from

134 es the activity of the mitotic exit network (MEN), a GTPase signaling pathway that promotes exit from

135 The mitotic exit network (MEN), a protein kinase cascade under the switch-like con

136 The mitotic exit network (MEN), a Ras-like signaling cascade, promotes the release

137 orks by inhibiting the mitotic exit network (MEN), a signaling cascade initiated and controlled by Te

138 ng yeast, inhibits the mitotic exit network (MEN), a signaling pathway that promotes exit from mitosi

139 Components of the mitotic exit network (MEN), a signaling pathway that triggers exit from mitosi

140 n anaphase because the mitotic exit network (MEN), an essential Ras-like GTPase signaling cascade, is

141 cascade, known as the mitotic exit network (MEN), controls this release.

142 n budding yeast by the mitotic exit network (MEN), where Cdc14p dephosphorylates key conserved Cdk1-s

143 nase is a component of mitotic exit network (MEN), which inactivates cyclin-dependent kinase (CDK) af

144 group of proteins, the mitotic exit network (MEN), which includes Lte1, Tem1, Cdc5, Cdc15, Dbf2/Dbf20

145 anaphase activates the mitotic exit network (MEN), which triggers dispersal of Cdc14 throughout the c

146 elongation delays the mitotic exit network (MEN)-dependent release of Cdc14, thus delaying spindle b

147 ylate Ace2 until after mitotic exit network (MEN)-initiated release of the phosphatase Cdc14.

148 ng the activity of the mitotic exit network (MEN).

149 x, an inhibitor of the mitotic exit network (MEN).

150 signaling cascade, the mitotic exit network (MEN).

151 osis by inhibiting the mitotic exit network (MEN).

152 exit, sitting atop the mitotic exit network (MEN).

153 timate effector of the mitotic exit network (MEN).

154 etworks named molecular ecological networks (MENs) through Random Matrix Theory (RMT)-based methods.

155 Nine MEN 1 kindreds were included in the study.

156 nts with de novo mutations when nonendocrine MEN 2B components are quickly appreciated and surgical i

157 Our studies identify a novel MEN-linked regulatory system that inhibits cytokinesis i

158 that ongoing maintenance enteral nutrition (MEN) can be beneficial in maintaining disease remission

159 hat daughter cells activate an Antagonist of MEN pathway (AMEN) in part through induction of the Amn1

160 Whereas binding of MEN components to spindle pole bodies (SPBs) is necessar

161 carriers of a RET mutation characteristic of MEN-2A had no evidence of persistent or recurrent medull

162 carriers of a RET mutation characteristic of MEN-2A underwent total thyroidectomy.

163 Comparisons of MEN 2B and MEN 2A MTCs revealed that genes involved in t

164 e position is sensed by a system composed of MEN-inhibitory and -activating zones and a sensor that m

165 ss of both is critical in the development of MEN tumors and that both p18 and p27 are regulated by RE

166 d treatment they had before the diagnosis of MEN 2.

167 mptoms 1 to 24 years before the diagnosis of MEN 2.

168 nts with de novo mutations, the diagnosis of MEN 2B was triggered by symptomatic MTC (28 patients) or

169 N 2B mutation does not cause any features of MEN 2B in mice.

170 rtained a patient with classical features of MEN 2B, but lacking either of the classical mutations in

171 24 amino acids results in hyperactivation of MEN and premature release of Cdc14 from the nucleolus, s

172 the key player in MEN pathway, indicative of MEN activation.

173 e Rad53 pathway alleviates the inhibition of MEN by Bfa1.

174 Knockdown of MEN epsilon/beta expression results in the disruption of

175 significantly higher than expected levels of MEN activity in knockout heterozygotes, which we attribu

176 Cutaneous manifestations of MEN 2A syndrome include macular amyloidosis, whereas MEN

177 onent Mob1p with the SPB acts as a marker of MEN activation.

178 Our findings indicate that multiple modes of MEN regulation occur through the protein kinase Cdc15.

179 le mechanisms underlying the pathogenesis of MEN 2A-related pheochromocytoma.

180 Distinct localization patterns of MEN and SPoC components mediate MEN inhibition.

181 ar invasion (P < 0.001), and the presence of MEN-1 (P = 0.035) were prognostically significant advers

182 To identify more negative regulators of MEN, we carried out a genetic screen for genes that are

183 syndrome was included within the spectrum of MEN 2A syndrome.

184 ation of Tem1, which acts at the very top of MEN pathway.

185 The familial MTC type of MEN 2 syndrome was included within the spectrum of MEN 2

186 of 11 individuals with familial MTC type of MEN 2A syndrome demonstrated the moderate risk RET p.Val

187 ns of patients with the familial MTC type of MEN 2A syndrome.

188 e), and (iii) the drug could be released off MENs on demand via application of an a.c. field (~50 Oe,

189 s of released Cdc14 have opposite effects on MEN activation.

190 We find that BBSR outperforms MEN at inferring GRNs from expression data and noisy str

191 and activates a signal transduction pathway, MEN, to allow mitotic exit.

192 rotubule (cMT)-bud neck interactions prevent MEN activity.

193 re examined for signs and symptoms prompting MEN 2B.

194 data, the Rad53 pathway negatively regulates MEN independently of Cdc5, a Polo-like kinase essential

195 The G protein Tem1 regulates MEN activity.

196 irty-six of the 61 patients (59%) responded (MEN 2A = 8, MEN 2B = 28) to the questionnaires.

197 the MEN kinase Cdc15 to accurately restrict MEN activation to late mitosis.

198 uring an unperturbed cell cycle, restricting MEN activity to anaphase can occur in a Tem1 GTPase-inde

199 ugh Bfa1p dephosphorylation and so restricts MEN activity to a short period in anaphase.

200 ude that A. nidulans has components of a SIN-MEN pathway, one of which, SEPH, is required for early e

201 idence for the existence of a functional SIN-MEN pathway outside budding and fission yeast.

202 may play a role in the tumorigenesis of some MEN 2A-related pheochromocytomas.

203 released by the FEAR network is to stimulate MEN activity.

204 ltiple endocrine neoplasia type 2B syndrome (MEN 2B).

205 Our analysis further shows that MEN signaling is modulated during meiosis in several key

206 ME property, for the first time we show that MENs can distinguish different cancer cells among themse

207 The MEN 2 syndromes are characterized by medullary thyroid c

208 The MEN Cdc14p phosphatase is sequestered in the nucleolus a

209 The MEN GTPase Tem1 has been assumed to be the central switc

210 The MEN inhibitory zone is located in the mother cell, the M

211 The MEN is a signaling cascade that localizes to spindle pol

212 The MEN is conserved and in metazoans is known as the Hippo

213 The MEN kinase Cdc15 first phosphorylated the scaffold Nud1.

214 ns, which, we propose, directly activate the MEN GTPase Tem1.

215 this signal and show that Lte1 activates the MEN in at least two ways.

216 hese data indicate that Cdc14p activates the MEN in early anaphase but later inactivates it through B

217 with the cortex of the bud and activates the MEN upon the formation of an anaphase spindle.

218 suggests that Cdc14p initially activates the MEN.

219 e we show that the 3' ends of MALAT1 and the MEN beta long noncoding RNAs are protected from 3'-5' ex

220 ing Cdk activity is critical for ME, and the MEN contributes strongly to ME efficiency.

221 the MEN activators Tem1p and Cdc15p and the MEN regulator Bub2p in vivo.

222 a component of both the FEAR network and the MEN, in Cdc14 release from the nucleolus.

223 d Esp1 depended on spindle integrity and the MEN.

224 hrough the regulated interaction between the MEN kinase Dbf20 and its activating subunit Mob1.

225 urther show that only Cdc14 liberated by the MEN after completion of chromosome segregation, and not

226 tory zone is located in the mother cell, the MEN-activating zone in the bud, and the spindle pole bod

227 Only when an SPB escapes the MEN inhibitor Kin4 in the mother cell and moves into the

228 umor suppressor gene are responsible for the MEN 1 syndrome.

229 Consistent with a role for the MEN during meiosis II, we find that the signaling pathwa

230 We also found a novel role for the MEN: activating Cdc14 nuclear export, even in the absenc

231 proteins during mitotic exit, we imaged the MEN activators Tem1p and Cdc15p and the MEN regulator Bu

232 This inactivates the MEN and displaces Mob1p from SPBs.

233 ad53 prevents mitotic exit by inhibiting the MEN pathway, whereas the Chk1 pathway prevents FEAR path

234 c15p persistence at the dSPB to initiate the MEN signal cascade.

235 We show here that during meiosis, the MEN is dispensable for exit from meiosis I but contribut

236 le model to further study the effects of the MEN 2A RET mutation in vivo.

237 Finally, hyperactivation of the MEN by deletion of BUB2 restores defects in cytokinesis

238 We conclude that control of the MEN by spindle position is exerted by both negative and

239 arrest in anaphase due to inhibition of the MEN by the mother cell-restricted SPoC kinase Kin4.

240 The association of the MEN component Mob1p with the SPB acts as a marker of MEN

241 ly anaphase independent of the action of the MEN components Cdc15p, Dbf2p, and Tem1p.

242 terized the functional domains of one of the MEN components, the protein kinase Cdc15, and investigat

243 N mutants by promoting the activation of the MEN effector, the protein phosphatase Cdc14.

244 that the anaphase-specific activation of the MEN in the absence of Tem1 is controlled by the Polo kin

245 Most components of the MEN localize to spindle pole bodies.

246 l interactions between the components of the MEN remain largely unresolved.

247 pole body (SPB), where the components of the MEN reside, functions as the sensor.

248 Awareness of the components of the MEN syndromes, as well as careful preoperative preparati

249 of BFA1 or BUB2, negative regulators of the MEN, failed to remedy the cytokinetic defect of these mu

250 the yeast Polo kinase Cdc5 converge onto the MEN kinase Cdc15 to accurately restrict MEN activation t

251 th Tem1 and Cdc5 are required to recruit the MEN kinase Cdc15 to spindle pole bodies, which is both n

252 Unlike Net1/Cfi1, which regulates the MEN through the Cdc14 phosphatase, Dnt1 can inhibit SIN

253 dc14 phosphorylation and, by stimulating the MEN, Cfi1/Net1 phosphorylation.

254 Our findings indicate that the MEN epsilon/beta non-coding RNAs are essential structura

255 Here we present evidence that the MEN protein kinase complex Mob1p-Dbf2p localizes to mito

256 We found that signaling through the MEN kinase cascade was mediated by an unusual two-step p

257 pombe a signaling pathway homologous to the MEN and termed the septation initiation network (SIN) is

258 of two S. cerevisiae proteins related to the MEN proteins Mob1p and Dbf2p kinase.

259 f proteins that functions in parallel to the MEN to promote Cdc14 function.

260 at cells normally avoid this problem via the MEN-dependent release of Cdc14, which counteracts all cl

261 mother cell and moves into the bud where the MEN activator Lte1 resides can exit from mitosis occur.

262 refore central to the mechanism by which the MEN and Cdc14 initiate cytokinesis and block polarised g

263 Our results define a mechanism by which the MEN promotes exit from mitosis.

264 ssion of a human Ret proto-oncogene with the MEN 2B mutation does not cause any features of MEN 2B in

265 et cell tumors arise in association with the MEN-1 syndrome, the majority of these neoplasms are spor

266 Therefore, MEN protein localization fluctuates to switch from Bub2p

267 This MEN 2B MTC profile may explain the early onset of malign

268 drug (paclitaxel (PTX)) could be attached to MENs (30-nm CoFe2O4@BaTiO3 nanostructures) through surfa

269 asure indicates efficient Cdc14 release upon MEN activation; release driven by Esp1 in the absence of

270 Genetic testing for mutations in the VHL, MEN, and SDHB/C/D genes was performed on patients withou

271 t) facilitated response acquisition, whereas MEN-10,376 (NK2 antagonist) hindered acquisition.

272 yndrome include macular amyloidosis, whereas MEN 2B syndrome is traditionally linked to multiple muco

273 ultiple endocrine neoplasia [MEN] 2A, 4 with MEN 2B, 1 each with von Hippel-Lindau and neurofibromato

274 ny of the expected neoplasms associated with MEN 2B.

275 onset of malignancy in MEN 2B compared with MEN 2A patients.

276 and early malignancy in MEN 2B compared with MEN 2A syndrome.

277 HD 2 to 63 years before being diagnosed with MEN 2.

278 From 83 families with MEN 2A, eight patients with HD were identified (MEN 2A-H

279 asymptomatic young members of kindreds with MEN-2A who had a mutated allele of the RET proto-oncogen

280 One patient with MEN 2B underwent open adrenalectomy due to previous adre

281 chromocytoma developed in four patients with MEN 2 (33%); three of them underwent adrenalectomy.

282 RET lead to tumor formation in patients with MEN 2, it is not understood why only selected cells deve

283 ed four pheochromocytomas from patients with MEN 2A and RET germline mutations for the presence of al

284 In addition, some patients with MEN 2A develop Hirschsprung's disease (HD), and all pati

285 ns not previously described in patients with MEN 2A syndrome and to discuss the association of this d

286 ns not previously described in patients with MEN 2A syndrome.

287 Patients with MEN 2A-HD had a typical HD presentation and always requi

288 All patients with MEN 2A-HD had rectal biopsies with a diverting colostomy

289 All patients with MEN 2A-HD were operated on for HD 2 to 63 years before b

290 sm for tumor formation in some patients with MEN 2A-related MTC.

291 chanisms of tumor formation in patients with MEN 2A-related pheochromocytoma.

292 mechanisms of tumorigenesis in patients with MEN 2A-related pheochromocytoma.

293 These and all patients with MEN 2B followed at the authors' institution (n = 53) wer

294 Ninety-three percent of patients with MEN 2B had gastrointestinal symptoms 1 to 24 years befor

295 sprung's disease (HD), and all patients with MEN 2B have intestinal neuromas and megacolon that can c

296 Patients with MEN 2B have significant gastrointestinal symptoms, but l

297 ble to physicians have enabled patients with MEN, particularly those with the carcinoid syndrome or p

298 Seventy-one percent of patients with MEN-2B with gastrointestinal symptoms had radiographic i

299 oordinate Ace2p-dependent transcription with MEN activation.

300 R absorption spectra of cells incubated with MENs.