ライフサイエンスコーパス: mTc

1 s with advanced medullary thyroid carcinoma (MTC).

2 ced, or metastatic medullary thyroid cancer (MTC).

3 cal evidence of medullary thyroid carcinoma (MTC).

4 d cancer (PTC) and medullary thyroid cancer (MTC).

5 t metastasis of medullary thyroid carcinoma (MTC).

6 he pathogenesis of medullary thyroid cancer (MTC).

7 the presence of medullary thyroid carcinoma (MTC).

8 staging system for medullary thyroid cancer (MTC).

9 In or (131)I in medullary thyroid carcinoma (MTC).

10 ntraction using magnetic twisting cytometry (MTC).

11 ll lung cancer and medullary thyroid cancer (MTC).

12 ss myocardial motion and thickening changes (MTCs).

13 e a set of multisubunit tethering complexes (MTCs).

14 ated the role of aberrant Cdk5 activation in MTC.

15 e dissection seems worthwhile for persistent MTC.

16 e of surgical benefit and risk in persistent MTC.

17 sion-free survival in patients with advanced MTC.

18 ent of the disease in patients with residual MTC.

19 I study of patients with advanced hereditary MTC.

20 erse event profile in patients with advanced MTC.

21 for general practice in detecting recurrent MTC.

22 nageable hematologic toxicity in progressive MTC.

23 med partial response in 68% of patients with MTC.

24 n acceptable safety profile and is active in MTC.

25 ve patients were enrolled, including 37 with MTC.

26 clinical benefit for patients with sporadic MTC.

27 naling, in patients with advanced hereditary MTC.

28 antitumor activity in preclinical studies of MTC.

29 iagnosis, imaging, and treatment options for MTC.

30 he extent of surgery and lymphadenectomy for MTC.

31 en shown to be effective in the treatment of MTC.

32 r biology, imaging, and treatment options of MTC.

33 eening, diagnosis, imaging, and treatment of MTC.

34 dies in 11 members of a family with familial MTC.

35 ing evaluated in Phase II clinical trials in MTC.

36 tant, first identified in a sporadic case of MTC.

37 t models for the evolutionary history of the MTC.

38 th locally advanced or metastatic hereditary MTC.

39 cells and may have a therapeutic benefit in MTC.

40 ffective therapeutic target for treatment of MTC.

41 This suggests a homogeneous nature of MTC.

42 ly influenced the gene expression profile of MTC.

43 g mortalin as a novel therapeutic target for MTC.

44 thy (TMA), or HUS-like events, exceeding the MTCD.

45 pression profiles of hereditary and sporadic MTCs.

46 or beta pathway, were up-regulated in MEN 2B MTCs.

47 ressed at high levels specifically in MEN 2B MTCs.

48 TCs, compared with those treated at ATCs and MTCs.

49 nosis of MEN 2B was triggered by symptomatic MTC (28 patients) or pheochromocytoma (1 patient).

50 ATCs (20402 [68.9%]), with the remainder at MTCs (7572 [25.6%]) or PTCs (1639 [5.5%]).

51 mpared with those treated at ATCs (80.4%) or MTCs (84.6%).

52 Medullary thyroid carcinomas (MTC), a tumor of the thyroid parafollicular C cells, occ

53 rgery, there are no effective treatments for MTC, a neuroendocrine malignancy that frequently metasta

54 option in patients with advanced hereditary MTC, a rare disease for which there has been no effectiv

55 However, the S/MTC activity corresponding to a semantic anomaly was mor

56 iew and Bayesian mixed-treatment-comparison (MTC) aimed to compare the efficacy and safety of standar

57 mutations were detected in 10 of 12 sporadic MTCs analyzed.

58 for the rapid and accurate identification of MTC and clinically relevant nontuberculous mycobacteria.

59 suspected residual, recurrent, or metastatic MTC and elevated calcitonin who had been referred for (1

60 h only three subunits, is the simplest known MTC and is essential for the retrograde traffic of COPI-

61 ed from cells infected with VSV-PeGFP-DeltaM-Mtc and labeled with the biarsenical red dye (ReAsH) wer

62 The MTC and MBM simulations revealed that the model is incom

63 qualitative features of the cell response to MTC and MBM.

64 PFS in patients with progressive metastatic MTC and represents an important new treatment option for

65 rs p35 and p25 are highly expressed in human MTC and that Cdk5 activity promotes MTC proliferation.

66 m correlates with survival for patients with MTC and to suggest a possible revision.

67 All MTC and TPD measurements were derived automatically.

68 erated recombinant viruses (VSV-PeGFP-DeltaM-Mtc and VSV-DeltaM-Mtc) encoding M protein with a carbox

69 pid, brief nAChR-mediated excitation of both MTCs and ETCs in the mouse olfactory bulb.

70 GluRs and nAChRs blocked, increased IPSCs in MTCs and ETCs, indicating that mAChRs recruit glomerular

71 nt and lateral dendrodendritic inhibition of MTCs and to selective engage a subpopulation of interneu

72 en left superior/middle temporal cortices (S/MTC) and inferior frontal cortices (IFC) during the proc

73 CCR6 is expressed by memory T cells (mTC) and is a requirement for efficient arrest of a subs

74 Familial medullary thyroid cancer (MTC) and its precursor, C cell hyperplasia (CCH), is ass

75 ells using both magnetic twisting cytometry (MTC) and laser tracking microrheology (LTM) are describe

76 ll poking (CP), magnetic twisting cytometry (MTC) and magnetic bead microrheometry (MBM) measurements

77 e., both Mycobacterium tuberculosis complex (MTC) and nontuberculous mycobacteria (NTM), using surfac

78 or the therapy of medullary thyroid cancers (MTC) and of a subset of papillary thyroid cancers.

79 development of medullary thyroid carcinoma (MTC) and pathogenesis of multiple endocrine neoplasia ty

80 n patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), m

81 rmine the maximum-tolerated cumulative dose (MTCD) and evaluate safety, activity, pharmacokinetics, a

82 s directly excites both mitral/tufted cells (MTCs) and external tufted cells (ETCs), the two major ex

83 terogeneous in both mitral and tufted cells (MTCs) and GCs but relatively constant within each GC dur

84 n resulted in thyroid tumors mimicking human MTC, and additional p53 loss led to rapid tumor progress

85 reated at ATCs, 1.8% for children treated at MTCs, and 0.6% for children treated at PTCs.

86 lly prolonged by the intrinsic properties of MTCs; and (4) sniff frequency IGC activation in vivo gen

87 The current AJCC TNM staging system for MTC appears to be less than optimal in distinguishing ri

88 provement initiatives geared toward ATCs and MTCs are required to provide optimal care to injured chi

89 cfp32 gene sequence is conserved within the MTC, as no polymorphisms were found in the tested cfp32

90 with hereditary medullary thyroid carcinoma (MTC) associated with multiple endocrine neoplasia (MEN)

91 These recombinant viruses incorporated Mtc at levels similar to M in wt VSV, demonstrating reco

92 microg/kg for 10 doses (n = 11) exceeded the MTCD because of 2 HUS/TMA/HUS-like events.

93 hickness, vessel density, MTC(mannitol), and MTC(BSA) among the groups at the various time intervals

94 nts of mannitol (MTC(mannitol)) and albumin (MTC(BSA)), osmotic filtration flux (J(osm)), and hydrost

95 Vessel density, MTC(mannitol), MTC(BSA), and J(osm) were dependent on injection duratio

96 s the OB output neurons mitral/tufted cells (MTCs) by GABA release from SACs: (2) gap junction-mediat

97 Medullary thyroid cancer (MTC) can be caused by germline mutations of the RET prot

98 in a family with apparent predisposition to MTC/CCH and no identifiable RET mutation.

99 e ESR2 mutation as a novel cause of familial MTC/CCH and provide important insights into a novel mech

100 However, some rare families with apparent MTC/CCH predisposition do not have a detectable RET muta

101 To identify novel MTC/CCH predisposition genes we undertook exome resequen

102 Mechanistically, we show that MTC cell growth inhibition by NOTCH1 is mediated by cell

103 Activation of NOTCH1 resulted in significant MTC cell growth inhibition.

104 Notably, reduction in MTC cell growth was dependent on the level of NOTCH1 pro

105 3 cells expressing oncogenic RET, and of the MTC cell line TT in nude mice.

106 stly induces cell death and growth arrest in MTC cell lines in culture and in mouse xenografts.

107 signaling and metabolic pathways pivotal to MTC cell survival and proliferation, proposing mortalin

108 ug, CEP-2563, also inhibited tumor growth in MTC cell xenografts.

109 af in the human medullary thyroid carcinoma (MTC) cell line, TT, induces growth arrest and differenti

110 ine-inducible NOTCH1 intracellular domain in MTC cells (TT-NOTCH cells).

111 VPA activates Notch1 signaling in MTC cells and inhibits their growth by inducing apoptosi

112 that inhibiting RET can block the growth of MTC cells and may have a therapeutic benefit in MTC.

113 culture medium conditioned by Raf-activated MTC cells and was identified by mass spectrometry as leu

114 Notch1 was absent in MTC cells at baseline.

115 Importantly, VPA inhibited the growth of MTC cells in a dose-dependent manner.

116 They also blocked the growth of these MTC cells in culture.

117 Overexpression of ASCL1 in MTC cells indicated that CgA expression is highly depend

118 usly shown that over-expression of Notch1 in MTC cells inhibits cell growth and hormone production.

119 Human MTC cells were treated with VPA (0-5 mM) and Western blo

120 n and altered mitochondrial bioenergetics in MTC cells, as indicated by depolarized mitochondrial mem

121 ck changes in differentiation markers of the MTC cells, including calcitonin, RET, and cell morpholog

122 cient downstream effector for LIF effects in MTC cells, specifically required for the LIF/JAK/STAT pa

123 confirming that VPA is a Notch1 activator in MTC cells, we performed cell proliferation assay.

124 that VPA might activate Notch1 signaling in MTC cells, with antiproliferative effects.

125 h inhibitory pathway of Ras/Raf signaling in MTC cells.

126 vatives, CEP-701 and CEP-751, inhibit RET in MTC cells.

127 induce growth arrest and differentiation of MTC cells.

128 Medullary thyroid cancer (MTC) cells characteristically express the transcription

129 found, with human medullary thyroid cancer (MTC) cells, that activated Ras or c-Raf-1 can induce gro

130 MTC combined with TPD achieved 61% sensitivity for 3-ves

131 We observe that the MTC complex acts in a dynamic fashion with the moving re

132 ous words showed increased activity in the S/MTC (corresponding in time with the N400), followed by I

133 ng this drug to treat patients with advanced MTC could be initiated in the near future.

134 itute for ARS, and multiple elements, termed mtc, could substitute for CEN.

135 heir phase tuning relative to sensory-driven MTC discharges.

136 med by means of fluorescence measurements of MTC displacement.

137 Selective transcatheter delivery of the MTC-DOX to the hepatic artery was monitored by using int

138 netic targeted carrier bound to doxorubicin (MTC-DOX) by using a joint magnetic resonance (MR) imagin

139 The MTCs effectively inhibited the pharmacologically relevan

140 The location of one of these mtc elements overlaps the location of rep, and this appr

141 viruses (VSV-PeGFP-DeltaM-Mtc and VSV-DeltaM-Mtc) encoding M protein with a carboxy-terminal tetracys

142 Low concentrations of MTCs enhanced the rate of movement of fluorescent Ad2 to

143 sion of MT dynamics by low concentrations of MTCs enhances MT-dependent trafficking toward the minus

144 the fork protection complex Mrc1-Tof1-Csm3 (MTC) enhances the rate of the leading-strand replisome t

145 thyroid cancer (MTC), led to expansion of an MTC-enriched cohort, which is the focus of this article.

146 biphasic, involving an initial excitation of MTC/ETCs mediated by nAChRs followed by inhibition media

147 of the cases of medullary thyroid carcinoma (MTC) express the RET receptor tyrosine kinase.

148 In 3D-MTC, ferromagnetic beads are bound to the cell surface v

149 neoplasia (MEN) types 2A and 2B and familial MTC (FMTC) have mutations in the RET proto-oncogene.

150 bining the total perfusion deficit (TPD) and MTC for each vessel territory.

151 e Dsl1 complex, the only other CATCHR-family MTC for which subunit interactions have been characteriz

152 ncluded in this study were 715 patients with MTC for whom histopathologic information was available f

153 Normal limits were used to quantify the MTCs for each map, and the accumulated sample values wer

154 stations preceding medullary thyroid cancer (MTC) for early diagnosis of multiple endocrine neoplasia

155 o elucidate structural principles underlying MTC function, we have determined the structure of the Ds

156 ose that herpesviruses may have co-opted the MTC functionality of UL37 to bring capsids to cytoplasmi

157 Additionally, 15 (41%) of 37 patients with MTC had stable disease (SD) for at least 6 months, resul

158 Injured children treated at ATCs and MTCs had higher in-hospital mortality compared with thos

159 mited available data, the staging system for MTC has been largely extrapolated from staging for diffe

160 d therapies (vandetanib and cabozantinib) in MTC have led to approval by US Food and Drug Administrat

161 ic screen between proliferating and arrested MTC identified the retinoblastoma protein (Rb) as a cruc

162 We found that hyperintense (light) areas in MTC images were coextensive with the SN as delineated hi

163 with TPD alone, the combination of TPD with MTC improved the sensitivity for the detection of 3VD an

164 nt of targeted systemic therapies in DTC and MTC in the past 5 years is incredibly exciting in the fi

165 tients aged 18 years or older diagnosed with MTC in the United States between 1998 and 2012.

166 Screening for MTC in the United States with basal serum calcitonin for

167 nd red due to incorporation of ReAsH-labeled Mtc in the viral envelope.

168 y in patients with medullary thyroid cancer (MTC) in phase I.

169 n with a carboxy-terminal tetracysteine tag (Mtc) in place of the M protein.

170 d cancer (DTC) and medullary thyroid cancer (MTC) in the past 10 years.

171 Of the 3315 patients with MTC included in the analysis, 1941 (58.6%) were women.

172 d family, with homology to subunits of other MTCs including the Dsl1, exocyst, and Golgi-associated r

173 targeting multiple pathways of importance in MTC, including MET, VEGFR2, and RET.

174 Sequential labeling of VSV-DeltaM-Mtc-infected cells with the biarsenical dyes ReAsH and F

175 IGC activation in vivo generates persistent MTC inhibition.

176 RECENT FINDINGS: MTC is a neuroendocrine malignancy frequently associated

177 MTC is curable in patients with de novo mutations when n

178 MTC is more accurate than T2-weighting for localizing th

179 Medullary thyroid carcinoma (MTC) is a neuroendocrine cancer that originates from cal

180 Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor mainly caused by mutation

181 Medullary thyroid carcinoma (MTC) is a rare endocrine tumor arising from the C-cells

182 3D-magnetic twisting cytometry (3D-MTC) is a technique for applying local mechanical stress

183 Medullary thyroid cancer (MTC) is an uncommon malignancy.

184 Medullary thyroid cancer (MTC) is derived from the parafollicular cells of the thy

185 like other multisubunit tethering complexes (MTCs), is thought to function as a scaffold and/or chape

186 troduction of periods of fast replication by MTC leads to an average rate enhancement of a factor of

187 uded patients with medullary thyroid cancer (MTC), led to expansion of an MTC-enriched cohort, which

188 logical processes, genes associated with the MTC(M918T) group were involved mainly in proliferative,

189 MTC(mannitol) did not change significantly with the addi

190 mine mass transfer coefficients of mannitol (MTC(mannitol)) and albumin (MTC(BSA)), osmotic filtratio

191 1) differences in thickness, vessel density, MTC(mannitol), and MTC(BSA) among the groups at the vari

192 Vessel density, MTC(mannitol), MTC(BSA), and J(osm) were dependent on in

193 Our results suggest that even the simplest MTC may be capable of orchestrating vesicle capture, unc

194 ists of RET kinase activity in patients with MTC may result in effects on plasma calcitonin that are

195 The methodological quality of MTCs may be difficult for clinicians to interpret becaus

196 Multiple treatment comparison (MTC) meta-analysis uses both direct (head-to-head) rando

197 The integrated 3D-MTC-microscopy platform takes approximately 20 d to cons

198 s suggest that UL37 could be the first viral MTC mimic and provide a structural rationale for the imp

199 suggests that UL37 could be the first viral MTC mimic and provides a structural basis for the import

200 terval (CrI): 2.45-6.87] in the fixed-effect MTC model (10 studies) and by 4.82 letters [95% confiden

201 Inactivating other members of the MTC module also resulted in Sir2p-dependent life span ex

202 the yeast mitochondrial translation control (MTC) module, causes a robust Sir2-dependent extension of

203 By means of a computational study, the MTC moiety binding mode on the CAs was explained.

204 A conditional MTC mouse model was generated and corroborated the role

205 patients, running a high risk of metastatic MTC, must be diagnosed early for biochemical cure.

206 While mtc mutants cannot use methionine as a sulfur source on

207 the specificity were each 99% or greater for MTC (n = 96), MAC (n = 97), MCAG (n = 68), and M. mucoge

208 in the field and patients with advanced DTC/MTC now have new standard-of-care therapy options.

209 s (odds ratio, 4.19; 95% CI, 1.30-13.51) and MTCs (odds ratio, 6.68; 95% CI, 2.03-21.99) compared wit

210 a subspecies of the M. tuberculosis complex (MTC) of mycobacteria.

211 tion of center characteristics (PTC, ATC, or MTC) on mortality among patients aged 15 to 19 years who

212 s of the Mycobacterium tuberculosis complex (MTC) on the basis of genomic deletions.

213 dds ratio [OR], 1.57; 95% CI, 1.15-2.14) and MTCs (OR, 1.45; 95% CI, 1.05-2.01) compared with those t

214 ed at ATCs (OR, 1.75; 95% CI, 1.25-2.44) and MTCs (OR, 1.62; 95% CI, 1.15-2.29) had higher odds of de

215 response to an oscillatory magnetic torque (MTC) or due to random Brownian or ATP-dependent forces (

216 to determine if magnetic transfer contrast (MTC) or T2 contrast MRI was better at delineating the su

217 trauma centers (PTCs), mixed trauma centers (MTCs), or adult trauma centers (ATCs) offer a survival b

218 ta add to the genetic definitions of several MTC organisms as well as fine-tune current models for th

219 Recent advances in the biology of MTC, particularly in RET proto-oncogene signaling, are n

220 rated to determine the role of Rb and p53 in MTC pathogenesis and test the hypothesis that p53 suppre

221 d at quantifying a medullary thyroid cancer (MTC) patient's risk of lung, liver, or bone metastasis.

222 py (pRAIT) in rapidly progressing metastatic MTC patients and also how serum biomarker DTs correlate

223 Ga-labeled IMP288 for immuno-PET in relapsed MTC patients with calcitonin serum levels greater than 1

224 ence with (18)F-FDG PET in postthyroidectomy MTC patients with elevated calcitonin.

225 pretargeted anti-CEA immuno-PET in relapsed MTC patients, especially using optimized pretargeting pa

226 with calcitonin and CEA doubling times in 47 MTC patients.

227 effectively may improve overall survival of MTC patients.

228 upport in advanced medullary thyroid cancer (MTC) patients.

229 rk (i) by continuing the evaluation of known MTC phylogenetic markers in a larger collection of tuber

230 for detection of coronary artery disease for MTC plus TPD was compared with TPD alone.

231 The accuracy of 3VD detection by MTC plus TPD was higher (69%) than the accuracy of TPD p

232 This MEN 2B MTC profile may explain the early onset of malignancy in

233 ransfection point mutations have helped with MTC prognosis and have resulted in the establishment of

234 in human MTC and that Cdk5 activity promotes MTC proliferation.

235 phosphorylation at Ser807/Ser811 attenuated MTC proliferation.

236 aratus senses and responds to the absence of MTC proteins and that this response converges with a pat

237 One founder line developed compound MTC/PTC at low frequency (8%) and pancreatic cystadenoca

238 le locally advanced or metastatic hereditary MTC received initial treatment with once-daily oral vand

239 ective study of 334 patients with persistent MTC referred to a tertiary surgical center, who were com

240 with 367 patients with previously untreated MTC referred to that institution during the same time pe

241 h mutation and with non-RET-mutated sporadic MTC remains lacking.

242 The role of (18)F-FDG PET in MTC remains somewhat unclear.

243 The cfp32 gene is MTC restricted, and the gene product is expressed ex viv

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

245 The temporal variation of the MTC rocking amplitude is surprisingly large and manifest

246 We studied 86 MTC samples.

247 MTCs secrete calcitonin, a useful indicator of tumor bur

248 evel 6B (ie, 50 microg/kg x 6 doses) was the MTCD, selected as the recommended phase 2 dose.

249 Clinicians and others evaluating an MTC should be aware of the potential biases that can aff

250 Patients with advanced, progressive MTC should be considered for enrollment in clinical tria

251 temporal and cell-to-cell variations in the MTC signal amplitude, and assessing the statistical char

252 ) by evaluating additional recently reported MTC species-specific and interspecific polymorphisms, an

253 Using transcriptional profiling of 49 frozen MTC specimens classified as RET mutation, we identified

254 classifiers that should be incorporated into MTC staging systems for better risk stratification.

255 riminate Mycobacterium tuberculosis complex (MTC) strains from nontuberculous Mycobacteria (NTM) stra

256 ure for persistent medullary thyroid cancer (MTC) stratified by basal calcitonin levels before reoper

257 electrical coupling is strong for the SAC-->MTC synapse, but negligible for the SAC-->ETC synapse; (

258 of cysteine residues implicated in MEN2A and MTC syndromes.

259 higher among adolescents treated at ATCs and MTCs than those treated at PTCs (3.2% and 3.5% vs 0.4%;

260 ow concentrations of MT-targeting compounds (MTCs) that do not disrupt the MT network but are known t

261 development of medullary thyroid carcinoma (MTC), the dominant endocrinopathy in patients with these

262 lude the Mycobacterium tuberculosis complex (MTC), the M. avium complex (MAC), the M. chelonae-M. abs

263 For therapy of advanced MTC, the Food and Drug Administration recently approved

264 trial of sorafenib in patients with advanced MTC, the primary end point was objective response.

265 d approximately 40% of the sporadic cases of MTC, the RET kinase is constitutively activated by mutat

266 ress is being made toward effective targeted MTC therapy.

267 ber of HSP70 family, is upregulated in human MTC tissues and that its depletion robustly induces cell

268 uirement for efficient arrest of a subset of mTC to activated human dermal microvascular endothelial

269 p53 nuclear accumulation required binding of MTCs to MTs and enhanced the induction of p53-up-regulat

270 This methionine-to-cysteine (mtc) transsulfurylation pathway is activated by cysteine

271 acy, which have been incorporated in the new MTC treatment guidelines.

272 absent in human MTC tumor tissue samples and MTC-TT cells.

273 TCH1 intracellular domain is absent in human MTC tumor tissue samples and MTC-TT cells.

274 plicate Cdk5 signaling via Rb as critical to MTC tumorigenesis and progression.

275 and malignant (medullary thyroid carcinomas, MTCs) tumors from patients with multiple endocrine neopl

276 oss of ESR2-encoded ERbeta expression in the MTC tumour.

277 The familial MTC type of MEN 2 syndrome was included within the spect

278 This family of 11 individuals with familial MTC type of MEN 2A syndrome demonstrated the moderate ri

279 manifestations of patients with the familial MTC type of MEN 2A syndrome.

280 In vivo, immunostaining of CCH and MTC using an anti-RET antibody demonstrated increased RE

281 he prognosis of medullary thyroid carcinoma (MTC) varies from long- to short-term survival based on s

282 23 formalin-fixed, paraffin-embedded (FFPE) MTCs was used for validation by RT-qPCR.

283 was found then a mixed treatment comparison (MTC) was performed using Bayesian methods.

284 Patients with advanced MTC were randomly assigned in a 2:1 ratio to receive van

285 Two tissue microarrays containing 69 MTCs were available for IHC assays.

286 Myocardial MTCs were computed, and normal limits of change were det

287 Furthermore, a selection of MTCs were evaluated in a normotensive glaucoma rabbit mo

288 A series of monothiocarbamates (MTCs) were prepared from primary/secondary amines and CO

289 o be beneficial for patients with hereditary MTC, where currently there is no effective chemotherapy

290 h cellular multisubunit tethering complexes (MTCs), which control vesicular trafficking in eukaryotic

291 s in the RET proto-oncogene cause hereditary MTC, which provides a strong therapeutic rationale for t

292 d rapid C cell hyperplasia leading to lethal MTC, which was arrested by repressing p25 overexpression

293 an detect residual, recurrent, or metastatic MTC with a reasonable sensitivity of 78% when the calcit

294 re we describe a protocol for interfacing 3D-MTC with confocal fluorescence microscopy.

295 ement of the central compartment, and for an MTC with increased basal calcitonin level of 20-200 pg/m

296 Ten (29%) of 35 patients with MTC with measurable disease had a confirmed partial resp

297 more, including 17 (49%) of 35 patients with MTC with measurable disease.

298 sive central compartment involvement, and in MTC with preoperative basal calcitonin levels more than

299 analyse the whole-gene expression profile of MTC with regard to the type of RET gene mutation and the

300 portant studies in medullary thyroid cancer (MTC) with an emphasis on targeted preclinical and transl