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1 ll lung cancer and medullary thyroid cancer (MTC).
2 s with advanced medullary thyroid carcinoma (MTC).
3 ced, or metastatic medullary thyroid cancer (MTC).
4 cal evidence of medullary thyroid carcinoma (MTC).
5 d cancer (PTC) and medullary thyroid cancer (MTC).
6 t metastasis of medullary thyroid carcinoma (MTC).
7 he pathogenesis of medullary thyroid cancer (MTC).
8 ntraction using magnetic twisting cytometry (MTC).
9 ust 10% (-130 MtC) of the net change (-1,290 MtC).
10 the presence of medullary thyroid carcinoma (MTC).
11 staging system for medullary thyroid cancer (MTC).
12 In or (131)I in medullary thyroid carcinoma (MTC).
13 ss myocardial motion and thickening changes (MTCs).
14 e a set of multisubunit tethering complexes (MTCs).
15 lfactory bulb (OB), mitral and tufted cells (MTCs).
16 in patients with progressive and symptomatic MTC.
17 g mortalin as a novel therapeutic target for MTC.
18 ated the role of aberrant Cdk5 activation in MTC.
19 e dissection seems worthwhile for persistent MTC.
20 e of surgical benefit and risk in persistent MTC.
21 sion-free survival in patients with advanced MTC.
22 ent of the disease in patients with residual MTC.
23 I study of patients with advanced hereditary MTC.
24 erse event profile in patients with advanced MTC.
25  for general practice in detecting recurrent MTC.
26 nageable hematologic toxicity in progressive MTC.
27 med partial response in 68% of patients with MTC.
28 n acceptable safety profile and is active in MTC.
29 ve patients were enrolled, including 37 with MTC.
30  clinical benefit for patients with sporadic MTC.
31 naling, in patients with advanced hereditary MTC.
32 antitumor activity in preclinical studies of MTC.
33 iagnosis, imaging, and treatment options for MTC.
34 in patients with symptomatic and progressive MTC.
35 he extent of surgery and lymphadenectomy for MTC.
36 en shown to be effective in the treatment of MTC.
37 r biology, imaging, and treatment options of MTC.
38 eening, diagnosis, imaging, and treatment of MTC.
39 ing evaluated in Phase II clinical trials in MTC.
40 tant, first identified in a sporadic case of MTC.
41 t models for the evolutionary history of the MTC.
42 th locally advanced or metastatic hereditary MTC.
43 dies in 11 members of a family with familial MTC.
44        This suggests a homogeneous nature of MTC.
45 ly influenced the gene expression profile of MTC.
46 1N) is a suitable agent for the treatment of MTC.
47 thy (TMA), or HUS-like events, exceeding the MTCD.
48 pression profiles of hereditary and sporadic MTCs.
49 TCs, compared with those treated at ATCs and MTCs.
50 nosis of MEN 2B was triggered by symptomatic MTC (28 patients) or pheochromocytoma (1 patient).
51  ATCs (20402 [68.9%]), with the remainder at MTCs (7572 [25.6%]) or PTCs (1639 [5.5%]).
52 mpared with those treated at ATCs (80.4%) or MTCs (84.6%).
53 ofile of Mycobacterium tuberculosis complex (MTC), a causative agent of tuberculosis.
54 rgery, there are no effective treatments for MTC, a neuroendocrine malignancy that frequently metasta
55  option in patients with advanced hereditary MTC, a rare disease for which there has been no effectiv
56                               However, the S/MTC activity corresponding to a semantic anomaly was mor
57 iew and Bayesian mixed-treatment-comparison (MTC) aimed to compare the efficacy and safety of standar
58 mutations were detected in 10 of 12 sporadic MTCs analyzed.
59 arbon were lost from both ITs and PNAs (-434 MtC and -423 MtC, respectively), with degradation/distur
60 for the rapid and accurate identification of MTC and clinically relevant nontuberculous mycobacteria.
61 suspected residual, recurrent, or metastatic MTC and elevated calcitonin who had been referred for (1
62 h only three subunits, is the simplest known MTC and is essential for the retrograde traffic of COPI-
63 ed from cells infected with VSV-PeGFP-DeltaM-Mtc and labeled with the biarsenical red dye (ReAsH) wer
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           Familial medullary thyroid cancer (MTC) and its precursor, C cell hyperplasia (CCH), is ass
74 ells using both magnetic twisting cytometry (MTC) and laser tracking microrheology (LTM) are describe
75 e., both Mycobacterium tuberculosis complex (MTC) and nontuberculous mycobacteria (NTM), using surfac
76 or the therapy of medullary thyroid cancers (MTC) and of a subset of papillary thyroid cancers.
77  development of medullary thyroid carcinoma (MTC) and pathogenesis of multiple endocrine neoplasia ty
78 n patients with medullary thyroid carcinoma (MTC) and type 2A multiple endocrine neoplasia (MEN2A), m
79 rmine the maximum-tolerated cumulative dose (MTCD) and evaluate safety, activity, pharmacokinetics, a
80  decreasing number of microtubule complexes (MtCs) and a reducing diameter.
81 s directly excites both mitral/tufted cells (MTCs) and external tufted cells (ETCs), the two major ex
82 terogeneous in both mitral and tufted cells (MTCs) and GCs but relatively constant within each GC dur
83 n resulted in thyroid tumors mimicking human MTC, and additional p53 loss led to rapid tumor progress
84 reated at ATCs, 1.8% for children treated at MTCs, and 0.6% for children treated at PTCs.
85 lly prolonged by the intrinsic properties of MTCs; and (4) sniff frequency IGC activation in vivo gen
86      The current AJCC TNM staging system for MTC appears to be less than optimal in distinguishing ri
87                                 The axonemal MtCs are cross-linked by previously unrecognized fibrous
88     Results showed that polycyclic musks and MTCS are present in mangrove ecosystems and can accumula
89 provement initiatives geared toward ATCs and MTCs are required to provide optimal care to injured chi
90                                              MTCs are thought to organize membrane trafficking by med
91            Multisubunit-tethering complexes (MTCs) are large (250 to >750 kDa), conserved macromolecu
92  (177)Lu-PP-F11N accumulates specifically in MTC at a dose that is sufficient for a therapeutic appro
93       These recombinant viruses incorporated Mtc at levels similar to M in wt VSV, demonstrating reco
94 microg/kg for 10 doses (n = 11) exceeded the MTCD because of 2 HUS/TMA/HUS-like events.
95 hickness, vessel density, MTC(mannitol), and MTC(BSA) among the groups at the various time intervals
96 nts of mannitol (MTC(mannitol)) and albumin (MTC(BSA)), osmotic filtration flux (J(osm)), and hydrost
97               Vessel density, MTC(mannitol), MTC(BSA), and J(osm) were dependent on injection duratio
98 s the OB output neurons mitral/tufted cells (MTCs) by GABA release from SACs: (2) gap junction-mediat
99                    Medullary thyroid cancer (MTC) can be caused by germline mutations of the RET prot
100  in a family with apparent predisposition to MTC/CCH and no identifiable RET mutation.
101 e ESR2 mutation as a novel cause of familial MTC/CCH and provide important insights into a novel mech
102    However, some rare families with apparent MTC/CCH predisposition do not have a detectable RET muta
103                            To identify novel MTC/CCH predisposition genes we undertook exome resequen
104                Mechanistically, we show that MTC cell growth inhibition by NOTCH1 is mediated by cell
105 Activation of NOTCH1 resulted in significant MTC cell growth inhibition.
106                        Notably, reduction in MTC cell growth was dependent on the level of NOTCH1 pro
107 3 cells expressing oncogenic RET, and of the MTC cell line TT in nude mice.
108 stly induces cell death and growth arrest in MTC cell lines in culture and in mouse xenografts.
109  signaling and metabolic pathways pivotal to MTC cell survival and proliferation, proposing mortalin
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                         Notch1 was absent in MTC cells at baseline.
113     Importantly, VPA inhibited the growth of MTC cells in a dose-dependent manner.
114                   Overexpression of ASCL1 in MTC cells indicated that CgA expression is highly depend
115 usly shown that over-expression of Notch1 in MTC cells inhibits cell growth and hormone production.
116                                        Human MTC cells were treated with VPA (0-5 mM) and Western blo
117 n and altered mitochondrial bioenergetics in MTC cells, as indicated by depolarized mitochondrial mem
118 confirming that VPA is a Notch1 activator in MTC cells, we performed cell proliferation assay.
119  that VPA might activate Notch1 signaling in MTC cells, with antiproliferative effects.
120                    Medullary thyroid cancer (MTC) cells characteristically express the transcription
121 rosophila model of Medullary Thyroid Cancer (MTC) characterized by a transformation network activated
122                                              MTC combined with TPD achieved 61% sensitivity for 3-ves
123                          We observe that the MTC complex acts in a dynamic fashion with the moving re
124          These results support the idea that MTCs contribute different aspects to encoding odor infor
125 ous words showed increased activity in the S/MTC (corresponding in time with the N400), followed by I
126 ng this drug to treat patients with advanced MTC could be initiated in the near future.
127 itute for ARS, and multiple elements, termed mtc, could substitute for CEN.
128 heir phase tuning relative to sensory-driven MTC discharges.
129 med by means of fluorescence measurements of MTC displacement.
130                                          The MTCs effectively inhibited the pharmacologically relevan
131 viruses (VSV-PeGFP-DeltaM-Mtc and VSV-DeltaM-Mtc) encoding M protein with a carboxy-terminal tetracys
132  the fork protection complex Mrc1-Tof1-Csm3 (MTC) enhances the rate of the leading-strand replisome t
133 thyroid cancer (MTC), led to expansion of an MTC-enriched cohort, which is the focus of this article.
134 biphasic, involving an initial excitation of MTC/ETCs mediated by nAChRs followed by inhibition media
135                                        In 3D-MTC, ferromagnetic beads are bound to the cell surface v
136                             The reduction in MTC firing during optogenetic stimulation was confirmed
137 bining the total perfusion deficit (TPD) and MTC for each vessel territory.
138 e Dsl1 complex, the only other CATCHR-family MTC for which subunit interactions have been characteriz
139 ncluded in this study were 715 patients with MTC for whom histopathologic information was available f
140      Normal limits were used to quantify the MTCs for each map, and the accumulated sample values wer
141 stations preceding medullary thyroid cancer (MTC) for early diagnosis of multiple endocrine neoplasia
142 ry bulb (OB), where mitral and tufted cells (MTCs) form parallel output streams of odor information p
143 o elucidate structural principles underlying MTC function, we have determined the structure of the Ds
144 ose that herpesviruses may have co-opted the MTC functionality of UL37 to bring capsids to cytoplasmi
145   Additionally, 15 (41%) of 37 patients with MTC had stable disease (SD) for at least 6 months, resul
146         Injured children treated at ATCs and MTCs had higher in-hospital mortality compared with thos
147 mited available data, the staging system for MTC has been largely extrapolated from staging for diffe
148 d therapies (vandetanib and cabozantinib) in MTC have led to approval by US Food and Drug Administrat
149 ts with metastatic medullary thyroid cancer (MTC) have limited systemic treatment options.
150 ic screen between proliferating and arrested MTC identified the retinoblastoma protein (Rb) as a cruc
151  We found that hyperintense (light) areas in MTC images were coextensive with the SN as delineated hi
152  with TPD alone, the combination of TPD with MTC improved the sensitivity for the detection of 3VD an
153 nt of targeted systemic therapies in DTC and MTC in the past 5 years is incredibly exciting in the fi
154 tients aged 18 years or older diagnosed with MTC in the United States between 1998 and 2012.
155                                Screening for MTC in the United States with basal serum calcitonin for
156 nd red due to incorporation of ReAsH-labeled Mtc in the viral envelope.
157                            The nine axonemal MtCs in a cilium are found to differ significantly in le
158 y in patients with medullary thyroid cancer (MTC) in phase I.
159 n with a carboxy-terminal tetracysteine tag (Mtc) in place of the M protein.
160 d cancer (DTC) and medullary thyroid cancer (MTC) in the past 10 years.
161                    Of the 3315 patients with MTC included in the analysis, 1941 (58.6%) were women.
162 d family, with homology to subunits of other MTCs including the Dsl1, exocyst, and Golgi-associated r
163 targeting multiple pathways of importance in MTC, including MET, VEGFR2, and RET.
164            Sequential labeling of VSV-DeltaM-Mtc-infected cells with the biarsenical dyes ReAsH and F
165  IGC activation in vivo generates persistent MTC inhibition.
166                             RECENT FINDINGS: MTC is a neuroendocrine malignancy frequently associated
167                                              MTC is curable in patients with de novo mutations when n
168                                              MTC is more accurate than T2-weighting for localizing th
169                 Medullary thyroid carcinoma (MTC) is a neuroendocrine cancer that originates from cal
170                 Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor mainly caused by mutation
171                 Medullary thyroid carcinoma (MTC) is a rare endocrine tumor arising from the C-cells
172           3D-magnetic twisting cytometry (3D-MTC) is a technique for applying local mechanical stress
173                    Medullary thyroid cancer (MTC) is an uncommon malignancy.
174                    Medullary thyroid cancer (MTC) is derived from the parafollicular cells of the thy
175 s with advanced medullary thyroid carcinoma (MTC) is still a challenge.
176 like other multisubunit tethering complexes (MTCs), is thought to function as a scaffold and/or chape
177 troduction of periods of fast replication by MTC leads to an average rate enhancement of a factor of
178 uded patients with medullary thyroid cancer (MTC), led to expansion of an MTC-enriched cohort, which
179 logical processes, genes associated with the MTC(M918T) group were involved mainly in proliferative,
180 mine mass transfer coefficients of mannitol (MTC(mannitol)) and albumin (MTC(BSA)), osmotic filtratio
181 1) differences in thickness, vessel density, MTC(mannitol), and MTC(BSA) among the groups at the vari
182                              Vessel density, MTC(mannitol), MTC(BSA), and J(osm) were dependent on in
183   Our results suggest that even the simplest MTC may be capable of orchestrating vesicle capture, unc
184 ists of RET kinase activity in patients with MTC may result in effects on plasma calcitonin that are
185                The methodological quality of MTCs may be difficult for clinicians to interpret becaus
186               Multiple treatment comparison (MTC) meta-analysis uses both direct (head-to-head) rando
187                            The integrated 3D-MTC-microscopy platform takes approximately 20 d to cons
188 s suggest that UL37 could be the first viral MTC mimic and provide a structural rationale for the imp
189  suggests that UL37 could be the first viral MTC mimic and provides a structural basis for the import
190 terval (CrI): 2.45-6.87] in the fixed-effect MTC model (10 studies) and by 4.82 letters [95% confiden
191            Inactivating other members of the MTC module also resulted in Sir2p-dependent life span ex
192 the yeast mitochondrial translation control (MTC) module, causes a robust Sir2-dependent extension of
193       By means of a computational study, the MTC moiety binding mode on the CAs was explained.
194                                A conditional MTC mouse model was generated and corroborated the role
195  patients, running a high risk of metastatic MTC, must be diagnosed early for biochemical cure.
196                                        While mtc mutants cannot use methionine as a sulfur source on
197 tro evaluation was performed using the human MTC MZ-CRC-1 and the transfected A431-CCK2R(+) cell line
198 the specificity were each 99% or greater for MTC (n = 96), MAC (n = 97), MCAG (n = 68), and M. mucoge
199  in the field and patients with advanced DTC/MTC now have new standard-of-care therapy options.
200 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
201 2016 but were responsible for just 10% (-130 MtC) of the net change (-1,290 MtC).
202  PNAs stored more than one-half (58%; 41,991 MtC) of the region's carbon in 2016 but were responsible
203 tion of center characteristics (PTC, ATC, or MTC) on mortality among patients aged 15 to 19 years who
204 s of the Mycobacterium tuberculosis complex (MTC) on the basis of genomic deletions.
205 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
206 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
207  response to an oscillatory magnetic torque (MTC) or due to random Brownian or ATP-dependent forces (
208  to determine if magnetic transfer contrast (MTC) or T2 contrast MRI was better at delineating the su
209 trauma centers (PTCs), mixed trauma centers (MTCs), or adult trauma centers (ATCs) offer a survival b
210 ta add to the genetic definitions of several MTC organisms as well as fine-tune current models for th
211            Recent advances in the biology of MTC, particularly in RET proto-oncogene signaling, are n
212 rated to determine the role of Rb and p53 in MTC pathogenesis and test the hypothesis that p53 suppre
213 ages of (177)Lu-DOTA-PP-F11N in a metastatic MTC patient were also acquired.
214 d at quantifying a medullary thyroid cancer (MTC) patient's risk of lung, liver, or bone metastasis.
215 py (pRAIT) in rapidly progressing metastatic MTC patients and also how serum biomarker DTs correlate
216 Ga-labeled IMP288 for immuno-PET in relapsed MTC patients with calcitonin serum levels greater than 1
217 ence with (18)F-FDG PET in postthyroidectomy MTC patients with elevated calcitonin.
218  pretargeted anti-CEA immuno-PET in relapsed MTC patients, especially using optimized pretargeting pa
219 with calcitonin and CEA doubling times in 47 MTC patients.
220  effectively may improve overall survival of MTC patients.
221 rk (i) by continuing the evaluation of known MTC phylogenetic markers in a larger collection of tuber
222 for detection of coronary artery disease for MTC plus TPD was compared with TPD alone.
223             The accuracy of 3VD detection by MTC plus TPD was higher (69%) than the accuracy of TPD p
224  musk fragrance compounds, methyl triclosan (MTCS), polychlorinated biphenyls, organochlorine pestici
225 ransfection point mutations have helped with MTC prognosis and have resulted in the establishment of
226 in human MTC and that Cdk5 activity promotes MTC proliferation.
227  phosphorylation at Ser807/Ser811 attenuated MTC proliferation.
228 aratus senses and responds to the absence of MTC proteins and that this response converges with a pat
229 le locally advanced or metastatic hereditary MTC received initial treatment with once-daily oral vand
230                                  Single-unit MTC recordings revealed that optogenetic activation of g
231 ective study of 334 patients with persistent MTC referred to a tertiary surgical center, who were com
232  with 367 patients with previously untreated MTC referred to that institution during the same time pe
233 h mutation and with non-RET-mutated sporadic MTC remains lacking.
234                 The role of (18)F-FDG PET in MTC remains somewhat unclear.
235 st from both ITs and PNAs (-434 MtC and -423 MtC, respectively), with degradation/disturbance account
236 t the impact of repeated odorant sampling on MTC responses, we used two-photon imaging in anesthetize
237                The temporal variation of the MTC rocking amplitude is surprisingly large and manifest
238 n of point mutations in the sequences of the MTC rpoB, katG, and gyrA genes, which are responsible fo
239                                We studied 86 MTC samples.
240                                              MTCs secrete calcitonin, a useful indicator of tumor bur
241 evel 6B (ie, 50 microg/kg x 6 doses) was the MTCD, selected as the recommended phase 2 dose.
242          Clinicians and others evaluating an MTC should be aware of the potential biases that can aff
243          Patients with advanced, progressive MTC should be considered for enrollment in clinical tria
244  temporal and cell-to-cell variations in the MTC signal amplitude, and assessing the statistical char
245 ) by evaluating additional recently reported MTC species-specific and interspecific polymorphisms, an
246 Using transcriptional profiling of 49 frozen MTC specimens classified as RET mutation, we identified
247  the OB transiently decreased sensory-evoked MTC spiking, regardless of the strength or polarity of t
248 classifiers that should be incorporated into MTC staging systems for better risk stratification.
249 riminate Mycobacterium tuberculosis complex (MTC) strains from nontuberculous Mycobacteria (NTM) stra
250 ure for persistent medullary thyroid cancer (MTC) stratified by basal calcitonin levels before reoper
251 n Cancer Genes, Medullary Thyroid Carcinoma (MTC) Surveillance Study, Osteosarcoma Surveillance Study
252  electrical coupling is strong for the SAC-->MTC synapse, but negligible for the SAC-->ETC synapse; (
253 of cysteine residues implicated in MEN2A and MTC syndromes.
254 higher among adolescents treated at ATCs and MTCs than those treated at PTCs (3.2% and 3.5% vs 0.4%;
255 ted the excitability of mitral/tufted cells (MTCs) that relay olfactory input to the cortex.
256  development of medullary thyroid carcinoma (MTC), the dominant endocrinopathy in patients with these
257 lude the Mycobacterium tuberculosis complex (MTC), the M. avium complex (MAC), the M. chelonae-M. abs
258                      For therapy of advanced MTC, the Food and Drug Administration recently approved
259 trial of sorafenib in patients with advanced MTC, the primary end point was objective response.
260 ress is being made toward effective targeted MTC therapy.
261 ber of HSP70 family, is upregulated in human MTC tissues and that its depletion robustly induces cell
262  polymerase II, thereby delivering the m(6)A MTC to actively transcribed nascent RNAs to deposit m(6)
263 in turn facilitates the binding of the m(6)A MTC to adjacent RNA polymerase II, thereby delivering th
264 ents with advanced medullary thyroid cancer (MTC) to assess the efficacy and safety of vandetanib in
265                 This methionine-to-cysteine (mtc) transsulfurylation pathway is activated by cysteine
266 acy, which have been incorporated in the new MTC treatment guidelines.
267 absent in human MTC tumor tissue samples and MTC-TT cells.
268 TCH1 intracellular domain is absent in human MTC tumor tissue samples and MTC-TT cells.
269 plicate Cdk5 signaling via Rb as critical to MTC tumorigenesis and progression.
270 oss of ESR2-encoded ERbeta expression in the MTC tumour.
271                                 The familial MTC type of MEN 2 syndrome was included within the spect
272  This family of 11 individuals with familial MTC type of MEN 2A syndrome demonstrated the moderate ri
273 manifestations of patients with the familial MTC type of MEN 2A syndrome.
274           In vivo, immunostaining of CCH and MTC using an anti-RET antibody demonstrated increased RE
275 he prognosis of medullary thyroid carcinoma (MTC) varies from long- to short-term survival based on s
276 EMRI showed excellent agreement with PET and MTC viability.
277  23 formalin-fixed, paraffin-embedded (FFPE) MTCs was used for validation by RT-qPCR.
278 was found then a mixed treatment comparison (MTC) was performed using Bayesian methods.
279    Structural models for kinases relevant to MTC were generated for virtual screening to identify uni
280                       Patients with advanced MTC were randomly assigned in a 2:1 ratio to receive van
281 uantification of viability by MEMRI, PET and MTC were similar, irrespective of manganese agent.
282         Two tissue microarrays containing 69 MTCs were available for IHC assays.
283                                   Myocardial MTCs were computed, and normal limits of change were det
284                  Furthermore, a selection of MTCs were evaluated in a normotensive glaucoma rabbit mo
285              A series of monothiocarbamates (MTCs) were prepared from primary/secondary amines and CO
286 nent of the m(6)A methyltransferase complex (MTC), which in turn facilitates the binding of the m(6)A
287 h cellular multisubunit tethering complexes (MTCs), which control vesicular trafficking in eukaryotic
288 f the yeast Dsl1 complex, the simplest known MTC, which is essential for coat protein I (COPI) mediat
289 s in the RET proto-oncogene cause hereditary MTC, which provides a strong therapeutic rationale for t
290 d rapid C cell hyperplasia leading to lethal MTC, which was arrested by repressing p25 overexpression
291 male and female mice to record activation of MTCs while precisely varying inhalation frequency.
292 an detect residual, recurrent, or metastatic MTC with a reasonable sensitivity of 78% when the calcit
293 re we describe a protocol for interfacing 3D-MTC with confocal fluorescence microscopy.
294 ement of the central compartment, and for an MTC with increased basal calcitonin level of 20-200 pg/m
295                Ten (29%) of 35 patients with MTC with measurable disease had a confirmed partial resp
296 more, including 17 (49%) of 35 patients with MTC with measurable disease.
297 sive central compartment involvement, and in MTC with preoperative basal calcitonin levels more than
298 r is a promising target for the treatment of MTC with radiolabeled minigastrin analogs.
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

 
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