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1                                              MCC binding to the second molecule of Cdc20 is mediated
2                                              MCC binds APC/C-bound CDC20 to inhibit substrate access.
3                                              MCC formation inhibits the anaphase-promoting complex/cy
4                                              MCC inhibits the anaphase-promoting complex/cyclosome (A
5                                              MCC inhibits the ubiquitin ligase anaphase promoting com
6                                              MCC is a critical checkpoint inhibitor of the anaphase-p
7                                              MCC is composed of the checkpoint proteins BubR1, Bub3,
8                                              MCC is composed of the checkpoint proteins Mad2, BubR1,
9                                              MCC levels in IEC increase in colitis and colitis-associ
10                                              MCC velocity was most dramatically accelerated by the sy
11                                              MCC, which contains a second molecule of CDC20, blocks A
12                                              MCC-K3 also exhibited excellent cyclic stability, facile
13                                              MCCs frequently contain Merkel cell polyomavirus (MCPyV)
14                   A total of 53 of 282 (19%) MCC tumors in this cohort were virus-negative using this
15 utagenic harman was observed (CMC: 1.2-13.2; MCC: 5.2-11.4ng/g) for increasing levels of fibers and a
16 MCV-positive (n = 13) and -negative (n = 21) MCC tumors and cell lines.
17 d for MCC activated with a KOH/C ratio of 3 (MCC-K3).
18                  Low-fat patties with 0.5-3% MCC/CMC were prepared using 90% of beef and 10% of an aq
19 g models were approximately as accurate as a MCC model in describing the experimental results.
20 well as a validation cohort of 14 additional MCC cases (n = 16).
21 ent computational studies showed that CC and MCC behavioral patterns could be explained by reinforcem
22 ration and disease, mucus concentrations and MCC were compared with FEV1, and both were significantly
23 erences in the active site region of GCC and MCC explain their distinct substrate preferences.
24      Specific subtype rates for SCC, MM, and MCC were 812, 75, and 2 per 100000 person-years, respect
25 ant skin cancer overall and for SCC, MM, and MCC were calculated per 100000 person-years.
26 icrocrystalline cellulose particles (NCC and MCC, respectively) were prepared, followed by freeze-dry
27 nt roles to play in checkpoint signaling and MCC generation.
28 ession was observed in MCC tumor tissues and MCC cell lines.
29 e more likely to have chronic conditions and MCCs compared with adults without a history of cancer.
30 ributed to individual chronic conditions and MCCs.
31 tal enhancers, they largely bind together at MCC gene promoters.
32  show that Mps1 promotes APC/C inhibition by MCC components through phosphorylating Bub1 and Mad1.
33 3 and p31(comet) prevent APC/C inhibition by MCC components, but cannot reactivate APC/C already boun
34  with this co-regulation, cilia extension by MCCs is more severely compromised in foxn4 and foxj1 dou
35 tructure of a human APC/C-MCC complex (APC/C(MCC)).
36 atomic resolution structure of a human APC/C-MCC complex (APC/C(MCC)).
37 d eisosomes or membrane compartment of Can1 (MCC), which correspond to approximately 200-nm-long furr
38 rboxylases 3-methylcrotonyl-CoA carboxylase (MCC) and propionyl-CoA carboxylase (PCC).
39 racterize how closely Merkel cell carcinoma (MCC) cell lines model native tumors.
40 ), melanoma (MM), and Merkel cell carcinoma (MCC) in a cohort of US OTRs receiving a primary organ tr
41                       Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine skin cancer w
42                       Merkel cell carcinoma (MCC) is a malignant neuroendocrine skin tumor frequently
43                       Merkel cell carcinoma (MCC) is a rare and aggressive cutaneous neuroendocrine n
44                       Merkel cell carcinoma (MCC) is a rare and aggressive, yet highly immunogenic sk
45                       Merkel cell carcinoma (MCC) is a rare but highly aggressive cutaneous neuroendo
46                       Merkel cell carcinoma (MCC) is an aggressive cutaneous neuroendocrine carcinoma
47                       Merkel cell carcinoma (MCC) is an uncommon, but highly malignant, cutaneous tum
48 o the primary site in Merkel cell carcinoma (MCC) is not uncommon.
49                       Merkel cell carcinoma (MCC) tumor cells express several markers detected in nor
50 s (MCPyV) can lead to Merkel cell carcinoma (MCC), a lethal form of skin cancer.
51 s of such pathways in Merkel cell carcinoma (MCC), a rare but lethal cutaneous neuroendocrine (NE) ma
52  majority of cases of Merkel cell carcinoma (MCC), an aggressive skin cancer with a high metastatic p
53  an important role in Merkel cell carcinoma (MCC).
54 initive treatment for Merkel cell carcinoma (MCC).
55 ng the proportion of Merkel cell carcinomas (MCCs) that contain the Merkel cell polyomavirus (MCPyV)
56  development of most Merkel cell carcinomas (MCCs) through several canonical mechanisms.
57 BCB5) confers resistance to standard-of-care MCC chemotherapeutic agents and provide proof-of-princip
58 mation of the mandibular condylar cartilage (MCC) and its subchondral bone is an important but unders
59 ineage of the mandibular condylar cartilage (MCC) are not well understood.
60 ther the data indicate that the beta-catenin MCC is needed for mucosal repair and carcinogenesis.
61 he Cdc20 subunit intrinsic to the MCC (Cdc20(MCC)) is ubiquitinated, a process that results in APC/C
62 that conformational dynamics of APC/C(CDC20)-MCC modulate E2 activation and determine distinctive ubi
63 als conformational variation of APC/C(CDC20)-MCC underlying this multifaceted regulation.
64            However, rotation about the CDC20-MCC assembly and conformational variability of APC/C mod
65                          Multiciliated cell (MCC) differentiation involves extensive organelle biogen
66                  Motile multiciliated cells (MCCs) have critical roles in respiratory health and dise
67       Micro- and nano-crystalline cellulose (MCC and NCC, respectively) particles isolated from cellu
68                  Microcrystalline cellulose (MCC) or carboxymethyl cellulose (CMC) can be used as fat
69 o high-aspect-ratio, micro-coating channels (MCCs) followed by topical application of powder drug-coa
70 arity to MCC tumor samples, we characterized MCC cell lines via gene expression microarrays.
71 howed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, wher
72                       Mucociliary clearance (MCC) in subjects with CB was negatively correlated with
73                       Mucociliary clearance (MCC) is a critical host innate defense mechanism in airw
74                       Mucociliary clearance (MCC) is a major airway host defence system that is impai
75 d in both established MCC lines and clinical MCC specimens at levels significantly higher than those
76 hich poses a significant barrier to clinical MCC treatment.
77           The HAAs in patties containing CMC(MCC) were found in the following concentrations; MeIQx (
78 ta gave a Matthews' correlation coefficient (MCC) of 0.53 (accuracy, 75%).
79  (ACC) and Matthews Correlation Coefficient (MCC) of Rice_Phospho 1.0 to be 82.0% and 0.64, significa
80 oved by replacing the multicapillary column (MCC) with a capillary column (CC).
81             Microporous carbon compartments (MCCs) were developed via controlled carbonization of whe
82 roduction of the mitotic checkpoint complex (MCC) consisting of BubR1, Bub3, Mad2, and Cdc20.
83  assembly of the mitotic checkpoint complex (MCC) consisting of BubR1-Bub3, Mad2, and Cdc20, which in
84              The mitotic checkpoint complex (MCC) coordinates proper chromosome biorientation on the
85              The mitotic checkpoint complex (MCC) is formed from two sub-complexes of CDC20-MAD2 and
86 Bub3 to form the mitotic checkpoint complex (MCC), a potent inhibitor of the anaphase-promoting compl
87 int is active, a mitotic checkpoint complex (MCC), composed of the checkpoint proteins Mad2, BubR1, B
88 inhibited by the Mitotic Checkpoint Complex (MCC), which assembles when the checkpoint is activated.
89 roduction of the Mitotic Checkpoint Complex (MCC), which inhibits Cdc20 to inactivate the Anaphase Pr
90 porated into the mitotic checkpoint complex (MCC), which inhibits the anaphase-promoting complex/cycl
91 AC generates the mitotic checkpoint complex (MCC), which inhibits the APC/C and delays chromosome seg
92  the form of the mitotic checkpoint complex (MCC), with the APC/C. apc14Delta mutants display increas
93 /C(Cdc20) is the mitotic checkpoint complex (MCC).
94 mplex called the mitotic checkpoint complex (MCC).
95 formation of the mitotic checkpoint complex (MCC: Cdc20-Mad3-Mad2 [13-15]).
96 eate a novel multiprotein cytosolic complex (MCC) involved in beta-catenin signaling in the intestine
97 g produces the "mitotic checkpoint complex" (MCC), which prevents anaphase by targeting Cdc20, the ac
98 reduced on a dataset of transient complexes (MCC=0.303).
99 a new class of metal-coordination complexes (MCCs) as anolytes for NRFBs.
100 and asthma) and multiple chronic conditions (MCCs) and the incremental annual health care use, medica
101 ns are managing multiple chronic conditions (MCCs), and trends are particularly alarming in youth.
102                                 In contrast, MCC blending augmented the specific surface area and por
103 ariant called moody conditional cooperation (MCC), with which they basically tend to cooperate when m
104 ng to Mad2 and Mad3/BubR1 (forming the "core MCC") and the other one (Cdc20(A)) through additional bi
105 tion: (1) sequestration of Cdc20 in the core MCC, sufficient at low Cdc20 concentrations; (2) inhibit
106  the bilateral ACC, median cingulate cortex (MCC) and right SFG.
107        Malformations of the cerebral cortex (MCCs) are devastating developmental disorders.
108                 The cell line designated CTC-MCC-41 has been cultured for more than one year, and the
109       This thorough analysis showed that CTC-MCC-41 cells resemble characteristics of the original tu
110 , the development of an additional cutaneous MCC tumor is clinically consistent with a second primary
111 nd 'bulk' drug powder inside relatively deep MCCs are crucial to induce the sustained drug release.
112 to initiate development of epidermis-derived MCC-like tumors in mice.
113 is a specific feature of well-differentiated MCC cell lines that express NE markers.
114 , may promote viral infection and thus drive MCC.
115 4 complements Foxj1 transcriptionally during MCC differentiation, thereby shaping the levels of gene
116             Mutating these motifs eliminates MCC binding to the APC/C, thereby abolishing the SAC and
117 n4 activity is inhibited in Xenopus embryos, MCCs show transient ciliogenesis defects similar to thos
118  expression was detected in both established MCC lines and clinical MCC specimens at levels significa
119 e Drosophila cell polarity gene lgl, exhibit MCCs resembling severe periventricular heterotopia (PH).
120                             ABCB5-expressing MCC cells in heterogeneous cancers preferentially surviv
121 thods with improvement between 0.02-0.07 for MCC, 4.18-21.47% for ST and 0.013-0.131 for AUC.
122  for binding of the MCC to the APC/C and for MCC disassembly.
123 reas UISO xenograft tumors were atypical for MCC.
124 am checkpoint signals and is dispensable for MCC assembly.
125 atients undergoing (18)F-FDG PET imaging for MCC between January 1997 and October 2010 at the Peter M
126 ght decrease of the content of norharman for MCC (0.5-1.6ng/g).
127 mol kg(-1) at 25 degrees C were obtained for MCC activated with a KOH/C ratio of 3 (MCC-K3).
128  APC/C and whether Mad2 is required only for MCC assembly and not for its action on the APC/C.
129 downstream target of Multicilin required for MCC differentiation in Xenopus skin.
130 -p31(comet) intercepts and disassembles free MCC not bound to APC/C through mediating the local unfol
131 TP-dependent factor that releases Cdc20 from MCC and identified it as chaperonin containing TCP1 or T
132 fidence interval = 1.20-2.62) and death from MCC (hazard ratio = 1.85, 95% confidence interval = 1.19
133                          MCPyV isolated from MCC typically contains wild-type ST but truncated forms
134  We also found that the release of Mad2 from MCC caused a marked (although not complete) decrease in
135 vious work showed that Mad2 is released from MCC by the joint action of the TRIP13 AAA-ATPase and the
136 scents with asthma in the US who suffer from MCCs have increased asthma symptoms, missed school days,
137 es (UISO, MCC13, and MCC26) and fresh frozen MCC tumors.
138 le; and (3) occupancy of the APC/C with full MCC, where Mad3 and Apc15 are involved.
139 may be a major proximate mechanism governing MCC behavior.
140 revisiae - KF551990 and Pichia gummiguttae - MCC 1273) and influence of jamun seeds on the physico-ch
141 verse asthma outcomes associated with having MCCs.
142 riae 2 + 3 (FIMs), diphtheria, tetanus, Hib, MCC and PCV13 serotypes were compared to responses in a
143 boplatin and etoposide in vitro and in human MCC xenograft-bearing mice in vivo.
144 nciple that ABCB5 blockade can inhibit human MCC tumor growth through sensitization to drug-induced c
145 reconstitution studies have shown that human MCC-APC/C can contain two molecules of Cdc20 [5-7].
146 d structural studies revealed that the human MCC binds two Cdc20 molecules, one (Cdc20(M)) through we
147 tients 18 years or older with stage I to III MCC of the extremities and/or trunk treated with definit
148  for extremities and/or trunk stage I to III MCC, with OS equivalent to that found at higher-dose reg
149                                To illustrate MCC-Seq, we use whole-genome bisulfite sequencing on adi
150  a novel therapeutic regimen to help improve MCC in smoking-related chronic bronchitis.
151 tility of this molecular target for improved MCC therapy.
152 allele-specific expression (ASE) analysis in MCC gene.
153  three groups, highest frequencies of ASE in MCC were concordantly found in CRC group, whereas lowest
154  differentiation and cancer cell behavior in MCC.
155  mutant lacking these motifs is defective in MCC maintenance in mitotic human cells but is capable of
156 s suggest a potential ontologic dichotomy in MCC, characterized by either viral-dependent or UV-depen
157 n has emerged as the key oncogenic driver in MCC carcinogenesis.
158 ablished that miR-375 is highly expressed in MCC tumors, but its biological role in MCC remains unkno
159              To determine TrkA expression in MCC as a rationale for potential targeted therapy.
160 -infiltrating lymphocytes (TIL) and PD-L1 in MCC tumors.
161 ibitory action, suggesting a role of Mad2 in MCC for APC/C inhibition.
162 lish ABCB5 as a chemoresistance mechanism in MCC and suggest utility of this molecular target for imp
163 duced HLA class-I expression was observed in MCC tumor tissues and MCC cell lines.
164  but the role of these putative oncogenes in MCC development, and this tumor's cell of origin, are un
165 oration of new targeted treatment options in MCC, especially for patients who do not respond to anti-
166 sidue in GCC is replaced by phenylalanine in MCC, which blocks access by the larger geranyl-CoA subst
167 ed in MCC tumors, but its biological role in MCC remains unknown.
168  APC/C. apc14Delta mutants display increased MCC association with the APC/C and are unable to silence
169 n budding yeast, APC:Cdc20 and its inhibitor MCC at the mitotic checkpoint, and PP2A:B55 and its inhi
170 ssion mimicking that of human intraepidermal MCC.
171 yses and complete ciliary rescue of knockout MCCs identify TAp73 as the conserved central transcripti
172 -talk, we have synthesized bivalent ligands (MCC series) that contain mu opioid agonist and CCR5 anta
173 y (RT) dose following resection of localized MCC of the extremities or trunk.
174 s, whereas WaGa and Mkl-1 more closely model MCC.
175 helial fluid secretion and absorption modify MCC velocity (MCCV).
176                                         Most MCC tumors contain integrated copies of the viral genome
177 Our University of Michigan Multidisciplinary MCC Program database was used to obtain characteristics
178 C were identified from the multidisciplinary MCC Program at the University of Michigan, a tertiary ca
179 the molecular pathogenesis of MCPyV-negative MCC is largely unexplored.
180 ve sequencing on two cases of MCPyV-negative MCC, as well as a validation cohort of 14 additional MCC
181 nto the underlying biology of viral-negative MCC and paves the road for further investigation into ne
182 s with virus-positive tumors, virus-negative MCC patients had significantly increased risk of disease
183 driven by MCPyV and that such virus-negative MCCs, which can be quite reliably identified by immunohi
184                                   This novel MCC may be an attractive therapeutic target in preventin
185 inds to both Cdc20 and Mad2, thus nucleating MCC formation.
186                                  We observed MCC behavior in both games, but the MCC that we observed
187       To determine the oncogenic activity of MCC tumor-derived T antigens in vivo, a conditional, tis
188 trumentation types promoting the adoption of MCC-IMS technology in a wide range of diverse applicatio
189 is developed and employed in the analysis of MCC-IMS spectra from 264 breath and ambient air samples.
190 he intermediary processes in the assembly of MCC are not sufficiently understood.
191                              The assembly of MCC in active checkpoint is initiated by the conversion
192 ical design principles for future classes of MCC-based anolytes.
193                                 Diagnosis of MCC was confirmed by staining positive for cytokeratin 2
194 , and motility during the differentiation of MCC progenitors.
195               Conversely, the disassembly of MCC that takes place when the checkpoint is turned off i
196  ATPase promotes the complete disassembly of MCC, necessary for the inactivation of the mitotic check
197 mooligomers, also promote the disassembly of MCC.
198 l enable detailed, mechanistic dissection of MCC generation and checkpoint silencing.
199 ion also alleviated CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated
200 ced pulmonary inflammation and impairment of MCC.
201  polyomavirus (MCPyV) causes the majority of MCC cases due to the expression of the MCPyV small and l
202 s (MCV) has been implicated in a majority of MCC tumors; however, viral-negative tumors have been rep
203 role in ongoing post-treatment management of MCC.
204 d in human cells by independent mediators of MCC-APC/C binding.
205                        Different moieties of MCC are disassembled by different ATP-requiring processe
206 he virus and the highly metastatic nature of MCC.
207 pression and the highly metastatic nature of MCC.
208 , provide insight into the cell of origin of MCC, and suggest that miR-375 silencing may promote aggr
209  Due to their large data size, processing of MCC-IMS spectra is still the main bottleneck of data ana
210 ng multiple primary MCCs from progression of MCC clinically resembling multiple primaries, allowing a
211 sition TAp73 as a novel central regulator of MCC differentiation.
212 d MCC26 cell lines are not representative of MCC tumors, whereas WaGa and Mkl-1 more closely model MC
213 ata analysis strategies in which the size of MCC-IMS data is reduced to enable further analysis.
214              A previously unknown species of MCC, which consists of Mad2, BubR1, and two molecules of
215 ot clear whether or not some subcomplexes of MCC inhibit the APC/C and whether Mad2 is required only
216 rther binds and disassembles subcomplexes of MCC that lack Mad2.
217 sely represented the global transcriptome of MCC tumors.
218 C modulate UBE2C-catalyzed ubiquitination of MCC's CDC20 molecule.
219         We confirm that approximately 20% of MCCs are not driven by MCPyV and that such virus-negativ
220                            KOH activation of MCCs was conducted at 700 degrees C with varying mass ra
221    When the checkpoint signal is turned off, MCC is disassembled, a process required for exit from ch
222 le the impact of MCV and viral T-antigens on MCC development has been extensively investigated, littl
223 opomyosin receptor kinase A was expressed on MCC tumor cells in 100% of evaluable specimens.
224 ry, restoration of HLA class-I expression on MCC cells by epigenetic priming is an attractive approac
225 s restored HLA class-I surface expression on MCC cells.
226 olding compounds, the impact of added CMC or MCC was studied concerning the formation of heterocyclic
227 AA-levels with increasing addition of CMC or MCC.
228  1 or 2 meningococcal C vaccine (MCC-CRM- or MCC-TT) doses at 3-4 months had blood samples taken at 2
229          To establish overall survival (OS), MCC-specific survival (MCCSS), and disease-free survival
230  of obligate complexes enhanced performance (MCC=0.381) while performance is somewhat reduced on a da
231  having slightly better overall performance (MCC=0.410, ACC=0.759, SPEC=0.783, SENS=0.676), but consi
232 nts yields essentially the same performance (MCC of 0.43) as a method that was specifically trained f
233 rticularly badly, increased the performance (MCC = 0.61, Acc = 79%).
234 es of clinically designated multiple primary MCC were characterized by tumor sequencing and targeted
235  with clinically designated multiple primary MCC were identified from the multidisciplinary MCC Progr
236 es of clinically designated multiple primary MCC were identified; 4 cases met inclusion criteria for
237  clinically consistent with a second primary MCC tumor rather than a cutaneous metastasis, which has
238 ion for 55 men and 49 women with 105 primary MCCs was obtained; 19 patients developed recurrent disea
239 tcome measures for 104 patients (105 primary MCCs) with tumors less than 2 cm in diameter.
240 is useful in distinguishing multiple primary MCCs from progression of MCC clinically resembling multi
241 h the clinical diagnosis of multiple primary MCCs.
242                        For tumor progression MCC has to escape the host's immuno-surveillance, e.g. b
243 ein p31(comet) and the ATPase TRIP13 promote MCC disassembly and checkpoint silencing.
244 approximately 0.71) and TATA-less promoters (MCC approximately 0.80, F1-score approximately 0.89 vers
245  prediction program for both TATA promoters (MCC approximately 0.84 and F1-score approximately 0.91 v
246  by numerous groups have failed to reproduce MCC in mice using oncoproteins from this polyomavirus.
247         Carboplatin- and etoposide-resistant MCC cell lines exhibited increased expression of ABCB5,
248         Importantly, ABCB5 blockade reversed MCC drug resistance and impaired tumor growth in xenotra
249                                  In selected MCC patients with primary tumors less than 2 cm in diame
250 bined with multicapillary column separation (MCC-IMS) is a well-known technology for detecting volati
251 ective approach, methylC-capture sequencing (MCC-Seq), for sequencing functional methylomes, while si
252 ulation of airway surface hydration may slow MCC in CB and contribute to disease pathogenesis.
253 mediated secretion (and possibly synergistic MCC) is lost, ENaC inhibition via exogenous agents may p
254                  Our study demonstrates that MCC-Seq provides comparable accuracy to alternative appr
255           We provide a first indication that MCC might confer alterative genetic susceptibility to CR
256                           This suggests that MCC risk factors such as UV radiation and aging, which a
257                                          The MCC contains p85alpha, the class IA subunit of PI3K, alo
258                                          The MCC-like tumor phenotype was dependent on the FBXW7-bind
259 ffusible 'wait anaphase' signal could be the MCC itself, and explain how reactivating the SAC can rap
260 ants display reduced association between the MCC and APC/C, are defective in poly-ubiquitination of C
261                                     Both the MCC and NCC particles were rod-shaped and had higher cry
262 observed MCC behavior in both games, but the MCC that we observed was different from that observed in
263 n of individual complex members disrupts the MCC and reduces beta-catenin signaling.
264 ntified ABBA motif class are crucial for the MCC to recognize active APC/C-Cdc20.
265  amino-terminal KEN box required to form the MCC.
266 se that the ABBA-KEN-ABBA cassette holds the MCC onto the APC/C by binding the two Cdc20 molecules in
267                              We show how the MCC inhibits active APC/C and that this is essential for
268 eased expression of pSMAD158 and VEGF in the MCC and subchondral bone.
269 /C by binding the two Cdc20 molecules in the MCC-APC/C complex.
270      This case series study investigated the MCC specimens of 55 patients treated at the Department o
271                 Degron-like sequences of the MCC subunit BubR1 block degron recognition sites on Cdc2
272 ind additionally required for binding of the MCC to the APC/C and for MCC disassembly.
273 ycan distribution, and mineralization of the MCC.
274      To investigate the role of I-PTH on the MCC and subchondral bone, we carried out our studies usi
275 mens expressed CK20 and synaptophysin on the MCC tumor cells (100% expression).
276                     Under this paradigm, the MCC and its underlying bone are thought to result from 2
277  surface hydroxyl groups on the NCC than the MCC particles and complete digestion of hemicellulose on
278                       Here, we show that the MCC can inhibit a second CDC20 that has already bound an
279 shows how the Cdc20 subunit intrinsic to the MCC (Cdc20(MCC)) is ubiquitinated, a process that result
280 but cannot reactivate APC/C already bound to MCC.
281 -Cdc20 interaction indirectly contributes to MCC homeostasis.
282 nism that is parallel, but not redundant, to MCC formation.
283 d immunosuppression showed that, relative to MCC patients with virus-positive tumors, virus-negative
284 beta6 holoenzyme of GCC, which is similar to MCC but strikingly different from PCC.
285             To determine their similarity to MCC tumor samples, we characterized MCC cell lines via g
286 lated in highly aggressive, undifferentiated MCC cell lines.
287 4 months and 1 or 2 meningococcal C vaccine (MCC-CRM- or MCC-TT) doses at 3-4 months had blood sample
288 ely 0.80, F1-score approximately 0.89 versus MCC approximately 0.29 and F1-score approximately 0.50).
289  0.84 and F1-score approximately 0.91 versus MCC approximately 0.51 and F1-score approximately 0.71)
290 plexes, our IntPred predictor performs well (MCC=0.370, ACC=0.811, SPEC=0.916, SENS=0.411) and compar
291 yed by human participants to examine whether MCC is observed across different types of game and the p
292                        It is unclear whether MCC suffices to inhibit all cellular APC/C.
293  highly metastatic phenotype associated with MCC.
294  immunophenotypical features consistent with MCC, whereas UISO xenograft tumors were atypical for MCC
295                       The data obtained with MCC-IMS and CC-IMS were evaluated, studying both the glo
296                      Moreover, patients with MCC also exhibited enhanced ABCB5 positivity after carbo
297      Our findings suggest that patients with MCC may develop a second genetically distinct primary tu
298 ) relationships in a cohort of patients with MCC.
299  after definitive treatment in patients with MCC.
300 We first genotyped four polymorphisms within MCC in 312 CRC patients, 270 schizophrenia patients and

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