ライフサイエンスコーパス: MCC

1 MCC binding to the second molecule of Cdc20 is mediated

2 MCC diagnoses have tripled over the past 20 years, but e

3 MCC dysfunction is associated with human diseases of the

4 MCC formation inhibits the anaphase-promoting complex/cy

5 MCC inhibits the ubiquitin ligase anaphase promoting com

6 MCC is a rare, clinically aggressive neuroendocrine tumo

7 MCC-SP has powerful and robust performance in identifyin

8 MCCs frequently contain Merkel cell polyomavirus (MCPyV)

9 MCCs from different tissues exhibited defective synchron

10 A total of 53 of 282 (19%) MCC tumors in this cohort were virus-negative using this

11 utagenic harman was observed (CMC: 1.2-13.2; MCC: 5.2-11.4ng/g) for increasing levels of fibers and a

12 Low-fat patties with 0.5-3% MCC/CMC were prepared using 90% of beef and 10% of an aq

13 ith an ACC value of 0.959, F-value of 0.958, MCC value of 0.917 and AUC value of 0.956, which compreh

14 tion, StackDPPred achieved an ACC of 89.96%, MCC of 0.799 and AUC of 94.50%.

15 g models were approximately as accurate as a MCC model in describing the experimental results.

16 cell death-1 pathway inhibitors for advanced MCC (aMCC) demonstrate increased progression-free surviv

17 ation-approved targeted therapy for advanced MCC.

18 ce for application of copanlisib in advanced MCC with aberrant PI3K activation for which immunotherap

19 cal screen to identify molecules that affect MCC ontogeny in the zebrafish embryo kidney, and found p

20 Although MCC has a high propensity for metastasis, little is know

21 nsitivity of 92.2%, specificity of 83.6% and MCC of 0.69, outperforming the current gold-standard Gen

22 P = 1.6 x 10-7), HTR1B (P = 1.9 x 10-7), and MCC (P = 2.1 x 10-7) genes.

23 ent computational studies showed that CC and MCC behavioral patterns could be explained by reinforcem

24 totic response in MCV-positive MCC cells and MCC-derived xenografts in mice.

25 Specific subtype rates for SCC, MM, and MCC were 812, 75, and 2 per 100000 person-years, respect

26 ant skin cancer overall and for SCC, MM, and MCC were calculated per 100000 person-years.

27 s, error rate (0.08%), Kappa stats, PRC, and MCC are (0.98%), precision, recall, and F-matrix are (0.

28 nt roles to play in checkpoint signaling and MCC generation.

29 7% and 0.48 for sensitivity, specificity and MCC respectively, with an area under the receiver operat

30 ession was observed in MCC tumor tissues and MCC cell lines.

31 e more likely to have chronic conditions and MCCs compared with adults without a history of cancer.

32 ributed to individual chronic conditions and MCCs.

33 Finally, we applied MCC-SP to analyze one real dataset from the Religious Or

34 prevention of virus-derived cancers such as MCC.

35 We termed this method as "MCC-SP".

36 te during the same developmental window, but MCCs complete intercalation prior to ICs.

37 show that Mps1 promotes APC/C inhibition by MCC components through phosphorylating Bub1 and Mad1.

38 3 and p31(comet) prevent APC/C inhibition by MCC components, but cannot reactivate APC/C already boun

39 Most centrioles amplified by MCCs grow on the surface of organelles called deuterosom

40 n A2 is ubiquitinated by the repressed APC/C-MCC, mediated by the cooperative engagement of its KEN a

41 The trimeric Mon1-Ccz1-C18orf8 (MCC) GEF therefore plays a central role in cellular chol

42 gregated into the Micro-Compartment-of-Can1 (MCC) and Pma1 (MCP), which have different lipid composit

43 Nitrogen-doped multichamber carbon (MCC) microspheres with a refined hierarchical structure

44 elopment, its role in Merkel cell carcinoma (MCC) carcinogenesis remains controversial.

45 ), melanoma (MM), and Merkel cell carcinoma (MCC) in a cohort of US OTRs receiving a primary organ tr

46 Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine skin cancer w

47 Merkel cell carcinoma (MCC) is a lethal skin cancer that metastasizes rapidly.

48 Merkel cell carcinoma (MCC) is a malignant neuroendocrine skin tumor frequently

49 Merkel cell carcinoma (MCC) is a rare and aggressive cutaneous neuroendocrine n

50 Merkel cell carcinoma (MCC) is a rare and aggressive, yet highly immunogenic sk

51 Merkel cell carcinoma (MCC) is a rare, aggressive skin cancer commonly driven b

52 Merkel cell carcinoma (MCC) is a rare, highly aggressive skin cancer for which

53 Merkel cell carcinoma (MCC) is an aggressive cutaneous neuroendocrine carcinoma

54 Merkel cell carcinoma (MCC) is an aggressive skin cancer often caused by the Me

55 tervention.IMPORTANCE Merkel cell carcinoma (MCC) is the most aggressive cutaneous tumor without clea

56 Merkel cell carcinoma (MCC) tumor cells express several markers detected in nor

57 cally associated with Merkel cell carcinoma (MCC), a rare and aggressive form of skin cancer.

58 ed in 80% of cases of Merkel cell carcinoma (MCC), a rare but aggressive form of human skin cancer, s

59 ogic role of MCPyV in Merkel cell carcinoma (MCC), an extremely lethal form of skin cancer.

60 es of piezo2 in human Merkel cell carcinoma (MCC)-13 cells; piezo2 is a low-threshold, positive press

61 Merkel cell carcinoma (MCC)-a neuroendocrine cancer of the skin-is caused by th

62 ressive human cancer, Merkel cell carcinoma (MCC).

63 form of skin cancer, Merkel cell carcinoma (MCC).

64 or the development of Merkel cell carcinoma (MCC).

65 plasm consistent with Merkel cell carcinoma (MCC).

66 ng the proportion of Merkel cell carcinomas (MCCs) that contain the Merkel cell polyomavirus (MCPyV)

67 Human Merkel cell carcinomas (MCCs) that harbor a clonally integrated Merkel cell poly

68 oximately 80% of all Merkel cell carcinomas (MCCs), a highly aggressive neuroendocrine carcinoma of t

69 mation of the mandibular condylar cartilage (MCC) and its subchondral bone is an important but unders

70 ineage of the mandibular condylar cartilage (MCC) are not well understood.

71 cells of the mandibular condylar cartilage (MCC) is rich in type VI collagen.

72 Multiciliated cells (MCC) contain hundreds of motile cilia used to propel flu

73 Multiciliated cells (MCCs) amplify large numbers of centrioles that convert i

74 Multiciliated cells (MCCs) are specialized epithelia with apical bundles of m

75 Motile cilia on multiciliated cells (MCCs) function in fluid clearance over epithelia.

76 zed beating of cilia on multiciliated cells (MCCs) generates a directional flow of mucus across epith

77 etory roles, as well as multiciliated cells (MCCs) that govern fluid flow.

78 In Xenopus skin, multiciliated cells (MCCs), which contain ~150 centrioles, and ionocytes (ICs

79 o the apical surface of multiciliated cells (MCCs).

80 Microcrystalline cellulose (MCC) or carboxymethyl cellulose (CMC) can be used as fat

81 olution concept called Markov-Conley chains (MCCs).

82 o high-aspect-ratio, micro-coating channels (MCCs) followed by topical application of powder drug-coa

83 ession, whereas ATOH1 knockdown in classical MCC cell lines reduced miR-375 expression.

84 e neuroendocrine growth pattern of classical MCC cell lines.

85 howed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, wher

86 on of Gas2l2 impaired mucociliary clearance (MCC) and led to mucus accumulation.

87 Mucociliary clearance (MCC) is a major airway host defence system that is impai

88 The HAAs in patties containing CMC(MCC) were found in the following concentrations; MeIQx (

89 having the Matthews Correlation Coefficient (MCC) >= 0.5 improves threading performance in nearly 30%

90 chieved a Matthew's Correlation Coefficient (MCC) of up to 0.77 and 0.73, outperforming previously de

91 troduce the maximal correlation coefficient (MCC) to represent the between-node connection, and then

92 assembly of the mitotic checkpoint complex (MCC) consisting of BubR1-Bub3, Mad2, and Cdc20, which in

93 The mitotic checkpoint complex (MCC) is formed from two sub-complexes of CDC20-MAD2 and

94 point (SAC), the mitotic checkpoint complex (MCC) represses APC/C's activity towards cyclin B1, but n

95 int is active, a mitotic checkpoint complex (MCC), composed of the checkpoint proteins Mad2, BubR1, B

96 he assembly of a Mitotic Checkpoint Complex (MCC), which inhibits the action of the ubiquitin ligase

97 porated into the mitotic checkpoint complex (MCC), which inhibits the anaphase-promoting complex/cycl

98 2 to produce the mitotic checkpoint complex (MCC), which is the diffusible wait anaphase signal [9, 1

99 the form of the mitotic checkpoint complex (MCC), with the APC/C. apc14Delta mutants display increas

100 formation of the mitotic checkpoint complex (MCC: Cdc20-Mad3-Mad2 [13-15]).

101 g produces the "mitotic checkpoint complex" (MCC), which prevents anaphase by targeting Cdc20, the ac

102 reduced on a dataset of transient complexes (MCC=0.303).

103 ch can influence soil microbial composition (MCC) and enzyme activities, and hence soil health.

104 by renneting of micellar casein concentrate (MCC), with modulation of salt and pH levels by adding sa

105 Multiple chronic conditions (MCC) are highly prevalent worldwide, especially among ol

106 and asthma) and multiple chronic conditions (MCCs) and the incremental annual health care use, medica

107 where threading using high-quality contacts (MCC >= 0.5) significantly improves the performance of 22

108 at etv5a acts downstream of irx2a to control MCC ontogeny.

109 including 1336 CRC cases and 2744 controls (MCC-Spain).

110 ariant called moody conditional cooperation (MCC), with which they basically tend to cooperate when m

111 ng to Mad2 and Mad3/BubR1 (forming the "core MCC") and the other one (Cdc20(A)) through additional bi

112 tion: (1) sequestration of Cdc20 in the core MCC, sufficient at low Cdc20 concentrations; (2) inhibit

113 the bilateral ACC, median cingulate cortex (MCC) and right SFG.

114 Malformations of the cerebral cortex (MCCs) are devastating developmental disorders.

115 , the development of an additional cutaneous MCC tumor is clinically consistent with a second primary

116 Upregulation of the methylcitrate cycle (MCC) is required to assimilate and detoxify propionyl-Co

117 nd 'bulk' drug powder inside relatively deep MCCs are crucial to induce the sustained drug release.

118 to initiate development of epidermis-derived MCC-like tumors in mice.

119 +/- 1) and regions with intrinsic disorder (MCC = 0.59 +/- 0.03) were predicted significantly better

120 n about the underlying mechanisms that drive MCC invasion and metastatic progression.

121 ription factor ets variant 5a (etv5a) during MCC fate choice, where modulating prostaglandin E(2) (PG

122 correspondence we establish to the dynamical MCC solution concept when the underlying evolutionary mo

123 To template these cilia, each MCC produces between 100-600 centrioles by a process ter

124 bryos had reduced expression of an essential MCC gene ets variant 5a (etv5a), and were rescued by etv

125 e Drosophila cell polarity gene lgl, exhibit MCCs resembling severe periventricular heterotopia (PH).

126 For MCC, one immune escape mechanism is insufficient for rec

127 thods with improvement between 0.02-0.07 for MCC, 4.18-21.47% for ST and 0.013-0.131 for AUC.

128 for binding of the MCC to the APC/C and for MCC disassembly.

129 a previously unrecognized two-step model for MCC development: GMNC functions in the initial step for

130 ght decrease of the content of norharman for MCC (0.5-1.6ng/g).

131 ng (GMNC), was also shown to be required for MCC formation.

132 antigen genes, viral oncogenes required for MCC tumor growth.

133 id and sterol concentrations are similar for MCC and MCP, but sphingolipids are enriched in MCP.

134 ment: GMNC functions in the initial step for MCC precursor specification.

135 -p31(comet) intercepts and disassembles free MCC not bound to APC/C through mediating the local unfol

136 TP-dependent factor that releases Cdc20 from MCC and identified it as chaperonin containing TCP1 or T

137 fidence interval = 1.20-2.62) and death from MCC (hazard ratio = 1.85, 95% confidence interval = 1.19

138 kt activities in mouse models generated from MCC cell xenografts and patient-derived tumor xenografts

139 vious work showed that Mad2 is released from MCC by the joint action of the TRIP13 AAA-ATPase and the

140 le; and (3) occupancy of the APC/C with full MCC, where Mad3 and Apc15 are involved.

141 may be a major proximate mechanism governing MCC behavior.

142 revisiae - KF551990 and Pichia gummiguttae - MCC 1273) and influence of jamun seeds on the physico-ch

143 Yet, how MCC regulate the precise number of centrioles and cilia

144 ously found PI3K pathway activation in human MCC cell lines and tumors and demonstrated complete clin

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 ious simulations are conducted to illustrate MCC is a better measurement of the between-node connecti

150 ic defect in ciliary orientation and impairs MCC and results in PCD.

151 a novel therapeutic regimen to help improve MCC in smoking-related chronic bronchitis.

152 5.6% in ACC value, 5.7% in F-value, 12.4% in MCC value and 5.8% in AUC value.

153 omatinostat's efficacy and mode of action in MCC.

154 -attached mode, activated piezo2 currents in MCC-13 and human embryonic kidney 293 T cells where piez

155 )/AKT/mTOR pathway is frequently detected in MCC, making it an attractive therapeutic target.

156 ion and stimulating its activity by DMXAA in MCC cells reactivates their antitumor inflammatory cytok

157 LSD, a known E3 ligase-targeting domain, in MCC.

158 To determine TrkA expression in MCC as a rationale for potential targeted therapy.

159 duced HLA class-I expression was observed in MCC tumor tissues and MCC cell lines.

160 regarded as a lineage-dependent oncogene in MCC.

161 hat ATOH1 is a lineage-dependent oncogene in MCC.

162 but the role of these putative oncogenes in MCC development, and this tumor's cell of origin, are un

163 oration of new targeted treatment options in MCC, especially for patients who do not respond to anti-

164 transcription of key genes prpC and prpD in MCC is activated by MtPrpR, a member of a family of prok

165 To reactivate STING in MCC, we developed an application of a human STING mutant

166 ered approximately 4 weeks before surgery in MCC was generally tolerable and induced pCRs and radiogr

167 osuppressive pathway is often upregulated in MCC, and advanced metastatic MCC frequently responds to

168 base of axonemes and at the basal bodies in MCCs.

169 These phenotypes were further confirmed in MCCs of Xenopus embryos when CAMSAP3 expression was knoc

170 62A/G230I/Q266I) causes robust cell death in MCCs as well as several other STING-silenced cancers.

171 ich is one of the most abundant microRNAs in MCCs.

172 suggest that massive centriole production in MCCs is a robust process that can self-organize.

173 IFN genes (STING) is completely silenced in MCCs.

174 apical actin polymerization and stability in MCCs.

175 APC/C. apc14Delta mutants display increased MCC association with the APC/C and are unable to silence

176 CCs mimicked T antigen knockdown by inducing MCC cell growth arrest and neuron-like differentiation.

177 n budding yeast, APC:Cdc20 and its inhibitor MCC at the mitotic checkpoint, and PP2A:B55 and its inhi

178 between-node connection, and then integrate MCC with K shortest paths algorithm to rank and identify

179 ssion mimicking that of human intraepidermal MCC.

180 ted complete clinical response in a Stage IV MCC patient treated with PI3K inhibitor idelalisib.

181 educed expression of key Merkel cell lineage/MCC marker genes, including HES6, SOX2, ATOH1, and KRT20

182 y (RT) dose following resection of localized MCC of the extremities or trunk.

183 ed to the developing pronephros and maturing MCCs, and loss of function altered formation of two segm

184 Here, we showed that MCV(+) MCC cells cocultured with keratinocytes undergo neuron-l

185 The knockdown of Sox2 in MCV(+) MCCs mimicked T antigen knockdown by inducing MCC cell g

186 lagen are observed on the central and medial MCC and are associated with significantly higher levels

187 mentation, and the control of etv5a mediated MCC formation.

188 upregulated in MCC, and advanced metastatic MCC frequently responds to PD-1 blockade.

189 vel approach for the treatment of metastatic MCC.

190 s are available for patients with metastatic MCC.

191 Our University of Michigan Multidisciplinary MCC Program database was used to obtain characteristics

192 C were identified from the multidisciplinary MCC Program at the University of Michigan, a tertiary ca

193 e and abnormal ciliary morphologies in nasal MCCs.

194 In contrast, virus-negative MCC contains inactivating mutations in TP53 and RB1.

195 s with virus-positive tumors, virus-negative MCC patients had significantly increased risk of disease

196 driven by MCPyV and that such virus-negative MCCs, which can be quite reliably identified by immunohi

197 We observed MCC behavior in both games, but the MCC that we observed

198 r pivotal health importance, many aspects of MCC development remain poorly understood.

199 patients and care partners in the context of MCC.

200 31(comet) by Plk1 prevents a futile cycle of MCC assembly and disassembly during the active mitotic c

201 s mechanistic insight into the dependence of MCC on LSD1 and a tumour suppressor role for ncBAF in ca

202 sidase activity were the key determinants of MCC.

203 Diagnosis of MCC was confirmed by staining positive for cytokeratin 2

204 ATPase promotes the complete disassembly of MCC, necessary for the inactivation of the mitotic check

205 totic checkpoint requires the disassembly of MCC.

206 mooligomers, also promote the disassembly of MCC.

207 l enable detailed, mechanistic dissection of MCC generation and checkpoint silencing.

208 he characteristic neuroendocrine features of MCC via induction of ATOH1; thus, ATOH1 can be regarded

209 h1) kinase, enabling efficient generation of MCC complexes.

210 LSD1 inhibition reduces the growth of MCC in vitro and in vivo.

211 care are recommended to reduce the impact of MCC and improve patients' outcomes.

212 ced pulmonary inflammation and impairment of MCC.

213 d in human cells by independent mediators of MCC-APC/C binding.

214 Different moieties of MCC are disassembled by different ATP-requiring processe

215 e phenotype and suggest that the ontology of MCC arises from a neuronal cell precursor.

216 to understand the molecular pathogenesis of MCC.

217 duce the migratory and invasive phenotype of MCC cells through the transcriptional activation of the

218 ng multiple primary MCCs from progression of MCC clinically resembling multiple primaries, allowing a

219 (MCI), in the transcriptional regulation of MCC specification and differentiation.

220 rther binds and disassembles subcomplexes of MCC that lack Mad2.

221 eat therapeutic promise for the treatment of MCC and many other STING-deficient cancers.

222 We confirm that approximately 20% of MCCs are not driven by MCPyV and that such virus-negativ

223 tributes to the immune suppressive nature of MCCs.

224 When the checkpoint signal is turned off, MCC is disassembled, a process required for exit from ch

225 opomyosin receptor kinase A was expressed on MCC tumor cells in 100% of evaluable specimens.

226 ry, restoration of HLA class-I expression on MCC cells by epigenetic priming is an attractive approac

227 o restores HLA class I surface expression on MCC cells, therefore, restoring surviving MCC cells' sus

228 s restored HLA class-I surface expression on MCC cells.

229 olding compounds, the impact of added CMC or MCC was studied concerning the formation of heterocyclic

230 AA-levels with increasing addition of CMC or MCC.

231 ression in hTERT-MCPyV gene-expressing HK or MCC cells resulted in a decrease in the number of cells

232 lta isoforms are abundantly expressed in our MCC cell lines and clinical samples; we therefore examin

233 of obligate complexes enhanced performance (MCC=0.381) while performance is somewhat reduced on a da

234 having slightly better overall performance (MCC=0.410, ACC=0.759, SPEC=0.783, SENS=0.676), but consi

235 lution concept based solely on fixed points, MCCs are a dynamical solution concept based on the Marko

236 In MCPyV-positive MCC cells, the expression of NDRG1 was downregulated by

237 rved that depletion of EP400 in MCV-positive MCC cell lines led to increased p53 target gene expressi

238 ing to an apoptotic response in MCV-positive MCC cells and MCC-derived xenografts in mice.

239 In addition, MCV-positive MCC cells expressed high levels of MDM4.

240 MCV-positive MCC expresses small T antigen (ST) and a truncated form

241 targeting of MDM2 and MDM4 in virus-positive MCC and other p53 wild-type tumors.

242 d activation are major barriers that prevent MCC eradication by the immune system.

243 es of clinically designated multiple primary MCC were characterized by tumor sequencing and targeted

244 with clinically designated multiple primary MCC were identified from the multidisciplinary MCC Progr

245 es of clinically designated multiple primary MCC were identified; 4 cases met inclusion criteria for

246 clinically consistent with a second primary MCC tumor rather than a cutaneous metastasis, which has

247 tcome measures for 104 patients (105 primary MCCs) with tumors less than 2 cm in diameter.

248 is useful in distinguishing multiple primary MCCs from progression of MCC clinically resembling multi

249 h the clinical diagnosis of multiple primary MCCs.

250 For tumor progression MCC has to escape the host's immuno-surveillance, e.g. b

251 ein p31(comet) and the ATPase TRIP13 promote MCC disassembly and checkpoint silencing.

252 approximately 0.71) and TATA-less promoters (MCC approximately 0.80, F1-score approximately 0.89 vers

253 prediction program for both TATA promoters (MCC approximately 0.84 and F1-score approximately 0.91 v

254 ation of two segment populations and reduced MCC number.

255 dues rendered MtPrpR incapable of regulating MCC gene transcription.

256 Remarkably, MCCs lacking parent centrioles and deuterosomes also amp

257 landin signaling is essential both for renal MCC progenitor formation and terminal differentiation.

258 that prostaglandin signaling mediates renal MCC development has broad implications for other tissues

259 Further, the appearance of renal MCCs has been cataloged in several kidney conditions, wh

260 g prostaglandin E(2) (PGE(2)) levels rescued MCC number.

261 -1 in the neoadjuvant setting for resectable MCC.

262 Committee on Cancer stage IIA-IV resectable MCC received >= 1 nivolumab dose.

263 iated cancer types, patients with resectable MCC received nivolumab 240 mg intravenously on days 1 an

264 regionally advanced, "borderline-resectable" MCC.

265 Here we apply methylC-capture sequencing (MCC-Seq) in a clinical population of ~200 adipose tissue

266 ew, we find that Mci mutant mice can specify MCC precursors.

267 Spanish multicenter multicase-control study (MCC-Spain).

268 on MCC cells, therefore, restoring surviving MCC cells' susceptibility to recognition and elimination

269 The as-synthesized MCC with a highly microporous shell, a multichamber inne

270 Principal component analysis indicated that MCC under manure differed from those under the INF treat

271 Here, we show that MCCs lacking deuterosomes amplify the correct number of

272 The MCC binds and inhibits the mitotic E3 ubiquitin ligase,

273 The MCC precursor is not the traditional phenolic resol but

274 The MCC-like tumor phenotype was dependent on the FBXW7-bind

275 ants display reduced association between the MCC and APC/C, are defective in poly-ubiquitination of C

276 observed MCC behavior in both games, but the MCC that we observed was different from that observed in

277 eased expression of pSMAD158 and VEGF in the MCC and subchondral bone.

278 I collagen in superficial layer cells in the MCC perichondrium but is present at high levels in the c

279 This case series study investigated the MCC specimens of 55 patients treated at the Department o

280 ind additionally required for binding of the MCC to the APC/C and for MCC disassembly.

281 ycan distribution, and mineralization of the MCC.

282 To investigate the role of I-PTH on the MCC and subchondral bone, we carried out our studies usi

283 mens expressed CK20 and synaptophysin on the MCC tumor cells (100% expression).

284 Under this paradigm, the MCC and its underlying bone are thought to result from 2

285 yV is constantly shed from healthy skin, the MCC incidence increases among aging and immunocompromise

286 glucono delta-lactone, respectively, to the MCC solutions prior to renneting.

287 tional array of basal bodies of cilia on the MCCs.

288 However, in Camsap3 (tm1a/tm1a) , MCCs lacked CAMSAP3 at the ciliary base.

289 but cannot reactivate APC/C already bound to MCC.

290 STING molecule was efficiently delivered to MCC cells via an AAV vector.

291 d immunosuppression showed that, relative to MCC patients with virus-positive tumors, virus-negative

292 In response to MCC cells with restored STING, cocultured T cells expres

293 Overexpression of ATOH1 in variant MCC cell lines and fibroblasts induced miR-375 expressio

294 ely 0.80, F1-score approximately 0.89 versus MCC approximately 0.29 and F1-score approximately 0.50).

295 0.84 and F1-score approximately 0.91 versus MCC approximately 0.51 and F1-score approximately 0.71)

296 plexes, our IntPred predictor performs well (MCC=0.370, ACC=0.811, SPEC=0.916, SENS=0.411) and compar

297 yed by human participants to examine whether MCC is observed across different types of game and the p

298 y 30% cases, while low-quality contacts with MCC <0.35 degrades the performance for 50% cases.

299 A sample of 340 patients with MCC and care partner dyads was recruited between 2017 an

300 adic approach when focusing on patients with MCC and their care partners.

301 Our findings suggest that patients with MCC may develop a second genetically distinct primary tu