ライフサイエンスコーパス: MSS

1 MSS also allows for accurate prediction of the number an

2 MSS BRAF(V600E) mCRC with baseline MAPK activation and i

3 MSS HNPCC tumors displayed a significantly lower degree

4 MSS HNPCC tumors had KRAS mutations exclusively in codon

5 MSS HTA provides a rapid and sensitive approach for dete

6 MSS promoters are defined by the lack of a TATA box and

7 MSS provides a straightforward approach for modeling hig

8 MSS reduced distress scores during the examination perio

9 MSS was used to define multi-marker panels that were rob

10 MSS-2 provides 9 Mb coverage of the canine genome with n

11 rithmic CRP; 95% CI, 1.30 to 1.59; P < .001; MSS hazard ratio, 1.51 per unit increase of logarithmic

12 and hMSH2 expression, as well as 9 of the 10 MSS cases, lacked methylation of the hMLH1 promoter.

13 integration in a manner consistent with a 12 MSS model.

14 le the results presented here confirm the 12 MSS model, they also indicate that the integration of NK

15 for intraspecific sperm competitiveness.(13) MSS is lost in self-fertile lineages, likely as a respon

16 in 8 of 12 MSI cancers whereas only 3 of 16 MSS cancers were methylated.

17 efforts in the dog, Minimal Screening Set 2 (MSS-2) of 327 canine microsatellite markers has been mul

18 2 (50%) of 4 MSI-L tumors, and 8 (35%) of 23 MSS tumors demonstrated HPP1 hypermethylation.

19 ors (5 of 5 MSI-H, 2 of 4 MSI-L, and 1 of 23 MSS) showed evidence of hMLH1 hypermethylation.

20 mean CORE-OM scores of 0.87 (SD 0.50) in 237 MSS participants versus 1.11 (0.57) in 216 support as us

21 MSI-H, 1 (6%) of 16 MSI-L, and 4 (15%) of 27 MSS lesions showed hMLH1 hypermethylation (P = 0.013).

22 tation, negative for KRAS mutation); type 3 (MSS or MSI low, non-CIMP, negative for BRAF mutation, po

23 volved and found elevations in 5 of 15 (33%) MSS CRC cell lines analyzed.

24 tation, positive for KRAS mutation); type 4 (MSS or MSI-low, non-CIMP, negative for mutations in BRAF

25 during the examination period and 182 (59%) MSS participants completed at least half of the course.

26 e-free survival (HR, 6.6; 95% CI, 2.9-14.6), MSS (HR, 6.2; 95% CI, 2.6-14.4), and OS (HR, 2.8; 95% CI

27 These findings may reflect a MSS mutator phenotype contributing to the development of

28 In addition, MSS-A and MSS-N tumors were associated with somatic muta

29 In adulthood, MSS decreased mRNA levels for both the alpha-2(A) adrene

30 ncreased immobility time, but did not affect MSS immobility.

31 chial epithelial (HBE) cells exposed to air, MSS from 1R5F tobacco reference cigarettes, and e-vapor

32 ACVR2, 62% lacked protein expression but all MSS and MSI-H tumors with wild-type ACVR2 expressed prot

33 KRAS mutation negative; n = 170), alternate (MSS, CIMP low, BRAF mutation negative, and KRAS mutation

34 tly, MSS patients with Chr20q amplification (MSS-A) were associated with better recurrence-free survi

35 h MSS patients without Chr20q amplification (MSS-N; P = 0.03).

36 The predictive value of normal IHC for an MSS/MSI-L phenotype was 96.7%, and the predictive value

37 utator phenotype was reported recently in an MSS CRC cell line.

38 ence-free survival (HR = 1.70, P = .046) and MSS (HR = 1.88, P = .043) in a multivariable analysis.

39 16S rRNA gene sequencing (r(2) = -0.60) and MSS (r(2) = -0.55).

40 In addition, MSS-A and MSS-N tumors were associated with somatic mutations in d

41 To ask whether the cytoplasmic domain and MSS of each protein serve only as a membrane anchor or h

42 differences were noted between the MSI-L and MSS group for any of the parameters tested.

43 15% of colorectal cancers, whereas MSI-L and MSS tumors appear to be phenotypically similar.

44 is distinct from tumor phenotypes MSI-L and MSS, with no apparent differences between MSI-L and MSS.

45 th no apparent differences between MSI-L and MSS.

46 phism has differential influences on MSI and MSS CRC risk.

47 ur findings support a model in which MSI and MSS preferentially target different genes and pathways i

48 expression signature distinguishing MSI and MSS samples.

49 o poorly differentiated histology in MSI and MSS tumors.

50 re missed 69% of samples detected by MSS and MSS missed 54% of samples detected by culture.

51 CRP level was associated with poorer OS and MSS in the initial, confirmatory, and combined data sets

52 Es was associated with impaired PFS, OS, and MSS in patients with advanced melanoma treated with firs

53 A Cox regression model compared PFS, OS, and MSS.

54 ding selectivity, poor pharmacokinetics, and MSS liability.

55 istant metastasis disease-free survival, and MSS after CLND in patients with SLN metastasis.

56 RNA knocking down MRE11 in the wild-type and MSS cell line SW-480 and a second cell line model transf

57 As MSS and HSS mice differ in several immunologic character

58 f this group, 129 (68.6%) were classified as MSS, 17 (9.0%) as MSI-L, and 42 (22.3%) as MSI-H.

59 old/poorly immunogenic solid tumors, such as MSS mCRC.

60 s subgroups indicated a significantly better MSS for SNB patients with T2 and T3 melanomas (>1.0 to 4

61 2- and BRAF(V600E)-mutated patients in both MSS (adjusted HR = 2.06 and 1.15; both P < 0.05) and MSI

62 ormation, and whole-exome sequencing of both MSS and MSI serrated tumors derived from these mouse mod

63 Culture missed 69% of samples detected by MSS and MSS missed 54% of samples detected by culture.

64 Detection of SA by MSS or culture missed over half of the SA detected by th

65 In obligately outcrossing Caenorhabditis, MSS is dispensable for baseline fertility but required f

66 microsatellite stable colorectal carcinoma (MSS-CRC) given flat doses of cibisatamab and atezolizuma

67 patients without mismatch repair deficiency (MSS HNPCC) have certain molecular features, including gl

68 first appear in mice that eventually develop MSS, sera from infected animals were monitored for CRI f

69 In mice that eventually developed MSS, CRI were detected by 5 to 6 wk after infection, pla

70 with AJCC stage IIIB and stage IIIC disease, MSS outcomes were similar to those of patients with stag

71 ining the AQP1 sequence truncated after each MSS.

72 e rat model of musculoskeletal side effects (MSS) was used to assess whether selective MMP-13 inhibit

73 ViroCap substantially enhances MSS for a comprehensive set of viruses and has utility f

74 -Sandri-Sarkar Maximum Likelihood Estimator (MSS-MLE) method, (ii) Lea-Coulson method of the median (

75 to insufficient data on most MS, only a few MSS predictive models have been developed so far.

76 ve patients (P < 0.001 for OS, P < 0.001 for MSS).

77 (95% CI, 1.01 to 1.04; P = .0051), 1.02 for MSS (95% CI, 1.00 to 1.04; P = .048), and 1.02 for DFS (

78 S, 0.70 to 0.74 for RFS and 0.72 to 0.76 for MSS.

79 paper we propose an efficient algorithm for MSS and evaluate it on both synthetic and real data.

80 e propose a noncanonic circular geometry for MSS, which better aligns with the polar nature of MSS an

81 A mouse model for MSS was previously produced by disrupting Sil1 using gen

82 S (HR, 1.60; 95% CI, 1.01-2.50), but not for MSS (HR, 0.80; 95% CI, 0.35-1.71).

83 5% confidence interval: 2.76, 8.91) than for MSS tumors (odds ratio = 2.33, 95% confidence interval:

84 rs were suggestively stronger than those for MSS tumors; the risk with high (>/=30) body mass index (

85 so that this protein initially adopts a four MSS topology.

86 the Mass Spec Studio development framework (MSS-CLEAN).

87 ility, distinguishing most CRC with MSI from MSS CRC.

88 For FtsQ, MSS swaps supported cell division but cytoplasmic domain

89 Further, MSS+ sperm appear to derive their competitive advantage

90 However, MSS can lack sensitivity and may yield insufficient data

91 Importantly, MSS patients with Chr20q amplification (MSS-A) were asso

92 ms some previously identified aberrations in MSS CRC and provides in silico evidence for some novel c

93 ociated with better survival in MSI-H and in MSS/MSI-L patient subgroups.

94 d TP53 in MSS-A and mutated KRAS and BRAF in MSS-N.

95 T with OX effectively induced RNA editing in MSS CRC cell lines (HT29 and Caco2, p < 0.001) via the i

96 When MTHFR C677T genotype frequencies in MSS CRC cases were compared to controls, individuals wit

97 icular are major targets for inactivation in MSS colon cancers as well as in colon cancers with micro

98 Instead, LC inhibition in MSS mice increased climbing time.

99 loss of heterozygosity at the ACVR2 locus in MSS tumors.

100 Although ADAR1 expression was low in MSS CRC, CRT including oxaliplatin (OX) treatment upregu

101 LK4) protein kinase is frequently mutated in MSS CRC with approximately 50% of the mutations occurrin

102 ion therapy (CRT) to generate neoantigens in MSS CRCs.

103 ional analyses, the increased OS observed in MSS-CRC warrants further exploration in larger randomize

104 y of the cell toxicity responses observed in MSS-exposed HBE cells, e-vapor exposure is not benign, b

105 embrane was prognostic for poorer outcome in MSS patients.

106 (eg, CCND1, FGF genes) was more prevalent in MSS-TMB-H tumours than in the dMMR/MSI-H or MSS-TMB-L su

107 es, with high frequencies of mutated TP53 in MSS-A and mutated KRAS and BRAF in MSS-N.

108 2, 16.1%); and those showing no instability (MSS, n = 317, 62.4%).

109 )(,)(15)(,)(16) However, restoration of just MSS to the self-fertile C. briggsae is sufficient to ind

110 The risk of MSI-L/MSS tumors was not elevated among long-duration smokers

111 current smoking than there was within MSI-L/MSS tumors.

112 I-H) or MSI-low/microsatellite stable (MSI-L/MSS), was assessed in tumors of 1,202 cases.

113 ght into the mechanisms regulating TATA-less MSS promoters has been hampered by the lack of an in vit

114 At the behavioral level, MSS increased locomotion in approach-avoidance explorato

115 Median MSS was not reached for the SLN-only positive group and

116 olizumab (anti-PD-L1) in advanced metastatic MSS-CRC.

117 those reported for primate models and mimic MSS in humans.

118 Although most MSS HNPCC tumors had some degree of CpG island methylati

119 mmunotherapy can reprogram BRAF-V600E mutant MSS colorectal cancers toward immune responsiveness.

120 ally, we showed that inhibiting the LC in No MSS mice increased immobility time, but did not affect M

121 olyadenine tract of exon 10 compared with no MSS tumors.

122 e association of rs1800734 with MSI+ but not MSS cancer risk in our own data and by meta-analysis.

123 D colorectal carcinoma compared with 0.4% of MSS/MMR-P colorectal carcinoma (P < 0.001) and 15% of MS

124 Moreover, another 55% of MSS colon cancers demonstrate a transforming growth fact

125 viral pathogen, we evaluate the accuracy of MSS for real-time parameter estimation and prediction du

126 However, a stratified univariate analysis of MSS for different thickness subgroups indicated a signif

127 all 19 cases of MSI-L and 35 of 82 cases of MSS exhibited EMAST.

128 BAP were identified to be the major cause of MSS.

129 epigenetic alterations to the development of MSS HNPCC tumors.

130 ption system optimized for the expression of MSS promoters, termed the multiple promoter comparison (

131 The majority of MSS CRCs demonstrate chromosomal instability (CIN) with

132 This simple and sensitive model of MSS is an attractive alternative for studying the pathol

133 which better aligns with the polar nature of MSS and allows changing the field-to-flow.

134 ve alternative for studying the pathology of MSS.

135 We compare the performance of MSS to three state-of-the-art benchmark 1) a likelihood

136 and KRT16 remained significant predictors of MSS in a joint analysis (HR = 2.3, P = 0.03) although, H

137 mitoses were the most powerful predictors of MSS.

138 sex (P = .01) were independent predictors of MSS.

139 CRC by characterizing the immune profiles of MSS and MSI tumor models.

140 ression and immunohistochemical profiling of MSS and MSI CRC cell lines and tumors revealed significa

141 ion event involving a 180-degree rotation of MSS 3 from an N(lum)/C(cyt) to an N(cyt)/C(lum) orientat

142 The severity of MSS, as judged by clinical criteria (2 blinded observers

143 red and scored for the onset and severity of MSS, using clinical and histologic parameters.

144 insic MSI signature, recognizing a subset of MSS patients with MSI transcriptional traits, endowed wi

145 harmacological treatment of certain types of MSS by specifically stabilizing the mutant SIL1 protein.

146 To demonstrate the versatility of MSS HTA, we also constructed a probe sensitive to change

147 replacement of the cytoplasmic domain and/or MSS resulted in the loss of the ability to support cell

148 vary in regard to their MSI status (MSI-H or MSS), their hMLH1 protein expression (MLH- or MLH+), and

149 MSS-TMB-H tumours than in the dMMR/MSI-H or MSS-TMB-L subgroups.

150 nical course than are stage-matched MSI-L or MSS tumors.

151 IMP-high or MSI subtypes than in CIMP-low or MSS subtypes, and is positively correlated with its para

152 ociations of lower vitamin D with poorer OS, MSS, and DFS were independent of this association.

153 Our MSS algorithm outperforms the algorithm of Kuksa and Pav

154 100% had confirmed pMMR/MSS tumors.

155 was also an independent predictor of poorer MSS (hazard ratio [HR] = 1.55, P < 0.001).

156 ) microsatellite stable, Amsterdam-positive (MSS HNPCC) (N = 22); (2) Lynch syndrome cancers (identif

157 -negative polyposis and early-onset proximal MSS CRC in whom detection rates will be highest, the exp

158 was not performed had significantly reduced MSS (HR = 2.10; P < 0.001), DFS (P < 0.001), RNRFS (P <

159 ly improved the predictive accuracy for RFS, MSS and OS when added to a comprehensive suite of establ

160 late sampling/culture and skin tape sampling/MSS: double negative, sequencing only positive, contact

161 o sensory analysis (Mixed Structured Scale - MSS) and seven formulations were selected in respect to

162 call this version as the Motif Stems Search (MSS) problem.

163 domain, a single membrane-spanning segment (MSS), and a large periplasmic domain that probably encod

164 soot measured with an AVL microsoot sensor (MSS) reflected black carbon.

165 In molecular-stream separation (MSS), a stream of a multicomponent mixture is separated

166 uencing, and metagenomic shotgun sequencing (MSS) for Clostridium difficile identification in diarrhe

167 Metagenomic shotgun sequencing (MSS) is an important tool for characterizing viral popul

168 4; 95% CI, 1.48-3.40; P < .001), and shorter MSS (HR, 2.23; 95% CI, 1.46-3.07; P < .001).

169 l, after which males and females had similar MSS.

170 those that initiate at multiple start sites (MSS).

171 4 into the membrane results in the final six MSS topology.

172 less risky alternative to main stream smoke (MSS) of conventional tobacco cigarettes.

173 d on the dorsal skin of the Mack Super Snow (MSS) leopard geckos.

174 Marker State Space (MSS) defines "marker states" based on all possible patte

175 his approach, termed multiple-site-specific (MSS) HTA, was directed toward the detection of mutations

176 rate a multichannel smartphone spectrometer (MSS) as an optical biosensor that can simultaneously opt

177 tch repair mutations) (N = 21); (3) sporadic MSS (N = 92); and (4) sporadic MSI (N = 46).

178 th microsatellite instable (MSI) and stable (MSS) phenotypes and had a high density of tumor-associat

179 e distinction between microsatellite stable (MSS) and low frequency MSI (MSI-L) can only be accomplis

180 ty and those that are microsatellite stable (MSS) but chromosomally unstable.

181 profiles for MSI and microsatellite stable (MSS) cancers, which suggest that cancers with MSI develo

182 d-type cell lines and microsatellite stable (MSS) cell lines.

183 onsistent with EMT in microsatellite stable (MSS) colon cancer cells, whereas cells with MSI and muta

184 Among microsatellite stable (MSS) colon cancers, we now find that non-BAT-RII point m

185 lity of MSI-H but not microsatellite stable (MSS) colorectal and endometrial cancer cell lines.

186 ork for patients with microsatellite stable (MSS) colorectal cancer.

187 kely to have MSI than microsatellite stable (MSS) CRC [odds ratio (OR) 1.90; 95% confidence interval

188 mutator phenotypes in microsatellite stable (MSS) CRC carcinogenesis.

189 ity (MSI), but not in microsatellite stable (MSS) CRC cell lines and tumors.

190 lity (MSI-H) CRCs and microsatellite stable (MSS) CRC demonstrate similar pathway activations at the

191 eatment in a model of microsatellite stable (MSS) CRC.

192 ptional landscapes of microsatellite stable (MSS) CRCs with or without nuclear HES1 expression, we in

193 y, whereas and in the microsatellite stable (MSS) group, these were detected in 7.7%, 38.6%, and 53.8

194 approaches to detect microsatellite stable (MSS) HNPCC tumors are unclear.

195 vity in patients with microsatellite stable (MSS) metastatic colorectal cancer need to be identified.

196 mains unclear whether microsatellite stable (MSS) patients with colorectal cancer can be further stra

197 identification, among microsatellite stable (MSS) patients, of a subset of MSI-like tumors with commo

198 , comparing MSI-H and microsatellite stable (MSS) patients.

199 liver metastases and microsatellite stable (MSS) primary CRC have a similar paucity of T cells and d

200 nalysis combining all microsatellite stable (MSS) samples demonstrated a clear prognosis value both f

201 ajor driving force of microsatellite stable (MSS) sporadic CRC.

202 ICIs than those with microsatellite stable (MSS) tumors (odds ratio [OR], 22.66 [95% CI, 17.30-29.73

203 cancers and 20 random microsatellite stable (MSS) tumors from a population-based cohort of 503 patien

204 dic CRCs, its role in microsatellite stable (MSS) tumors is debated.

205 However, microsatellite stable (MSS) tumors, are intrinsically resistant to immunotherap

206 ntly mutated genes in microsatellite stable (MSS) tumours and 16 in microsatellite instable (MSI) tum

207 Of these, 680 were microsatellite stable (MSS), 27 were MSI-H, and 111 were MSI-L.

208 es have been defined: microsatellite stable (MSS), low-frequency MSI, and high-frequency MSI (MSI-H).

209 characterized them as microsatellite stable (MSS), MSI high or MSI low, CIMP high or CIMP low, CIMP n

210 (CIN); herein termed microsatellite stable (MSS).

211 infected with EBV and microsatellite stable (MSS).

212 ubgroups of MSI-H and microsatellite stable (MSS)/low-frequency MSI (MSI-L) tumors, diploidy was asso

213 (MSI) and differ from microsatellite-stable (MSS) colorectal cancers in both prognosis and response t

214 e limited activity in microsatellite-stable (MSS) or mismatch repair-proficient (pMMR) colorectal can

215 ying MSI-H, MSI-L, or microsatellite-stable (MSS) tumors have never been evaluated.

216 l as in a subgroup of microsatellite-stable (MSS) tumors.

217 icrosatellite status (microsatellite-stable (MSS) vs. microsatellite-instable (MSI)) and histology (t

218 if unstable at only one locus, or MS-stable (MSS) if showing no instability at any loci.

219 AS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, positive for BRAF mutati

220 romosome instability (microsatellite stable; MSS), are best understood in the context of colon cancer

221 fectiveness of detecting viruses in standard MSS versus MSS following targeted sequence capture.

222 irmed the independent effect of NSLN status (MSS; P = .04).

223 urine specimens from middle-school students (MSS) were tested individually by LCR, and then the proce

224 y students (Mindfulness Skills for Students [MSS]) plus mental health support as usual, or mental hea

225 articularly the Mesovoid Shallow Substratum (MSS), an understudied subterranean environment.

226 ncluded the following groupings of subtypes: MSS = 337 and MSI = 130; type I = 458 and type II = 66.

227 e, mitochondrial local constraint score sum (MSS) and find it associated with all-cause mortality, an

228 In summary, MSS is a promising method that may improve on current ap

229 Conditional melanoma-specific survival (MSS) estimates up to 5 years after diagnosis were adjust

230 The 5-year melanoma-specific survival (MSS) for ulcerated and nonulcerated melanomas was 77.6%

231 nt in predicting melanoma specific survival (MSS) in a univariate analysis, which was also consistent

232 CCv8 cohort, the melanoma-specific survival (MSS) rates at 5 years were 67% versus 77%, and at 10 yea

233 Melanoma-specific survival (MSS) was not significantly different for patients in the

234 urvival (OS) and melanoma-specific survival (MSS) were 82% and 94%, respectively, for histopathology-

235 vival (RFS), and melanoma-specific survival (MSS) were analyzed.

236 e-free survival, melanoma-specific survival (MSS), and overall survival.

237 l survival (OS), melanoma-specific survival (MSS), and recurrence-free survival (RFS) were compared b

238 ficantly reduced melanoma-specific survival (MSS), DFS, regional node recurrence-free survival (RNRFS

239 e recurrence and melanoma-specific survival (MSS).

240 rvival (RFS) and melanoma-specific survival (MSS).

241 y reduced OS and melanoma-specific survival (MSS).

242 (OS; P < .001), melanoma-specific survival (MSS; P = .0025), and disease-free survival (DFS; P = .04

243 Marinesco-Sjogren syndrome (MSS) is an autosomal recessive, neurodegenerative, multi

244 his gene lead to Marinesco-Sjogren syndrome (MSS), a debilitating autosomal recessive disease charact

245 of mice with moderate splenomegaly syndrome (MSS) at 20 wk after infection.

246 splay either moderate splenomegaly syndrome (MSS) or hypersplenomegaly syndrome (HSS).

247 d, Multiple Shooting for Stochastic systems (MSS), applies a linear noise approximation to describe t

248 We demonstrate that MSS HTA is sensitive and largely specific to all targete

249 We find that MSS significantly outperforms each of these three benchm

250 We show that MSS produces accurate estimates of key epidemic paramete

251 The MSS rates in the CMMR and EORTC cohorts over the entire

252 The MSS rates of the EORTC studies either overlapped with or

253 For stage IIIA, the MSS rates at 5 years were 80% versus 93%, and at 10 year

254 ars were 71% versus 88%; for stage IIIB, the MSS rates at 5 years were 75% versus 83%, and at 10 year

255 In the MSS group, 5-year TTR rates of 61.8%, 66.3%, and 72.9% w

256 In the MSS group, KRAS exon 2 mutations were associated with TT

257 red with 88 (37%) of 235 participants in the MSS group.

258 In the MSS population, the pool-by-4 algorithm was 95.8% sensit

259 rom ICIs compared to TP53-WT patients in the MSS subgroup (5 versus 21 months, HR = 2.39, 95% CI: 1.2

260 In the MSS tumors, exhausted CD8+ T cells co-expressed PD-1 and

261 None of the MSS and none of the MSI-L tumors had altered expression

262 95% CI four to ten) needed to be offered the MSS course to prevent one from experiencing clinical lev

263 16, we randomly assigned 616 students to the MSS group (n=309) or the support as usual group (n=307).

264 We validated the performance of this MSS via measuring the concentrations of protein and immu

265 t, the results sufficiently showed that this MSS can achieve the comparative analysis detection limit

266 In IE patients, SSS compared to MSS accurately upgraded the diagnosis from possible to d

267 Although most mutations leading to MSS result in deletion of the majority of the protein, t

268 , overexpression of the MSRP most similar to MSS, Cbr-MSRP-3, is insufficient to enhance competitiven

269 following integrated pathways: traditional (MSS, CIMP negative, BRAF mutation negative, and KRAS mut

270 with a subset of pathway-unassigned tumors (MSS or MSI low, CIMP negative, BRAF mutation negative, a

271 the accurate and robust transcription of two MSS promoters, pgp1 (hamster P-glycoprotein class I homo

272 Furthermore, we used MSS HTA in longitudinal studies of pro gene evolution in

273 86.3% of C. difficile-positive samples using MSS.

274 Hazard ratios (HR) for RFS for MSI-H versus MSS/MSI-L patients were 0.77 (95% CI, 0.40 to 1.48) in t

275 of detecting viruses in standard MSS versus MSS following targeted sequence capture.

276 , in patients with MSS-RNF43(mutated) versus MSS-RNF43(wild-type) tumors.

277 ree survival (RFS) for MSI-H patients versus MSS/MSI-L patients (P = .10), but showed no difference i

278 The remaining 118 neoplasms (80%) were MSS.

279 nocopies several pathologies associated with MSS, although its ability to assemble and secrete antibo

280 wn-regulated in MSI cancers as compared with MSS cancers.

281 etter recurrence-free survival compared with MSS patients without Chr20q amplification (MSS-N; P = 0.

282 pproximately 15% of cases, and compared with MSS tumors, more often arise in the proximal colon and d

283 phoblastoid cell lines from individuals with MSS, leading us to conclude that the BiP cofactor Sil1 i

284 study (NCT04017650) of 26 participants with MSS BRAF(V600E) mCRC who received encorafenib, cetuximab

285 Among patients with MSS and proficient mismatch repair, the HR for PFS was 0

286 mes in 148 heavily pre-treated patients with MSS mCRC (six from the dose-escalation cohort; 142 from

287 her investigational agents, in patients with MSS metastatic colorectal cancer and disease progression

288 this cohort study suggest that patients with MSS metastatic colorectal cancer and without liver metas

289 A total of 39 patients with MSS metastatic colorectal cancer whose disease progresse

290 igate PD-1/PD-L1 inhibitors in patients with MSS metastatic colorectal cancer without liver metastase

291 In addition, 29 out of 235 patients with MSS tumors (12.3%) experienced durable responses on ICI-

292 tant clinical implications for patients with MSS tumors who are generally unresponsive to immunothera

293 Among patients with MSS tumors, ICI-based therapy was associated with signif

294 CI, 0.10-0.71; P = 0.008), in patients with MSS-RNF43(mutated) versus MSS-RNF43(wild-type) tumors.

295 Males had significantly worse MSS outcomes for up to 2 years of conditional survival,

296 The 5-year MSS and RFS rates were 83% and 76%, respectively (median

297 The 5-year MSS for minimally/moderately ulcerated melanomas (</=70%

298 elanomas (>70% or >5 mm), which had a 5-year MSS of 66.4% and 59.3%.

299 0 months for the NSLN positive group (5-year MSS, 77.8% and 49.5%, respectively).

300 bility to classify both 5-year OS and 5-year MSS.