ライフサイエンスコーパス: CRC

1 CRC lines (HCT116 and SW480) were engineered to express

2 CRC screening tests are ranked in 3 tiers based on perfo

3 CRC was reported on questionnaires and ascertained by re

4 been generated for 10 KRAS-mutant ACF and 10 CRCs harboring a KRAS mutation, as well as matched sampl

5 599 patients diagnosed with stage 1, 2, or 3 CRC.

6 transcriptomic analyses were performed on 44 CRC cell lines, compared against primary CRCs (n=95) and

7 was a prospective case-control study of 613 CRC cases and 1190 matched controls nested within the No

8 presented a 4-fold change were considered a CRC proteomic signature.

9 In a CRC cell line and human CRC tissue exposed to hypoxia, i

10 hereditary cancer syndrome (51%) reported a CRC diagnosis in a first-degree relative.

11 h recurrently gained or lost activity across CRC specimens.

12 ling pathways that are important in advanced CRC.

13 ormal microRNA (miRNA) expression can affect CRC pathogenesis and development through targeting criti

14 m CRC survivors, regular use of NSAIDs after CRC diagnosis was significantly associated with improved

15 administration of the cholera vaccine after CRC diagnosis with decreased risk of death from CRC and

16 When coffee intake before vs after CRC diagnosis were examined, compared with patients cons

17 k of the IL1B (-3737C/-1464G/-511T/-31C) and CRC risk, and this association was exclusively observed

18 emonstrated that both colorectal adenoma and CRC are monoclonal in origin, and the CRCs further diver

19 ionship between CT colonography coverage and CRC screening.

20 Many activate known oncogenes, and CRC growth can be mitigated through pharmacologic inhibi

21 s) and 95% CIs for overall survival (OS) and CRC-specific survival.

22 een Western and prudent dietary patterns and CRC risk in the Health Professionals Follow-up Study and

23 , 1.28; 95% CI, 1.10-1.53, respectively) and CRC-related death (HR, 1.71; 95% CI, 1.39-2.12 and HR, 1

24 own about which lesion subtypes may serve as CRC precursors in young adults.

25 ogy, assisted by the Metafer-iFISH automated CRC imaging system, provides a platform for the analysis

26 nt efficacy of anti-VEGFR2 treatment in both CRC models.

27 Interval colorectal cancer (CRC) accounts for 3% to 8% of all cases of CRC in the Un

28 leading to high risks of colorectal cancer (CRC) and endometrial cancer mainly as a result of mutati

29 epsilon) cause hereditary colorectal cancer (CRC) and have been found in many sporadic colorectal and

30 e in protein abundance in colorectal cancer (CRC) and its contribution to tumorigenesis have not been

31 es have similar risks for colorectal cancer (CRC) as those diagnosed with serrated polyposis.

32 ong subjects screened for colorectal cancer (CRC) by the guaiac fecal occult blood test, interval can

33 tive splicing profiles of colorectal cancer (CRC) cells compared to adjacent normal tissues using dee

34 & AIMS: Relative risk of colorectal cancer (CRC) decreases with age among individuals with a family

35 veral clinically relevant colorectal cancer (CRC) gene expression signatures, we assessed the suscept

36 and tumor progression in colorectal cancer (CRC) has not been fully elucidated.

37 ory potential and risk of colorectal cancer (CRC) in 87,042 postmenopausal women recruited from 1993-

38 & AIMS: The incidence of colorectal cancer (CRC) in individuals younger than 50 years is increasing.

39 ng colonoscopy to prevent colorectal cancer (CRC) in persons aged 70 to 74 and those aged 75 to 79 ye

40 ever, the role of MLK3 in colorectal cancer (CRC) invasion is unknown.

41 Colorectal cancer (CRC) is a leading cause of death in the developed world,

42 Human colorectal cancer (CRC) is a major cause of cancer mortality and frequently

43 Colorectal cancer (CRC) is a worldwide health concern with respect to both

44 Colorectal cancer (CRC) is characterized by genome-wide alterations to DNA

45 patients with early-onset colorectal cancer (CRC) is largely undetermined.

46 teomic landscape of human colorectal cancer (CRC) is maintained in established CRC cell lines and the

47 Colorectal cancer (CRC) is one of the most common malignancies worldwide wi

48 Among cancer diagnoses, colorectal cancer (CRC) is prevalent, with a lifetime risk of developing CR

49 Akt survival proteins in colorectal cancer (CRC) metastasis and explored potential mechanisms of Akt

50 orylation correlates with colorectal cancer (CRC) metastasis and prognosis.

51 ce and mortality rates of colorectal cancer (CRC) of any ethnic group in the United States.

52 uencing (bulk WES) on two colorectal cancer (CRC) patients with normal or adenomatous polyps, we foun

53 ult to delineate in human colorectal cancer (CRC) patients.

54 n a cell culture model of colorectal cancer (CRC) progression, we observe accumulation of Alu RNA tha

55 oorly understood, role in colorectal cancer (CRC) progression.

56 d cell compartment drives colorectal cancer (CRC) progression.

57 Advanced colorectal cancer (CRC) remains a critical health care challenge worldwide.

58 play an important role in colorectal cancer (CRC) risk, yet the prevalence of germline cancer suscept

59 ult blood test (FOBT) for colorectal cancer (CRC) screening is supported by randomized trials demonst

60 genetically diverse human colorectal cancer (CRC) specimens.

61 io (LMR) in patients with colorectal cancer (CRC) undergoing curative resection and to compare it to

62 ong elderly patients with colorectal cancer (CRC) were because of differences in tumor characteristic

63 an orthotopically induced colorectal cancer (CRC) xenograft model.

64 with a decreased risk of colorectal cancer (CRC), but the association may be related to residual con

65 tivity in mouse models of colorectal cancer (CRC), CRC cell lines, and mouse and human normal and can

66 Colorectal cancer (CRC), the second leading cause of cancer-related deaths

67 ptional classification of colorectal cancer (CRC), with clinical and biological implications.

68 characteristic feature of colorectal cancer (CRC).

69 urvival for patients with colorectal cancer (CRC).

70 tations toward metastatic colorectal cancer (CRC).

71 polyps in mouse models of colorectal cancer (CRC).

72 rant WNT signaling drives colorectal cancer (CRC).

73 ed with the occurrence of colorectal cancer (CRC).

74 -coding risk variants for colorectal cancer (CRC).

75 as a tumor suppressor in colorectal cancer (CRC).

76 colon cancer 1 (MACC1) in colorectal cancer (CRC).

77 usceptibility to sporadic colorectal cancer (CRC).

78 l (5-FU)-chemotherapy for colorectal cancer (CRC).

79 variety of aneuploid circulating rare cells (CRCs), including CTCs and circulating tumor endothelial

80 with RSPO3 fusions and in tumors with common CRC mutations such as APC, beta-catenin, or RNF43.

81 First, we compiled CRC-related miRNAs, CRC-related genes, and human TFs fro

82 etrospective study recruited 509 consecutive CRC patients between January 2009 and December 2009.

83 Complete root coverage (CRC) for CAF + EMD was 70.59%, significantly superior to

84 Percentage of RC, complete root coverage (CRC), width, and thickness of keratinized tissue were as

85 in mouse models of colorectal cancer (CRC), CRC cell lines, and mouse and human normal and cancer co

86 In CT26 CRCs, highly resistant to anti-VEGFR2 therapy, CXCR4 blo

87 y repressed the MIR34A gene in p53-defective CRC cells, whereas expression of MIR34A was induced in p

88 erform or complement hemoglobin in detecting CRC and advanced adenomas.

89 FIT therefore detects CRC with 77% sensitivity.

90 ed a multi-stakeholder task force to develop CRC screening recommendations.

91 icant association between risk of developing CRC and selected SNPs.

92 revalent, with a lifetime risk of developing CRC being approximately 5%.

93 senchymal phenotype in poorly differentiated CRC cell lines as a consequence of repression of the KCN

94 ify protein combinations that differentiated CRC or advanced adenoma from control samples.

95 ns outperformed hemoglobin in discriminating CRC or advanced adenoma from control samples.

96 critical for the progression of disseminated CRCs.

97 tified a panel of 11 proteins to distinguish CRC from AT.

98 Dutch CRC screening program and published literature.

99 Enriched CRCs, maintained at high viability and suitable for prim

100 al cancer (CRC) is maintained in established CRC cell lines and the utility of proteomics for predict

101 Proteomes of established CRC cell line are representative of primary tumors.

102 tions, using sequence data from 863 familial CRC cases and 1604 individuals without CRC (controls).

103 eterious BRF1 variants with 1.4% of familial CRC cases, in individuals without mutations in high-pene

104 Through this approach, we identify five CRC intrinsic subtypes (CRIS) endowed with distinctive m

105 ead to the development of new biomarkers for CRC risk.

106 ified novel candidate protein biomarkers for CRC screening.

107 on Insurance coverage of CT colonography for CRC screening was associated with a greater likelihood o

108 rrant transcriptional programme critical for CRC growth and survival.

109 s under age 65 who were eligible and due for CRC screening and managed by the participating health sy

110 emonstrates that HIF-2alpha is essential for CRC growth and progression.

111 Our data provide evidence for CRC proteomic subtype-specific drug responses.

112 The age-adjusted hazard ratio (HR) for CRC among female immigrants was 0.63 (95% CI 0.59, 0.67)

113 hway) and ADCY3 (FGFR signaling pathway) for CRC evolution.

114 8-year risk for CRC and 30-day risk for adverse events.

115 We determined the relative risk for CRC for individuals based on age and number of affected

116 ies aged 70 to 74 years, the 8-year risk for CRC was 2.19% (95% CI, 2.00% to 2.37%) in the screening

117 id not differ significantly from the SIR for CRC in patients with multiple serrated polyps (0.74; 95%

118 The SIR for CRC in patients with serrated polyposis (0.51; 95% CI, 0

119 ted standardized incidence ratios (SIRs) for CRC in both groups, as well as in their first-degree rel

120 rker of prognosis and therapeutic target for CRC.

121 the application of epigenetic therapies for CRC patient treatment.

122 diagnosis with decreased risk of death from CRC and overall mortality.

123 ; this strategy prevented 79% of deaths from CRC.

124 ; this strategy prevented 79% of deaths from CRC.

125 in exosomes, plasma and tissue samples from CRC patients and healthy controls.

126 Nearly half of all GWAS CRC risk loci co-localize to recurrently activated enhan

127 ) had breast cancer only and 144 (27.3%) had CRC only.

128 subjects without CRC: subjects found to have CRC by colonoscopy had a median level of 86.0 pg IFNG/mL

129 tumor cells among enriched non-hematopoietic CRCs.

130 In a CRC cell line and human CRC tissue exposed to hypoxia, induced heat-shock 70-kDa

131 eered ex vivo, or from patient-derived human CRC organoids.

132 STEAP4 was increased in human CRC and predicted poor prognosis.

133 ial-to-mesenchymal transition (EMT) in human CRC cell lines of varying stages of differentiation.

134 GC32 was significantly up-regulated in human CRC tissues versus adjacent normal tissues.

135 n is associated with poor prognosis in human CRC.

136 n, migration and tumorigenic growth of human CRC cells in vitro and in vivo.

137 val status were collected for all identified CRC cases.

138 We identified CRC from the Ontario Cancer Registry between the index d

139 ormal FIT result, or treatment evaluation if CRC was detected.

140 iser Permanente patients with stage I to III CRC diagnosed from 2006 through 2011.

141 we describe a broadly usable immunocompetent CRC model that recapitulates the entire adenoma-adenocar

142 e importance of histone H4K16 acetylation in CRC.

143 he enhancers highly recurrently activated in CRC, most are constituents of super enhancers, are occup

144 on after hypoxia or HIF-2alpha activation in CRC are unclear.

145 Inducible loss of Akt2 in CRC cells robustly upregulated MTSS1 at the messenger RN

146 the metastasis-promoting effects of Akt2 in CRC cells.

147 one of the earliest signaling alterations in CRC, and the decreased expression of the bile acid apica

148 w details the DNA methylation alterations in CRC, the significance of CIMP status, the development of

149 R/Matrin 3 axis in response to DNA damage in CRC cells.

150 ancer Genome Atlas (TCGA) expression data in CRC, whereby we generated a core regulatory network cons

151 d epithelial-mesenchymal transition (EMT) in CRC via the Smad/Sip1 signaling pathway, as shown by dec

152 l effects on eliminating SRSF6 expression in CRC cells by inducing SRSF6(+intron 2) transcripts which

153 s associated with altered gene expression in CRC, this was not the case in ACF, suggesting the insuff

154 MPV was an independent prognostic factor in CRC (HR = 1.452, 95% CI = 1.118-1.884, p = 0.005).

155 SRP1 loss is an adverse prognostic factor in CRC.

156 tic strategies and disease-relevant genes in CRC and possibly other solid tumors.

157 To understand the role of oncogenic KRAS in CRC, we engineered a mouse model of metastatic CRC that

158 e plasma membrane, induced a patent lumen in CRC spheroids, and slowed CRC cell invasion.

159 ificance of systemic inflammatory markers in CRC such as the NLR, PLR, and mGPS has been well defined

160 els and activity of microRNA-34a (MIR34A) in CRC cells.

161 cidate the predictive significance of MPV in CRC.

162 ncurrent with CT, could substitute for OC in CRC surveillance.

163 imary end point was patient participation in CRC screening 1 year after the intervention.

164 The distribution of NLR, PLR and PC in CRC patients was compared with 5270 healthy blood donors

165 mbrane and a loss of epithelial phenotype in CRC spheroids.

166 Targeted deletion of PINCR in CRC cells significantly impaired G1 arrest and induced h

167 nhibitor restores regorafenib sensitivity in CRC cells with intrinsic or acquired resistance.

168 Together, our findings suggest that in CRC TIAM1 suppresses tumor progression by regulating YAP

169 ined SRSF6 (SRSF6(+intron 2)) transcripts in CRC tissues and cell lines.

170 CT colonography (CTC), when used in CRC screening, effectively identifies colorectal polyps

171 and a tumor suppressor frequently mutated in CRCs, contribute to resistance to targeted therapies.

172 and PAr were both associated with increased CRC risk [OR: 1.48 (95% CI: 1.08, 2.02) and OR: 1.50 (95

173 e to reduce risk for environmentally induced CRC with the realization that the extent of protection m

174 identify variants associated with inherited CRC.

175 t this pathway might be developed to inhibit CRC metastasis and overcome resistance to therapy associ

176 ransplant recipients with CF should initiate CRC screening at age 30 years within 2 years of the tran

177 To examine whether risk for interval CRC among Medicare patients differs by race/ethnicity an

178 ly Medicare enrollees, the risk for interval CRC was higher in black persons than in white persons; t

179 The probability of interval CRC by the end of follow-up was 7.1% in black persons an

180 Data on interval CRC by race/ethnicity are scant.

181 Likewise, CRC was stable with 61%/61% for CAF + CMX and 39%/39% fo

182 Twenty-eight (96.6%) of 29 available LS CRCs demonstrated abnormal MSI/MMR results.

183 s of (non-V600) BRAF mutations in metastatic CRC.

184 C, we engineered a mouse model of metastatic CRC that harbors an inducible oncogenic Kras allele (Kra

185 proximately 2.2% of patients with metastatic CRC and define a clinically distinct subtype of CRC with

186 e independent sets of primary and metastatic CRCs, with limited overlap on existing transcriptional c

187 First, we compiled CRC-related miRNAs, CRC-related genes, and human TFs from multiple data sour

188 oved outcome of anti-VEGFR2 therapy in mouse CRCs.

189 nsmigration across the endothelium in murine CRC tumors.

190 of the implementation of the Dutch national CRC screening program allowed for instant adjustment of

191 wever, these loci only explain around 14% of CRC heritability, highlighting the dire need of identify

192 r types of tumors that represent over 90% of CRC, RSPO3 is produced by stromal cells in the tumor mic

193 Immunohistochemical analyses of CRC tissues further corroborate the importance of histon

194 e identify TIAM1 as a critical antagonist of CRC progression through inhibiting TAZ and YAP, effector

195 MiR-210 was increased in hypoxic areas of CRC tissues and hypoxia-responsive miR-21 and miR-30d, b

196 ted 803 deaths, of which 188 were because of CRC.

197 (CRC) accounts for 3% to 8% of all cases of CRC in the United States.

198 CCL-21) and applied it to large datasets of CRC.

199 ional status as a key genetic determinant of CRC response to targeted therapies, and Mcl-1 as an attr

200 n variants in these genes and development of CRC in a systematic review of 11 publications, using seq

201 and decaffeinated coffee after diagnosis of CRC with lower risk of CRC-specific death and overall de

202 t overexpression of RGC32 facilitates EMT of CRC cells by activating Smad/Sip1 signaling.

203 DNA methylation alterations are hallmarks of CRC, and epigenetic driver genes have been identified th

204 We modeled the hazard of CRC using Cox proportional hazards regression, accountin

205 Persons with a family history of CRC or a documented advanced adenoma in a first-degree r

206 In an analysis of families with a history of CRC, we associated germline mutations in BRF1 with predi

207 e among individuals with a family history of CRC.

208 as associated with an increased incidence of CRC (Ptrend < .0001), with a relative risk (RR) of 1.31

209 EMD provides highest levels of CRC; however, the addition of CM increases gingival thic

210 icity play a major role in the modulation of CRC risk.

211 use was associated with a decreased odds of CRC, however this association may be due to residual con

212 The prevalence of CRC was similar between patients with confirmed serrated

213 ession, which manipulates the progression of CRC calls.

214 umor-promoting influence on a broad range of CRC.

215 th generic reminders about regional rates of CRC screening did not increase screening rates compared

216 ce diagnosis, 381 deaths (100 as a result of CRC) were observed.

217 We aimed to compare the risk of CRC among immigrants to Ontario, Canada, to its general

218 Decreased risk of CRC has been associated with physical activity, but prot

219 The risk of CRC in patients with multiple serrated polyps who do not

220 Because of the higher risk of CRC in these patients, screening should start at an earl

221 patterns are associated with a lower risk of CRC that does not vary according to anatomic subsite or

222 cups/day) had a significantly lower risk of CRC-specific death (multivariable HR, 0.63; 95% CI, 0.44

223 ee after diagnosis of CRC with lower risk of CRC-specific death and overall death.

224 that regulate ribosome synthesis and risk of CRC.

225 We calculated relative and absolute risks of CRC for PLP and the ratios 3-hydroxykynurenine:XA (HK:XA

226 In specimen of CRC patients, high-level expression of GM-CSF positively

227 ical models that mimic the natural stages of CRC progression are lacking.

228 and define a clinically distinct subtype of CRC with an excellent prognosis.

229 c anatomic subsites or molecular subtypes of CRC.

230 s the association with molecular subtypes of CRC.

231 l antibody therapies for targeted therapy of CRC.

232 Here, we show that treatment of CRC cells with fidarestat increases the efficacy of DOX-

233 e genotype and time-dependent progression of CRCs from adenocarcinoma (6 weeks), to local disseminate

234 f potential contributions of each subtype of CRCs to distinct clinical outcome.

235 ange (50-76 years), who had not been offered CRC screening.

236 to examine the effect of these haplotypes on CRC cell lines, our results suggest that inflammation an

237 Of 450 patients with early-onset CRC, 72 (16%) had gene mutations.

238 ne mutations among patients with early-onset CRC.

239 -effectiveness analysis to determine optimal CRC screening strategies for patients with cystic fibros

240 e DII group was at increased risk of overall CRC and proximal colon cancer.

241 o among nonusers of NSAIDs, risks of overall CRC, colon cancer, and proximal colon cancer were higher

242 re not substantially associated with overall CRC, but proximal colon cancer risk was higher in the pr

243 ic potential of IGF-2 in IGF2-overexpressing CRC models and the efficacy of MEDI-573, an IGF-1/2-neut

244 g overactivation of Wnt-signaling to prevent CRC malignancy.

245 Analysis of human primary CRC tumor patient databases showed a positive correlatio

246 44 CRC cell lines, compared against primary CRCs (n=95) and normal tissues (n=60), and integrated wi

247 sion of MIR34A was induced in p53-proficient CRC cells exposed to hypoxia.

248 We recruited 1,058 participants who received CRC care in a clinic-based setting without preselection

249 the mechanisms by which coffee might reduce CRC progression.

250 oncentrations were associated with a reduced CRC risk for the third compared with the first quartile

251 he surveillance intervals to 5 years reduced CRC mortality by 51.8% and increased colonoscopy demand

252 with CRC, but not of other recently reported CRC susceptibility variants.

253 re significantly increased in 5-FU resistant CRCs.

254 th incidence and mortality, and as a result, CRC tumorigenesis, progression and metastasis have been

255 y among subjects with SD-CRC and with non-SD-CRC.

256 istics, and mortality among subjects with SD-CRC and with non-SD-CRC.

257 geting ability even on a subcentimeter-sized CRC after spraying with a dose of 50 microg F-SERS dots.

258 a patent lumen in CRC spheroids, and slowed CRC cell invasion.

259 Conclusion Among long-term CRC survivors, regular use of NSAIDs after CRC diagnosis

260 scopy outreach to increase completion of the CRC screening process (screening initiation and follow-u

261 The national information system of the CRC screening program kept track of the number of invita

262 ple of 1370 healthy German volunteers of the CRC TRR58 MEGA study wave 1.

263 These findings indicate that the CRC epigenome is defined by highly recurrent epigenetic

264 ma and CRC are monoclonal in origin, and the CRCs further diversified into different subclones with h

265 9, and the median follow-up from baseline to CRC diagnosis was 8.2 y.

266 f risk prediction models for colon cancer to CRC.

267 s) a list of patients who are nonadherent to CRC screening enhances patient participation in fecal im

268 ine mutations in BRF1 with predisposition to CRC.

269 By using mice genetically prone to CRC, we show that SGG colonization is 1,000-fold higher

270 markers of vitamin B-6 status in relation to CRC risk.This was a prospective case-control study of 61

271 innate immune cells, which are recruited to CRCs upon anti-VEGFR2 treatment.

272 otential anti-cancer approaches for treating CRC patients.

273 ate-dissemination model of metastasis in two CRC patients and provide an unprecedented view of metast

274 oach to trace the metastatic lineages of two CRC patients with matched liver metastases.

275 eness of FIT relative to other commonly used CRC screening modalities.

276 utations in genes previously associated with CRC risk to identify variants associated with inherited

277 -penetrance genes previously associated with CRC.

278 spective study of individuals diagnosed with CRC at an age younger than 50 years, evaluated by the cl

279 dish Cancer Register who were diagnosed with CRC from July 2005 through December 2012.

280 most accurately identified individuals with CRC.

281 ity of the test to identify individuals with CRC.

282 disparities in black vs white patients with CRC 18-64 years old.

283 independent predictor of OS in patients with CRC undergoing curative resection and appears to be supe

284 sceptibility gene mutations in patients with CRC unselected for high-risk features (eg, early age at

285 whole blood samples identified patients with CRC with 87.0% sensitivity and a negative predictive val

286 test could be used to identify patients with CRC, using findings from colonoscopy as a reference stan

287 rvival times of black vs white patients with CRC.

288 advance personalized care for patients with CRC.

289 tations are carried by 9.9% of patients with CRC.

290 A reference group comprised all persons with CRC diagnosed in the Netherlands general population duri

291 ollected blood samples from 3 relatives with CRC in Spain (65, 62, and 40 years old at diagnosis) and

292 ion between variants in NTHL1 and RPS20 with CRC, but not of other recently reported CRC susceptibili

293 K cell activity between the 23 subjects with CRC (based on pathology analysis) and the 849 subjects w

294 cell activity test identified subjects with CRC with 87.0% sensitivity, 60.8% specificity, a positiv

295 egree relative diagnosed at >/=60 years with CRC or an advanced adenoma can be offered average-risk s

296 ilial CRC cases and 1604 individuals without CRC (controls).

297 -151.0 pg IFNG/mL), whereas subjects without CRC had a median level of 298.1 pg IFNG/mL (inter-quarti

298 ology analysis) and the 849 subjects without CRC: subjects found to have CRC by colonoscopy had a med

299 ll activity between subjects with vs without CRC.

300 Among colonoscopies yielding CRC precursor lesions in patients under 50 years, SSA/P