ライフサイエンスコーパス: colon cancer

1 links between inflammation and malignancy in colon cancer.

2 ting is an import strategy to treat advanced colon cancer.

3 mor-suppressing effects against experimental colon cancer.

4 ncer, 5508 with lung cancer, and 12,723 with colon cancer.

5 rapy among young and middle-aged adults with colon cancer.

6 nflammation is a significant risk factor for colon cancer.

7 for studying diseases including colitis and colon cancer.

8 n about the chemopreventive effect of KJT on colon cancer.

9 in several cancers including lung cancer and colon cancer.

10 h early-onset inflammatory bowel disease and colon cancer.

11 elated with markers of TGFbeta activation in colon cancer.

12 ribed as prognostic factors in patients with colon cancer.

13 that generates O2(), is highly expressed in colon cancer.

14 Main outcome was the event of colon cancer.

15 in a population-based cohort of early-stage colon cancer.

16 o affect survival of patients diagnosed with colon cancer.

17 treatment effects in a murine model of human colon cancer.

18 rbated by Stat-3-activation and help promote colon cancer.

19 s should undergo endoscopic surveillance for colon cancer.

20 t increased risk of overall CRC and proximal colon cancer.

21 ed invasive adenocarcinoma when subjected to colon cancer.

22 ygen contents on the metastatic potential of colon cancer.

23 R2 and XVX as a chemopreventive tool against colon cancer.

24 on between development of diverticulitis and colon cancer.

25 sible as diagnosis biomarker for early-stage colon cancer.

26 irmed using tumor samples from patients with colon cancer.

27 r Ser-165 phosphorylation or both of YBX1 in colon cancer.

28 f human malignancies, including melanoma and colon cancer.

29 ma exosomes of the patients with early stage colon cancer.

30 is in many systems, including microbe-driven colon cancer.

31 t of 10 in CXCR4 overexpressing leukemia and colon cancer.

32 mphocyte antigen-4 (CTLA-4) immunotherapy of colon cancer.

33 ), and 20 cases with newly diagnosed primary colon cancer.

34 us knockout mice have reduced development of colon cancer.

35 SNTI and BMM in patients with stage I to III colon cancer.

36 tumorigenic inflammatory microenvironment in colon cancer.

37 -ray-induced photodynamic therapy (X-PDT) of colon cancer.

38 for resistance to fluoropyrimidines in early colon cancer.

39 nutraceutical potential in the fight against colon cancer.

40 0.02) but not proximal (HR = 0.95; P = 0.72) colon cancer.

41 ly potent drug for several cancers including colon cancer.

42 r therapeutic targets especially in proximal colon cancer.

43 implicated in the suppression of colitis and colon cancer.

44 e defined as statin users after diagnosis of colon cancer.

45 rgeting might be a strategy for treatment of colon cancers.

46 with pooled gastrointestinal and right-side colon cancers.

47 y in preclinical models of breast, liver and colon cancers.

48 ithout drug treatments, and human breast and colon cancers.

49 HCGV, TCTE5, TCTEX5, or CFAP255) in 82 human colon cancers.

50 signaling target of metastasis-associated in colon cancer 1 (MACC1) in colorectal cancer (CRC).

51 dy identified 6365 patients with early-stage colon cancer (48.7% [3098 of 6365] female).

52 atients with high-risk stage II or stage III colon cancer, adjuvant chemotherapy with fluoropyrimidin

53 ined genotypes, we found the highest risk of colon cancer among individuals harbouring the SNP55TT or

54 rectal cancer cases: 690 cases with proximal colon cancer and 690 cases with distal colorectal cancer

55 k of colon cancer, particularly for proximal colon cancer and among nonusers of NSAIDs.

56 the elevated risks for lung, pancreatic, and colon cancer and encouraged to modify risk factors and a

57 potent tumour growth inhibition in melanoma, colon cancer and human papilloma virus-E6/E7 tumour mode

58 s-talk between LGR5 and TGFbeta signaling in colon cancer and identifies LGR5 as a new modulator of T

59 mary mouse colon tumour, liver metastasis of colon cancer and naive colon tissues.

60 tified an enrichment of SMAD4 alterations in colon cancer and other rare alterations predicted to hav

61 odes and BMM in patients with stage I to III colon cancer and the prognostic effect on disease-free s

62 k is to investigate the role of IRE1alpha in colon cancer and to determine whether IRE1alpha could se

63 measurement of a mouse bearing subcutaneous colon cancer and validated using histology.

64 CCDC66 expression was elevated in polyps and colon cancer and was associated with poor prognosis.

65 and is stabilized in both APC-mutated human colon cancers and Apc(min/+) intestinal polyps.

66 stability (CIN) is observed in 80% to 90% of colon cancers and is thought to contribute to colon canc

67 be over-expressed in oral, breast, lung, and colon cancers and plays important roles in regulation of

68 d for the survival of primary and metastatic colon cancers and that oncogenic K-RAS activates TGF-bet

69 ntaining the proliferative phenotype of some colon cancers and the potential of NOX1 as a therapeutic

70 , C-08, N0147, MOSAIC (Adjuvant Treatment of Colon Cancer), and XELOXA (Adjuvant XELOX) were pooled t

71 ng nonusers of NSAIDs, risks of overall CRC, colon cancer, and proximal colon cancer were higher in t

72 a functionally important molecular event in colon cancer, and that GRM3 is a promising molecular tar

73 all survival of patients with a diagnosis of colon cancer, and whether their effects were associated

74 ith prostate, renal, pancreatic, breast, and colon cancer as the most common diagnoses.

75 egulatory function of DDB2 is significant in colon cancer, as it regulates metastasis.

76 lantation because of the additional risk for colon cancer associated with immunosuppression.

77 ouse systems to engineer and study recurrent colon cancer-associated EIF3E-RSPO2 and PTPRK-RSPO3 chro

78 included all patients treated surgically for colon cancer at Massachusetts General Hospital from 2004

79 OM/DSS mice, a model of IBD and inflammatory colon cancer, augmented DSS-induced weight loss and incr

80 cancer often differ significantly from human colon cancer, being largely restricted to the small inte

81 h mRNA expression levels of Stat3 or Jab1 in colon cancer, breast cancer and glioblastoma are associa

82 otein 3(TMED3) is a metastatic suppressor in colon cancer, but its function in the progression of hep

83 condition associated with increased risk for colon cancer, but its role in the development of colorec

84 seases such as Crohn's disease, colitis, and colon cancer, but mechanistic insights into these proces

85 gher connectivity in the network of proximal colon cancer, but not in distal colorectal cancer.

86 connected with other biomarkers in proximal colon cancer, but not in distal colorectal cancer.

87 As GRM3 is upregulated in colon cancer, but rarely expressed in normal peripheral

88 g immunotherapies for patients with advanced colon cancer, but their durable response rate remains lo

89 pression patterns of all of the GalNAc-Ts in colon cancer by analyzing transcriptomic data.

90 progression-promoting function of GM-CSF in colon cancer by inducing EMT.

91 a can promote colitis and colitis-associated colon cancer (CAC) development using a CAC mouse model a

92 In human colon cancer Caco-2 cells, induction of cellular HD5 exp

93 Most colon cancer cases are initiated by truncating mutations

94 However, the side of origin of colon cancer (CC) still does not represent a prognostic

95 rrent standard combination therapies used in colon cancer (CC).

96 bination chemotherapies in three-dimensional colon cancer cell cultures, or spheroids.

97 onstrated decreased oxidative-stress induced colon cancer cell invasion, but increased interaction wi

98 sal cytosolic Ca(2+) concentration of HCT116 colon cancer cell line and modified the cytosolic Ca(2+)

99 In vitro experiments were performed with colon cancer cell line Colo320 (high Nrp-2 expression) a

100 consisting of four defined derivatives of a colon cancer cell line that resulted from consecutive ep

101 sed significantly by UbV.7.2 expression in a colon cancer cell line that was treated with the chemoth

102 , we used CRISPR to KO PPIP5Ks in the HCT116 colon cancer cell line.

103 els could be modeled in an APC-mutated human colon cancer cell line.

104 carcinoma proliferation, a) in vitro against colon cancer cell lines and b) in vivo on tumor growth i

105 uantify AKT1 and AKT2 from breast cancer and colon cancer cell lines and flash-frozen tumor lysates w

106 pression downstream of silenced NOX1 in both colon cancer cell lines and xenografts.

107 ease in protein phosphatase activity for two colon cancer cell lines in which NOX1 expression was kno

108 d precise gene targeting to produce isogenic colon cancer cell lines with a knockout/rescue system fo

109 eir antiproliferative activity against HT-29 colon cancer cell lines.

110 1 in YAMC mouse colonocytes and Caco-2 human colon cancer cell lines.

111 of human colonic adenocarcinomas tested and colon cancer cell lines.

112 e sets related to glycolysis, hypoxia, and a colon cancer cell phenotype, including genes regulated b

113 LGR5 ablation in colon cancer cells and crypt stem cells resulted in loss

114 of anthocyanin-rich plant extracts on human colon cancer cells and determine their mechanism of acti

115 (PKG2) to activate forkhead box O (FoxO) in colon cancer cells and in the colon epithelium of mice.

116 oter in HT1080 fibrosarcoma cells and HCT116 colon cancer cells and NME2-mediated transcriptional rep

117 increased proliferation and motility of both colon cancer cells and normal fibroblasts, increased the

118 ment leads to increased activin secretion in colon cancer cells and TGF-beta induced cellular migrati

119 firmed by coimmunoprecipitation in the HT115 colon cancer cells and was supported by a partial coloca

120 We found that metastatic colon cancer cells are able to transfer their amoeboid p

121 MYC-nick promotes the migration of colon cancer cells assayed in 3D cultures or grown as xe

122 ypes, we reconstituted its signaling axis in colon cancer cells harboring MLK4-inactivating mutations

123 d the metastatic dissemination capability of colon cancer cells HT29, including the migration and inv

124 JMJD2B enhanced subcutaneous tumor growth of colon cancer cells in a p53-dependent manner, and geneti

125 matous polyposis coli/beta-catenin wild-type colon cancer cells in a paracrine fashion, whereas no hy

126 of IRE1alpha suppressed the proliferation of colon cancer cells in vitro and xenograft growth in vivo

127 han its major constituents- proliferation of colon cancer cells in vitro, attenuated migration and do

128 rogenitor cell compartment of growth-fueling colon cancer cells in vivo Our results imply that differ

129 ockdown and suppresses the tumorigenicity of colon cancer cells in vivo.

130 and pharmacological inhibition of nCDase in colon cancer cells increases ceramide, and this is accom

131 We show that activation of PKG2 in colon cancer cells inhibited cell proliferation, inhibit

132 ium butyrate-induced differentiation of HT29 colon cancer cells is associated with a reduced CD133 ex

133 ction of the mechanism of action of SPRY2 in colon cancer cells is important to understand the upregu

134 Furthermore, GM-CSF stimulation renders colon cancer cells more resistant to cytotoxic agents.

135 pression or inhibition of GRM3 activation in colon cancer cells reduces cell survival and anchorage-i

136 Herein, we show that chronic exposure of colon cancer cells to GM-CSF, which harbor its receptor,

137 Colon cancer cells treated with low-dose PEITC for >1 mo

138 Here, we report that GRP78 is secreted from colon cancer cells via exosomes.

139 nhibited growth and tumorigenic potential of colon cancer cells, and DBC1 expression correlated with

140 cytotoxicity to Caco-2, HT-29, HCT-116 human colon cancer cells, and reduced inflammatory response ca

141 lassification of white blood T-cells against colon cancer cells, as well as lipid accumulating algal

142 hanced cancer cell killing in cultured human colon cancer cells, but also improved antitumor activity

143 operatively with TGFbeta type II receptor in colon cancer cells, enhancing TGFbeta-mediated growth in

144 r to results that our group has published in colon cancer cells, inhibition of ERK phosphorylation in

145 beta-catenin, inhibited the proliferation of colon cancer cells, repressed colon CSCs and prevented x

146 nt activated ERK1/2 and promoted invasion of colon cancer cells, which was attenuated by MLK3 siRNA k

147 itive feedback loop enhances the invasion of colon cancer cells.

148 crease NOX1 expression stably in HT-29 human colon cancer cells.

149 d consequently inhibits the proliferation of colon cancer cells.

150 ion, we investigated the protein partners in colon cancer cells.

151 fects of the combination chemotherapy on the colon cancer cells.

152 y contributing to the oncogenic phenotype of colon cancer cells.

153 owth arrest and a metabolic reprogramming in colon cancer cells.

154 mbined and tested for cytotoxicity in CaCo-2 colon cancer cells.

155 compared with TRAIL-sensitive human lung and colon cancer cells.

156 NA) contribute to the stem-like character of colon cancer cells.

157 dhesion in normal adult crypt stem cells and colon cancer cells.

158 tially explaining the decreased migration of colon cancer cells.

159 mbined and tested for cytotoxicity in CaCo-2 colon cancer cells.

160 f exosomes is affected by differentiation of colon cancer cells; exosomes might be used by differenti

161 had no colonoscopy, had an increased risk of colon cancer compared with those without both diverticul

162 ed association between adult weight gain and colon cancer could be primarily explained by attained ab

163 In patients with recurrence of stage III colon cancer, deficient MMR was significantly associated

164 we studied acid handling by myofibroblasts (colon cancer-derived Hs675.T, intestinal InMyoFib, embry

165 aling, with an important role in suppressing colon cancer development.

166 mation is believed to have a crucial role in colon cancer development.

167 ibition in APC(Min) mice, a model of FAP and colon cancer, diminished the number of small intestinal

168 fusion and sepsis were associated with worse colon cancer disease-specific survival [(+)transfusion:

169 e effects of blood transfusion and sepsis on colon cancer disease-specific survival, cardiovascular d

170 geneic blood transfusion, sepsis, and 5-year colon cancer disease-specific survival, cardiovascular d

171 ulation-based cohort of early-stage resected colon cancer, disease laterality was not associated with

172 Patients with primary diagnoses for colon cancer, diverticular disease, benign colonic neopl

173 altered consistently in six CRC cell lines (colon cancer: DLD-1, HCT116 and HT29; rectal cancer: HT5

174 We found that human breast, lung, and colon cancers expressed GARP aberrantly.

175 Colon cancers frequently bear inactivating mutations of

176 lands) and linked to patients diagnosed with colon cancer from 2002 through 2007, listed in the Eindh

177 ve cohort study of patients with early-stage colon cancer from the province of Ontario, Canada.

178 Determining the grade of colon cancer from tissue slides is a routine part of the

179 ver the key epigenetic regulators that drive colon cancer growth, we used a CRISPR loss-of-function s

180 To investigate the role that NOX1 plays in colon cancer growth, we used shRNA to decrease NOX1 expr

181 to-alanine) mutant in either HEK293 cells or colon cancer HT29 cells showed dramatically reduced NF-k

182 Migration of human colon cancer (HT29) cells was assessed with a wound-clos

183 aTa (REMBRANDT), caArray studies of lung and colon cancer, ImmPort and the 1000 genomes data sets.

184 e the association between diverticulitis and colon cancer in a large, nationwide cohort study.

185 val gains among patients diagnosed as having colon cancer in an equal-access health care system.

186 GSK-3beta independent manner, differentiated colon cancer in claudin-3-/- mice versus WT-mice.

187 The incidence of colon cancer in the group with diverticulitis (4.3%) and

188 18,186 patients with resected stage I to III colon cancer in the National Cancer Data Base (2004-2012

189 al, and metastasis in an orthotopic model of colon cancer in vivo Upon RSPO1 stimulation, LGR5 formed

190 Colon cancer induces a state of mucosal dysbiosis with a

191 ls with stem-like properties, referred to as colon cancer-initiating cells (CCIC), have high tumorige

192 indicate that carcinogenesis in a subset of colon cancer is consequent to a molecular mechanism driv

193 Surgery for colon cancer is not an exception.

194 ers in different locations of the gut, where colon cancer is primarily driven by inflammation and the

195 protects from distant metastases in primary colon cancer is unknown.

196 ting data on overall survival for left-sided colon cancer (LCC) compared with right-sided colon cance

197 ery for nonlocally advanced, nonmetastasized colon cancer, LR was associated with a significant lower

198 uggested that disease biology and outcome of colon cancer may differ between right-sided and left-sid

199 e LIGHT (TNFSF14) in the microenvironment of colon cancer metastases associates with improved patient

200 ulator of TGFbeta signaling able to suppress colon cancer metastasis.

201 half of hospitals perform well on these NQF colon cancer metrics concurrently, and high performance

202 ospitals on the National Quality Forum (NQF) colon cancer metrics.

203 Mechanisms to increase LIGHT in the colon cancer microenvironment warrant further investigat

204 lation were assessed in a colitis-associated colon cancer model (CAC).

205 Using an isogenic HCT116 colon cancer model of oxaliplatin resistance, we further

206 rs for CRC were consistent with those in our colon cancer model.

207 These findings represent an advance in colon cancer modeling and implicate enhancer-mediated ge

208 In colitis-associated colon cancer models, epithelial HIF-2alpha was essential

209 By studying colon cancer models, we found that bacteria can metaboli

210 In a colon cancer mouse model, gemcitabine resistance was ind

211 gh a prophylactic hydrogel patch leads, in a colon cancer mouse model, to complete tumour remission w

212 Thus the colon cancer mucosal microbiome evolves with cancer stag

213 g/year) was associated with a higher risk of colon cancer (multivariable-adjusted relative risk = 1.5

214 stering coefficient was 0.50 in the proximal colon cancer network and 0.30 in the distal colorectal c

215 We found that the proximal colon cancer network formed a denser network (total numb

216 greater clustering tendency of the proximal colon cancer network.

217 additional pharmacologic strategy to improve colon cancer outcomes.

218 mal (HR = 1.31) than with distal (HR = 1.04) colon cancer (P = 0.029).

219 iets are associated with an elevated risk of colon cancer, particularly for proximal colon cancer and

220 somal miRNA was isolated from 50 early-stage colon cancer patients and 50 matched healthy volunteers.

221 ls and was also found in primary tumors from colon cancer patients with distant metastases.

222 Human colon cancer patients with more advanced disease show hi

223 positive nodal status, and poor survival of colon cancer patients.

224 ses and was associated with poor survival of colon cancer patients.

225 RNAs as candidates for diagnostic markers in colon cancer patients.

226 uate Selumetinib response in tumours from 23 colon cancer patients.

227 ereditary mixed polyposis syndrome is a rare colon cancer predisposition syndrome caused by a duplica

228 btain functional foods or nutraceuticals for colon cancer prevention.

229 olon cancers and is thought to contribute to colon cancer progression and recurrence.

230 ght junction integral protein, in inhibiting colon cancer progression by serving as the common rheost

231 ehensively characterized a cellular model of colon cancer progression consisting of four defined deri

232 cells during human aging, in tissues during colon cancer progression, in telomere-related diseases s

233 We found that BRD4 is critical for colon cancer proliferation, and its knockdown led to dif

234 associated with neoplastic diseases such as colon cancer, prostate cancer and neuroblastoma.

235 ents, and AC within 4 months of diagnosis as colon cancer quality indicators.

236 For 4 of those 5 cancers (colon cancer: R = 0.61; P < .001; lung cancer: R = 0.62;

237 only diagnosed cancers in the United States (colon cancer: R = 0.61; P < .001; lung cancer: R = 0.73;

238 effect of colonoscopies and treatment on the colon cancer rate after diverticulitis.

239 colon cancer (LCC) compared with right-sided colon cancer (RCC).

240 In KRAS-mutant colon cancer, regulation of MAPK signaling was preserved

241 atment options for patients with young-onset colon cancer remain to be defined and their effects on p

242 orter survival, independent of sepsis, after colon cancer resection.

243 ative System were queried for stage I to III colon cancer resections from 2004 to 2011.

244 We expanded and updated our colon cancer risk model to evaluate colorectal cancer (C

245 ly associated with overall CRC, but proximal colon cancer risk was higher in the proinflammatory-chan

246 Colon cancer screening is being targeted toward patients

247 p of 1.5 years, 11.6% of patients received a colon cancer screening test (57.9 tests per 1000 person-

248 None of 17 colon cancers showed sst2 sites with the agonist, and on

249 d to promote development of prostate cancer, colon cancer, skin cancer, breast cancer, lung cancer an

250 , prospectively collected set of 278 primary colon cancers spanning diverse tumor stages and clinical

251 We constructed a tissue microarray of 999 colon cancer specimens from patients who underwent surgi

252 .5 mum for phosphorus and platinum in HCT116 colon cancer spheroids upon treatment with the clinicall

253 cNAc-mediated epigenetic regulation of human colon cancer stem cells (CCSC).

254 xpression of IRE1alpha decreased stemness of colon cancer stem cells (CSCs) and attenuated growth of

255 tion (EMT), and expressed markers related to colon cancer stem cells.

256 For colon cancer surgery (N = 4202), laparoscopic resection

257 duce sepsis rates and improve survival after colon cancer surgery.

258 pecific survival, and overall survival after colon cancer surgery.

259 S2R16 gene do not have a strong influence on colon cancer susceptibility, but a possible role in rect

260 results show a tumorigenic role of SPRY2 in colon cancer that is based on the dysregulation of tight

261 rious Slco2a1 genotypes in a murine model of colon cancer, the adenomatous polyposis (APC) mutant (Ap

262 nown to exhibit tumor suppressor activity in colon cancer, the mechanism of which is not understood.

263 lied to the dynamic (18)F-FDG measurement of colon cancer, the proposed algorithm accurately identifi

264 val for right-sided compared with left-sided colon cancer: the hazard ratios were 1.00 (95% CI, 0.92-

265 Restoring oxygen in metastatic colon cancer through ITPP inhibits tumor spread and mark

266 prove cisplatin efficacy in the treatment of colon cancer through the creation of orally administered

267 he application of risk prediction models for colon cancer to CRC.

268 hat GRM3 is a promising molecular target for colon cancer treatment.

269 attractive and specific molecular target for colon cancer treatment.

270 ovements have been reported in three phase 3 colon cancer trials when oxaliplatin was added to fluoro

271 ly that dual SHMT1/2 knockout blocks HCT-116 colon cancer tumor xenograft formation.

272 In proximal colon cancer, tumor biomarkers tended to be correlated w

273 prostaglandin transporter OATP2A1/SLCO2A1 in colon cancer tumorogenesis is unknown.

274 alysis, different miR expression patterns in colon cancer versus non tumour cells using the previousl

275 es beta-catenin signaling and cell growth in colon cancer via binding RXRalpha, which provide new str

276 Right-side colon cancer was also associated with gallstone disease

277 Right-sided colon cancer was defined as any tumor arising in the cec

278 Left-sided colon cancer was defined as any tumor arising in the spl

279 analysis of 999 patients with a diagnosis of colon cancer, we associated statin with reduced risk of

280 To investigate the function of GalNAc-T6 in colon cancer, we used precise gene targeting to produce

281 s of overall CRC, colon cancer, and proximal colon cancer were higher in the highest quintile compare

282 A total of 122 patients with stage I to III colon cancer were included.

283 Patients with right-sided colon cancer were more likely to be older (median age, 7

284 een (90 %) of the cases with newly diagnosed colon cancer were not known to have metastatic disease o

285 es were smaller in kidney cancer and in situ colon cancers were more common in patients diagnosed aft

286 Patients with resected stage III colon cancers were randomized to adjuvant FOLFOX (folini

287 ancer Registry to identify all patients with colon cancer who underwent resection between January 1,

288 separate cohort of 252 patients with primary colon cancer who underwent resection of CCLM without pre

289 The majority of patients with colon cancer will develop advanced disease, with the liv

290 atients had normal findings, one patient had colon cancer with a hepatic metastasis, one patient had

291 that miR-125a-3p abundant level may predict colon cancer with an area of under the curve (AUC) of 68

292 d the association between diverticulitis and colon cancer with inconclusive results.

293 NPP4B may function as an oncogenic driver in colon cancer, with potential implications for targeting

294 in patients undergoing elective surgery for colon cancer without mechanical bowel preparation (n = 1

295 Treatment of mice bearing a colon cancer xenograft with the antibiotic metronidazole

296 single treatment on nude mice bearing HT-29 colon cancer xenograft.

297 on antiangiogenic treatment effects in human colon cancer xenografts compared with ex vivo reference

298 3D matrix transducer to monitor response of colon cancer xenografts to antiangiogenic therapy with f

299 als and Methods Twenty-three mice with human colon cancer xenografts were randomized to receive eithe

300 mor-associated macrophages and the growth of colon cancer xenografts.