ライフサイエンスコーパス: colon tumor

1 and beta-catenin and CD44 expression in the colon tumor.

2 hways were recapitulated in both ovarian and colon tumors.

3 he therapeutic responsiveness of established colon tumors.

4 microbiota composition before development of colon tumors.

5 cancer cells of human prostate, breast, and colon tumors.

6 ess the development of breast, prostate, and colon tumors.

7 ere then administered azoxymethane to induce colon tumors.

8 and its expression was reduced in most human colon tumors.

9 ent to selectively enhance T(eff) entry into colon tumors.

10 s a regulator of the growth and apoptosis of colon tumors.

11 ermined that LIN28B overexpression occurs in colon tumors.

12 ALNT12, also recently shown to be altered in colon tumors.

13 receptor type 2 (LPA(2)) is overexpressed in colon tumors.

14 age of these genes were basally repressed in colon tumors.

15 ions in 64% of MSI cell lines and 69% of MSI colon tumors.

16 eminated, or metastatic CT26 and MC38 murine colon tumors.

17 tations in a set of 30 microsatellite stable colon tumors.

18 ic differences of KRAS and BRAF mutations in colon tumors.

19 des a growth advantage to this subset of MSI colon tumors.

20 y on the biological and clinical behavior of colon tumors.

21 ariant 2 in lung tumors but not in breast or colon tumors.

22 -associated and Apc tumor suppressor-related colon tumors.

23 uently deleted or inactive in pancreatic and colon tumors.

24 lation and Cables gene expression in primary colon tumors.

25 gated in colon cancer cell lines and primary colon tumors.

26 detected in 10 exons of Cables in 20 primary colon tumors.

27 XR knockout increases the size and number of colon tumors.

28 utants of beta-catenin found in PhIP-induced colon tumors.

29 lity, but it is implicated in the genesis of colon tumors.

30 rectum and left-colon tumors than for right-colon tumors.

31 PhIP 48 to 72 hours before surgery to remove colon tumors.

32 alian cells and is implicated in mammary and colon tumors.

33 methylation was also found in 12/14 primary colon tumors.

34 l proliferation and increase in apoptosis in colon tumors.

35 pathway genes have been identified in human colon tumors.

36 suggest ways to suppress Cox-2 expression in colon tumors.

37 r levels of COX-2 activity and expression in colon tumors.

38 ointestinal tract and downregulated in human colon tumors.

39 m2(+/+) but not Apc(min/+);Mdm2(C305F/C305F) colon tumors.

40 l, causes interleukin 17A (IL-17A)-dependent colon tumors.

41 erforin plus IFN-gamma compared to untreated colon tumors.

42 audin-7 and those of SPRY2 and ZEB1 in human colon tumors.

43 er, size and distribution of AOM/DSS-induced colon tumors.

44 married, higher tumor grade, and presence of colon tumors.

45 differentially methylated regions (DMRs) in colon tumors.

46 and KITLG are expressed by a subset of human colon tumors.

47 pressed heterogeneously by a subset of human colon tumors.

48 However, in mouse colon-tumors, 5'-promoter of DCLK1-gene remains unchange

49 ane/dextran sulfate sodium (AOM/DSS)-induced colon tumors, a mouse model for colitis-associated color

50 In primary human colon tumors, all of the epithelial cells also expressed

51 eased expression characterized half of human colon tumors, although not all tumors with elevated Wnt

52 g were identified as cancer-related, with 95 colon tumor and 67 lung tumor genes identified, respecti

53 e inflammation; high levels were detected in colon tumor and adjacent non-tumor tissues.

54 Metabolic profiling was also performed on colon tumor and adjacent nontumor tissues from 39 patien

55 ally unrelated embryos and a matched pair of colon tumor and adjacent normal colon tissue obtained fr

56 cancer, and the samples included breast and colon tumor and adjacent normal tissue.

57 high-coverage data from multiple samples of colon tumor and matched normal tissues.

58 performed RNA sequence analyses of pairs of colon tumor and nontumor tissues, each collected from 68

59 unction protein claudin-1 is dysregulated in colon tumors and associates with their progression.

60 g probiotic decreased the number and size of colon tumors and colonic uptake of [(18)F]-fluorodeoxygl

61 Messenger RNA levels of Smurf2 in colon tumors and control tissue were measured by quantit

62 We found an increased incidence of visible colon tumors and dysplastic microadenomas in ER-deficien

63 mutations were found in 34% of the proximal colon tumors and in 45% of the distal colon and rectal t

64 coexpressed in primary human liver, lung and colon tumors and in a subset of human colon cancer cell

65 creased protein expression of HDAC3 in human colon tumors and in duodenal adenomas from Apc1638(N/+)

66 ethane and regulates STAT3 activity in mouse colon tumors and in the HCT116 and young adult mouse col

67 phospholipase D2 (PLD2) was overexpressed in colon tumors and is secreted by cancer cells, inducing s

68 of tumor-infiltrating lymphocytes in primary colon tumors and liver metastases have improved outcomes

69 Here we integrated topological maps for colon tumors and normal colons with epigenetic, transcri

70 olon crypts) but was repressed in a panel of colon tumors and patient-derived colon cancer cell lines

71 n was detected in approximately 50% of human colon tumors and showed strong correlation with increase

72 s classical tumor suppressor is amplified in colon tumors and suggests a rationale for targeting Rb p

73 novel regulator of neutrophil recruitment to colon tumors and that it is essential in shaping the pro

74 An array of 137 patient-derived colon tumors and their associated xenografts were analyz

75 ferentiated colonosphere cultures from human colon tumors and used them to generate stably differenti

76 an hour in a large volume of mouse xenograft colon tumor, and 3) determine the impact of the HIFU/nan

77 an hour in a large volume of mouse xenograft colon tumor, and 3) determine the impact of the HIFU/nan

78 ne, respectively, accelerated development of colon tumors, and caused severe anemia.

79 ession of beta-catenin-target genes in mouse colon tumors, and interacted with beta-catenin to block

80 n/T-cell factor (TCF) complex occurs in most colon tumors, and its actions correlate with the neoplas

81 mors; they are believed to promote growth of colon tumors, and their numbers correlate with outcomes

82 s that predispose to development of skin and colon tumors are associated with accumulation in tissues

83 Colon tumors arise in a stepwise fashion from either dis

84 Similar results were seen in spontaneous colon tumors arising in genetically engineered mice.

85 ockout induces a marked 7.6-fold increase in colon tumors arising in the Min (multiple intestinal neo

86 cious against both wild-type and mutant KRAS colon tumors as a single agent and in combination with i

87 rexpressed in colon cancer cell lines and in colon tumors as compared to matched normal tissue sample

88 control mice (both WT and M(3)R(-/-)) had no colon tumors, azoxymethane-treated WT mice had 5.3 +/- 0

89 Furthermore, treatment of HCT-116 colon tumor-bearing ICR SCID mice with curcumin resulted

90 crease the antitumor immune response in CT26 colon tumor-bearing mice through the modulation of regul

91 CT26 colon tumor-bearing mice were imaged with FMT after intr

92 In addition, sampling of spatially distinct colon tumor biopsies revealed pTyr differences as dramat

93 from human colorectal cancer cell lines and colon tumor biopsies.

94 hibitors are specifically cytotoxic to human colon tumor biopsy cultures as well as colon cancer cell

95 ptosis and genetic deletion of Sam68 dampens colon tumor burden in mice.

96 form (SIM2-s), is specifically expressed in colon tumors but not in the normal colon.

97 iency increased the multiplicity and size of colon tumors but reduced the frequency of beta-catenin h

98 In conclusion, MAIT cells infiltrate colon tumors but their ability to produce IFN-gamma is s

99 Inhibition of colon tumors by celecoxib was associated with lower leve

100 ption factor (SPDEF) suppresses formation of colon tumors by unclear mechanisms.

101 Patients with KIT-expressing colon tumors can benefit from KIT RTK inhibitors.

102 small interfering RNA knockdown to suppress colon tumor cell growth with reduced sensitivity of norm

103 wth, invasion, and metastasis, of both human colon tumor cell lines and primary human colon cancer ti

104 (EPHB4) is aberrantly overexpressed in human colon tumor cell lines and selectively required for thei

105 Here we show that PDE10 is elevated in human colon tumor cell lines compared with normal colonocytes,

106 In matched colon tumor cell lines lacking Smad4 or expressing physi

107 -fluoro-2'-deoxyuridine (FdUrd) in two human colon tumor cell lines.

108 ntial contributor to PGC1beta expression and colon tumor cell survival.

109 increased acetylated alpha-tubulin in HCT116 colon tumor cells 253-fold but only modestly increased p

110 XR bound to the FGF19 promoter in both human colon tumor cells and "normal" intestinal crypt cells.

111 evels of CCL5 expression in human and murine colon tumor cells correlated with higher levels of apopt

112 vasion of human MDA-MB-231 breast and HCT116 colon tumor cells in vitro at concentrations less than t

113 and tumor formation induced by injection of colon tumor cells into NOD/SCID mice were positively ass

114 esting the cell cycle in isogenic breast and colon tumor cells lacking p53, suggesting the response i

115 These findings suggest that BRAF-mutant colon tumor cells may be less sensitive to the effect of

116 DLL4 inhibition in colon tumor cells reduces tumor growth and stem cell fre

117 -positive (CD133(+)) subpopulations of human colon tumor cells that exhibited more potent tumor-initi

118 d not convert TRAIL-sensitive Type II HCT116 colon tumor cells to a Type I death pattern as judged by

119 ession of CD44v6 depletes the ability of the colon tumor cells to signal through hyaluronan-CD44v6 in

120 Xenograft tumors from colon tumor cells with O-linked N-acetylglucosamine tran

121 of MYC target genes by CDK8 was observed in colon tumor cells, and increased expression of a CDK8-re

122 human B-lymphoblastoid TK6 cells and HCT116 colon tumor cells.

123 f (T-cell factor)-dependent transcription in colon tumor cells.

124 otential for silencing genes associated with colon tumor cells.

125 essed mTORC2 kinase activity and invasion in colon tumor cells.

126 ony formation and increases doubling time of colon tumor cells.

127 ell factor (TCF) transcriptional activity in colon tumor cells.

128 related with H2O2-stress signatures in human colon tumor cohorts, but positively correlated with diff

129 ression is elevated in both rodent and human colon tumors, collaborate to drive colon tumor formation

130 phosphotyrosine (pTyr) sites in ovarian and colon tumors collected under conditions of controlled is

131 SNRK transcript levels were reduced in human colon tumors compared to normal tissue by 35.82%, and st

132 at were dysregulated in neutrophil-deficient colon tumors compared with colon tumors from control mic

133 by an SPF microbiota had significantly more colon tumors compared with GF mice.

134 munostaining that Nur77 was overexpressed in colon tumors compared with normal colon tissue.

135 oth showed high protein levels of hnRNP F in colon tumors compared with normal colon tissues.

136 d by the down-regulation of UGT1A_i2 mRNA in colon tumors compared with normal tissues.

137 ong-term survival of mice bearing metastatic colon tumors compared with systemic administration of wi

138 Colon tumors contain a fraction of undifferentiated stem

139 hree oncogenic beta-catenin mutants from rat colon tumors containing substitutions adjacent to amino-

140 Tgifs, which are up-regulated in Apc mutant colon tumors, contribute to reprogramming metabolic gene

141 The effect of obesity on colon tumors could not be explained by differences in ab

142 In distal colon tumors, deletions causing loss of amino acids were

143 Sixty-five percent of primary colon tumors demonstrated chromosome 18q LOH.

144 mice with inflammation-induced and sporadic colon tumors, depletion of neutrophils increased the gro

145 ination of SFN and DBM treatment blocked the colon tumor development (P=0.002).

146 ts have a variety of activities that promote colon tumor development and progression; these include r

147 n DDB2 exhibited increased susceptibility to colon tumor development in a manner associated with high

148 to understand the role of the microbiota in colon tumor development in germ-free (GF) mice are limit

149 with calcium and vitamin D(3) that prevented colon tumor development, demonstrating profound interact

150 d obesity, without ongoing high fat diet, on colon tumor development.

151 t experiments with autologous and homologous colon tumors engineered to repress the ectopic secretion

152 VEGF directly promotes colon tumor epithelial cell survival through activation

153 ression decreased the proliferation of human colon tumor epithelial cells and blunted H(2)O(2)-induce

154 emokine CXCL1 gene was highly upregulated in colon tumor epithelium in a HIF-2alpha-dependent manner.

155 Moreover, using orthotopic mouse colon tumors estalished from human CRC cells or patient-

156 We have determined that human colon tumors exhibit decreased levels of mature let-7 is

157 rate in an immunocompetent murine model that colon tumors expressing LIGHT stimulate lymphocyte proli

158 that cellular proliferation was increased in colon tumors following HIF activation.

159 A priori screening of colon tumors for PTEN expression status and PIK3CA and R

160 and human colon tumors, collaborate to drive colon tumor formation and progression, respectively.

161 Colon tumor formation correlated with the presence of co

162 les of genomic and epigenomic instability in colon tumor formation has the potential to yield more ef

163 ive, human colon mucosal homogenates induced colon tumor formation in 3 mouse colon tumor models (ger

164 here that Tcf4 haploinsufficiency results in colon tumor formation in a mouse tumor model that normal

165 ndent cellular copper uptake is critical for colon tumor formation in a murine model of colitis-assoc

166 robustly decreased intestinal polyposis and colon tumor formation in Apc(Min)(/+) mice, suggesting a

167 e to its ability to induce colitis and cause colon tumor formation in mice through the production of

168 mone replacement therapy reduces the risk of colon tumor formation.

169 The intestinal flora may promote colon tumor formation.

170 p27, ATOH1 and MUC2 were upregulated in the colon tumors from AIB1-deficient mice compared with thos

171 Colon tumors from Apc(Min/+)Ffar2(-/-) mice had a higher

172 trophil-deficient colon tumors compared with colon tumors from control mice.

173 Colon tumors from either CR-infected ApcP (Min/+) or azo

174 pared with normal colonocytes, as well as in colon tumors from human clinical specimens and intestina

175 Colon tumors from IL-17RD-deficient mice are characteriz

176 in the composition of the microbiota between colon tumors from neutrophil-deficient vs control mice.

177 in was reisolated after infection of a human colon tumor growing in nude mice.

178 strate that Gal2 plays a suppressive role in colon tumor growth and highlights the therapeutic potent

179 lar mechanism that might underlie PXR-driven colon tumor growth and malignancy.

180 ut neutrophils, we found neutrophils to slow colon tumor growth and progression by restricting number

181 ays; and 3) CD44v6/short hairpin RNA reduces colon tumor growth in vivo.

182 e determined that beta1 integrins from human colon tumors have elevated levels of alpha2-6 sialylatio

183 tant role for tumor epithelial HIF-2alpha in colon tumors; however, the function of epithelial HIF-2a

184 ably expressing CXCR4 (U87-stb-CXCR4) and in colon tumors (HT-29) using dynamic and whole-body PET su

185 ression, we knocked down Pdcd4 expression in colon tumor HT29 cells using pdcd4 short hairpin RNA (sh

186 r growth inhibition or regression in a human colon tumor (HT29) xenograft model.

187 We found that Dnmt3b1 enhanced the number of colon tumors in Apc Min/+ mice approximately twofold and

188 antibody against IL27 reduced the numbers of colon tumors in Apc(Min/+) mice with colitis.

189 quencies of flat and polypoid tumors; 83% of colon tumors in I/LNJ mice are flat compared with only 1

190 ult mouse tissues and on spontaneous primary colon tumors in mice.

191 -phenylimidazo(4,5-b)pyridine (PhIP)-induced colon tumors in the rat have increased beta-catenin and

192 fed the HFFO diet showed significantly lower colon tumor incidence and multiplicity compared with rat

193 The colon tumor incidence and multiplicity were significantl

194 LB-RagMin mice had a significant increase in colon tumor incidence relative to uninfected BALB-RagMin

195 Increased colon tumor incidence, multiplicity, and reduced tumor l

196 ) in the colon exhibit a similar increase in colon tumor incidence, tumor size, and tumor burden in r

197 have been associated with the development of colon tumors, including Clostridium septicum, and decrea

198 ive reverse transcription-PCR analysis of 17 colon tumors indicated tumoral overexpression of OATP1B3

199 mined the expression of SK1 and COX-2 in rat colon tumors induced by azoxymethane (AOM) and the relat

200 ficantly increased the incidence and size of colon tumors induced by azoxymethane (AOM)/dextran sulfa

201 es the normal resistance of C57BL/6J mice to colon tumor induction by the carcinogen azoxymethane (AO

202 ere formation and viability of primary human colon tumor-initiating cells harboring mutant KRAS.

203 taurin potently reduces azoxymethane-induced colon tumor initiation and progression by inhibiting PKC

204 -cycle progression, genetic instability, and colon tumor initiation by modulating commensal TLR signa

205 indings indicate a noncanonical mechanism of colon tumor initiation that is mediated through activati

206 mechanisms contributing to IL-17A-dependent colon tumor initiation.

207 ay for Bcl-2 over-expression in PhIP-induced colon tumors involving beta-catenin, c-Myc and E2F1.

208 A striking feature of colon tumors is the significant reduction of goblet cell

209 d multiplicity were significantly higher and colon tumor latency was significantly shorter in Vparp-/

210 nt inhibitor of Src and Abl kinases, against colon tumor lines in vitro and in s.c. tumor xenograft m

211 -1 treatment led to sphere formation in some colon tumor lines.

212 ssion of GM-CSF and its receptor subunits by colon tumors may be a useful marker for prognosis as wel

213 To examine signaling pathways important for colon tumor metastasis, cells of increased migratory pot

214 rostaglandin synthesis that increases in the colon tumor microenvironment.

215 a significantly decreased neutrophils in the colon tumor microenvironment.

216 embled a set of peptide variants for a mouse-colon tumor model to determine how to improve T-cell res

217 r specificity was also observed in the HT-29 colon tumor model.

218 tes induced colon tumor formation in 3 mouse colon tumor models (germ-free ApcMinDelta850/+;Il10-/- o

219 veloped a significant (P < 0.05) increase in colon tumor multiplicity (7.2-fold and 5.5-fold, respect

220 testine-specific disruption of Vhl increased colon tumor multiplicity and progression from adenomas t

221 In proximal colon tumors, mutations in exon 5 showed a trend toward

222 Metabolomics analysis of patient colon tumors (n = 197) and normal tissues (n = 39) revea

223 animals that readily presented with multiple colon tumors, NFATc2-deficient mice were protected from

224 We observed a stepwise increase in median colon tumor numbers as the duration of ETBF colonization

225 ion of 600 ppm SFN and 1.0% DBM also reduced colon tumor numbers by 80% (P=0.016) and 60% (P=0.103),

226 etion of Dnmt3a in APC((Min/+)) mice reduced colon tumor numbers by ~40%.

227 WD increased colon tumor numbers, and mucosa proteomic analysis indic

228 Human colon tumors often lose Cdx2 expression, and heterozygou

229 significantly upregulated in differentiated colon tumors (P </= 0.0001) and correlates with K-Ras ex

230 th homocysteine was significant for proximal colon tumors (P = 0.008) but not for distal or rectal tu

231 factors and mechanisms contributing to human colon tumor pathogenesis, as well as work on tumor-promo

232 point to a function for LIN28B in promoting colon tumor pathogenesis, especially metastasis.

233 gest that beta1 hypersialylation may augment colon tumor progression by altering cell preference for

234 urate noninvasive longitudinal monitoring of colon tumor progression or response to various therapies

235 w beta1 hypersialylation might contribute to colon tumor progression.

236 l response and cell cycle gene expression in colon tumor recurrence.

237 a clinically significant proportion of human colon tumors relative to matched normal tissue.

238 and hnRNP F were expressed in 78% and 89% of colon tumors, respectively.

239 -) mice that normally develop intestinal and colon tumors resulted in GH-deficient double mutants wit

240 xpression patterns in normal human colon and colon tumors revealed that the pattern in proliferating,

241 d applied to the analysis of a pre-malignant colon tumor sample and late-stage colorectal adenocarcin

242 NTR1, miR-21, and miR-155 increase in human colon tumor samples and correlate with tumor stage.

243 and miR-155 increased significantly in human colon tumor samples, compared with normal tissues, where

244 din-1 correlated with that of ZEB-1 in human colon tumor samples.

245 ium, Fes expression was reduced or absent in colon tumor sections from most individuals.

246 Our recent efforts in sequencing colon tumors showed that 40% of the tumors sequenced pos

247 ably detected germline SNPs and discovered a colon tumor specific nonsense mutation in APC, a gene ca

248 a tissue microarray containing 93 evaluable colon tumor specimens, we detected immunostaining of OAT

249 For these colon tumor studies, we used either Rosa26-Foxm1b transg

250 while elevated expression of TIGAR in human colon tumors suggested that deregulated TIGAR supports c

251 subcellular levels of CKB were decreased in colon tumors, suggesting that the observed high CKB leve

252 GFbeta signaling, transcriptome profiling of colon tumors suggests minimal effect of Tgifs on the TGF

253 SPDEF is a colon tumor suppressor and a candidate therapeutic targe

254 th inflammation-induced colon carcinomas and colon tumor survival.

255 ice developed significantly more spontaneous colon tumors than Apc(Min/+) mice and had increased gut

256 1(DeltaIEC) mice developed fewer and smaller colon tumors than Apc(Min/+) mice.

257 association was stronger for rectum and left-colon tumors than for right-colon tumors.

258 /-) mice developed approximately 3-fold more colon tumors than Spdef(+/+) mice after administration o

259 /+) mice developed approximately 3-fold more colon tumors than Spdef(+/+); Apc(Min/+) mice.

260 Ptp4a3-null mice developed 50% fewer colon tumors than wildtype mice after exposure to azoxym

261 or the dominant peptide antigen from a mouse colon tumor that elicits a range of tumor protection fol

262 uld, therefore, target pancreatic, lung, and colon tumors that lack S1P(2) without affecting wild-typ

263 Similarly, 100% of the patients with human colon tumors that overexpressed GM-CSF and its receptor

264 er initially defined on endothelial cells in colon tumors that was discovered recently to be upregula

265 is markedly upregulated in human breast and colon tumors, that holo-RBP/STRA6 signaling promotes onc

266 In colon tumors, the transcription of many genes becomes de

267 lent immune cells in the microenvironment of colon tumors; they are believed to promote growth of col

268 Colon tumor tissue isolated from Ptp4a3-null mice reveal

269 We genotyped human colon tumor tissues and adjacent nontumor tissues collec

270 Primary colon tumor tissues from these mice were assessed by his

271 Expression of MAGI-3 and NHERF-2 in human colon tumor tissues was analyzed using tissue microarray

272 esponse to 5-FU in a small number of patient colon tumor tissues.

273 n MC38 tumors were implanted in liver, where colon tumors usually metastasize, SFV-IL-12 efficacy was

274 The median concentration in primary colon tumors was 0.016% injected dose per gram, compared

275 ulfate; formation of aberrant crypt foci and colon tumors was examined.

276 In a mouse model of inflammation-associated colon tumors, we found nuclear expression of beta-cateni

277 Colon tumor weights calculated from MRI in vivo correlat

278 of E-cadherin and up-regulation of ZEB-1 in colon tumors were associated with shorter survival times

279 t curative surgery for rectal and left-sided colon tumors were included in a program of pelvic survei

280 In mice where colon tumors were initiated by a ras-activating carcinog

281 Rats were killed 42 weeks later, and colon tumors were processed histopathologically and anal

282 Rats were killed 26 weeks later and colon tumors were subjected to histopathologic examinati

283 Balb-C mice, bearing ectopic and orthotopic colon tumors, were monitored for 3 weeks with high-resol

284 ression of KIT- and hypoxia-related genes in colon tumors, which was highest in relapse-prone mesench

285 -AAG induced CIMD in cell lines derived from colon tumors with chromosome instability, but not in cel

286 hromosome instability, but not in cells from colon tumors with microsatellite instability.

287 Integrating gene expression data from colon tumors with other gene expression and chromatin-bi

288 Colon tumors with RNF43-G659Vfs*41 had low Wnt/beta-cate

289 microarrays from 151 paraffin-embedded human colon tumors, with adjacent normal and adenoma tissues,

290 itis given the FFAR2 agonist developed fewer colon tumors, with fewer IL27(+) DCs, than mice not give

291 cer cells and inhibits mutant p53-associated colon tumor xenograft growth in a p73-dependent manner i

292 SKI-606 was orally active in s.c. colon tumor xenograft models and caused substantial redu

293 AS mutant tumors in a panel of early passage colon tumor xenograft models derived from patients.

294 protein level in two separate in vivo human colon tumor xenograft models, HCT116 and GEO, using immu

295 ession of KIT in cultured cells and in human colon tumor xenografts and this contributed to the clono

296 nt CFPAC-1 pancreatic as well as DLD-1 human colon tumor xenografts in mice.

297 ed activity in vitro and inhibited growth of colon tumor xenografts in vivo and effectively prevented

298 against human prostate, breast, bladder, and colon tumor xenografts, where its efficacy could be furt

299 , using either HCT116/p53(-/-) or DLD1 human colon tumor xenografts.

300 moderate in vivo efficacy against HT29 human colon tumor xenografts.