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 human tumor xenografts such as HCT-116 human colon tumor.

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

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

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

6 ermined that LIN28B overexpression occurs in colon tumors.

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

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

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

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

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

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

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

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

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

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

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

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

19 uently deleted or inactive in pancreatic and colon tumors.

20 lation and Cables gene expression in primary colon tumors.

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

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

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

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

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

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

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

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

29 l proliferation and increase in apoptosis in colon tumors.

30 pathway genes have been identified in human colon tumors.

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

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

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

34 iated with the degree of aneuploidy in human colon tumors.

35 t only in breast tumors but also in lung and colon tumors.

36 in the detection, recurrence, and therapy of colon tumors.

37 with the set of mutations reported in human colon tumors.

38 normal colon control tissue in 8 of 10 solid colon tumors.

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

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

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

42 differentially methylated regions (DMRs) in colon tumors.

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

44 pressed heterogeneously by a subset of human colon tumors.

45 hways were recapitulated in both ovarian and colon tumors.

46 he therapeutic responsiveness of established colon tumors.

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

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

49 ere then administered azoxymethane to induce colon tumors.

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

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

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

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

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

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

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

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

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

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

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

61 plotypes for FDXR were not different between colon tumor and normal samples.

62 fference in variant allele frequency between colon tumor and normal tissues (P > 0.05), and the commo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 d be used to identify and characterize novel colon tumor-associated antigens.

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 9 effectively suppressed the growth of SW480 colon tumors but not of A549 lung tumors.

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

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

100 as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is un

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

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

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

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

105 lones that were generated from an autologous colon tumor cell line cDNA library.

106 ition of cellular proliferation of the human colon tumor cell line DiFi.

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

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

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

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

111 -Met on in vitro and in vivo growth of human colon tumor cell lines, stable subclones of the high met

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

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

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

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

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

117 ion may be important in metastatic growth of colon tumor cells in the liver.

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

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

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

121 ermore, five of five irradiated CEA(+)/A2(+) colon tumor cells lines demonstrated significantly enhan

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

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

124 Early stage, non-progressed colon tumor cells show a down-regulation of TGFalpha in

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

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

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

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

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

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

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

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

133 otential for silencing genes associated with colon tumor cells.

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

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

136 ential efficacy among current candidates for colon tumor chemopreventive agents.

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

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

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

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

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

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

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

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

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

146 Colon tumors contain a fraction of undifferentiated stem

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

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

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

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

151 as performed in our recently established A/J colon tumor-derived cell line, AJ02-NM0.

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

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

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

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

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

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

158 On histological analysis, -/- colon tumors displayed more RBCs near the tumor surface,

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

160 VEGF directly promotes colon tumor epithelial cell survival through activation

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

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

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

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

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

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

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

168 polyunsaturated fatty acids (PUFAs) decrease colon tumor formation have not been fully elucidated.

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

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

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

172 The intestinal flora may promote colon tumor formation.

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

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

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

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

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

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

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

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

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

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

183 Colon tumors in 3-month-old Min mice that were null for

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

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

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

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

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

189 The colon tumor incidence and multiplicity were significantl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 -1 treatment led to sphere formation in some colon tumor lines.

207 ccination of BALB/c mice bearing murine CT26 colon tumor lung metastases or palpable s.c. tumors (>10

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

209 C liver metastasis model, we implanted mouse colon tumor MC-26 cells into the splenic subcapsule of B

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

211 rostaglandin synthesis that increases in the colon tumor microenvironment.

212 a significantly decreased neutrophils in the colon tumor microenvironment.

213 The azoxymethane (AOM)-induced mouse colon tumor model recapitulates many of the histopatholo

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

215 active as camptothecin (CPT)-11 in the HCT-8 colon tumor model, and compared favorably with CPT-11 an

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

217 o in mice bearing LS174T xenografts, a human colon tumor model.

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

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

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

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

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

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

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

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

226 Human colon tumors often lose Cdx2 expression, and heterozygou

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

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

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

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

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

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

233 w beta1 hypersialylation might contribute to colon tumor progression.

234 t evidence that the Ink4a/Arf locus inhibits colon tumor progression.

235 olecules have been shown to be recognized by colon tumor-reactive T cells, limiting the options for t

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 of Math1, was dramatically down-regulated in colon tumor samples and colon cancer cell lines.

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

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

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

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

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

248 In colon tumors, SIM2-s expression was seen in early stages

249 In colon tumor, SIMA135/CDCP1 expression appeared dysregula

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

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

252 mutations, we selected seven patients whose colon tumors stained negative for PMS2 and positive for

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

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

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

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

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

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

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

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

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

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

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

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

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

266 Colon tumor tissue isolated from Ptp4a3-null mice reveal

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

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

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

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

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

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

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

274 Rats bearing a s.c. implanted rat colon tumor were given eniluracil and injected i.v. with

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

276 More strikingly, one-half of the -/- colon tumors were grossly red in color, whereas most of

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

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

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

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

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

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

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

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

285 e (MTD) and for efficacy in the HCT116 human colon tumor xenograft assay.

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

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

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

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

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

291 MP 241 was successfully pretargeted to human colon tumor xenografts in athymic mice with both the che

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

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

294 In vivo studies in nude mice bearing human colon tumor xenografts showed that the radiolabeled pept

295 mors on the back, and mice with LS174T human colon tumor xenografts were prepared.

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

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

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

299 or growth inhibition in staged HCT-116 human colon tumor xenografts.

300 solid tumors, including 70-80% of breast and colon tumors, yet how it promotes cell transformation is