ライフサイエンスコーパス: colorectal tumor

1 that MDFI is up- and MDFIC downregulated in colorectal tumors.

2 effectors may lead to selective toxicity in colorectal tumors.

3 human tumor tissues and mice with orthotopic colorectal tumors.

4 nes and amounts equal to K-Ras4B in 17 human colorectal tumors.

5 ines closely resembled those seen in primary colorectal tumors.

6 2 and these TSGs in a large panel of primary colorectal tumors.

7 several cancers including hepatocellular and colorectal tumors.

8 or 1,2-dimethylhydrazine and DSS, to induce colorectal tumors.

9 een demonstrated to be a frequent feature of colorectal tumors.

10 DK8, which is amplified in a large number of colorectal tumors.

11 rtion of colon cancer cell lines and primary colorectal tumors.

12 magnesium are associated with lower risk of colorectal tumors.

13 t in gastric/esophageal adenocarcinomas than colorectal tumors.

14 accelerated the incidence and progression of colorectal tumors.

15 cancer-prone mice accelerates development of colorectal tumors.

16 ays interact in vivo and affect formation of colorectal tumors.

17 -2 common molecular events observed in human colorectal tumors.

18 lymerase chain reaction in a series of human colorectal tumors.

19 re effective in suppressing the formation of colorectal tumors.

20 previously uncharacterized gene (ZKSCAN3) in colorectal tumors.

21 ors, including a stage-dependent increase in colorectal tumors.

22 uppressor is inactivated by mutation in most colorectal tumors.

23 surface antigen expressed by the majority of colorectal tumors.

24 immunohistochemistry for binding to primary colorectal tumors.

25 tended the survival of mice with melanoma or colorectal tumors.

26 , we identify key events in the evolution of colorectal tumors.

27 al immunohistochemistry (IHC) on a cohort of colorectal tumors.

28 , and somatic mutations in APC and CTNNB1 in colorectal tumors.

29 subsets of pancreatic, ovarian, gastric, and colorectal tumors.

30 hibit the progression of neoantigen-specific colorectal tumors.

31 holog, which was increased in advanced human colorectal tumors.

32 in RSPO genes have been identified in human colorectal tumors.

33 have distinct genetic features from sporadic colorectal tumors.

34 opment of T-cell-driven colitis and sporadic colorectal tumors.

35 t-villus axis and compartmentalize incipient colorectal tumors.

36 e central bulk and invasive front regions of colorectal tumors.

37 ic, and phenotypic information from 12 human colorectal tumors (11 carcinomas, 1 adenoma) obtained th

38 dy that included 14 studies, 12,696 cases of colorectal tumors (11,870 cancer, 826 adenoma), and 15,1

39 mors from patients with IBD than in sporadic colorectal tumors (13% and 20% of cases, respectively).

40 m The Cancer Genome Atlas (113 patients with colorectal tumors, 178 endometrial tumors); 100% of doub

41 63 tag SNPs in 940 individuals with familial colorectal tumor (627 CRC, 313 advanced adenomas) and 96

42 with prevalence similar to that of sporadic colorectal tumors (63% of cases).

43 dian survival was 457 days for patients with colorectal tumors, 776 days for those with neuroendocrin

44 However, about 10% of colorectal tumors also exhibit increased CTNNB1 mRNA.

45 stry was used to examine levels of IL6 in 20 colorectal tumor and adjacent nontumor tissues.

46 ) to comprehensively profile a primary human colorectal tumor and adjacent normal colon tissue at sin

47 s and 96 genes (928 RNA probes) in lymphoid, colorectal tumor and autoimmune tissues by using the nCo

48 Using L1-targeted resequencing of 16 colorectal tumor and matched normal DNAs, we found that

49 de Wetering et al. (2015) derive biobanks of colorectal tumor and matching normal organoids and ident

50 We collected colorectal tumor and non-neoplastic tissues from 31 pati

51 NA expression profiling of 124 fresh, paired colorectal tumor and nontumor samples (30 CRC; 32 AAs) f

52 s to examine gene expression patterns in 260 colorectal tumor and normal colon samples.

53 ight technology, involving 295 primary human colorectal tumors and 16,785 separate quantitative analy

54 CpG sites in 3 macrodissected regions of 79 colorectal tumors and 23 associated liver metastases, ob

55 enome-scale DNA methylation profiling of 125 colorectal tumors and 29 adjacent normal tissues.

56 We screened 244 colorectal tumors and 40 cell lines for CDC4 mutations a

57 ssessed archived specimens from 732 incident colorectal tumors and characterized them as microsatelli

58 show that MMP-2 is up-regulated in resected colorectal tumors and degrades beta1 integrins with the

59 nesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the ge

60 rantly located within the nucleus of primary colorectal tumors and human colon cancer cells, and onco

61 hibition of PCs enhanced CTL infiltration in colorectal tumors and increased tumor clearance in synge

62 of 10 Gy significantly reduces the growth of colorectal tumors and increases the survival time as com

63 pG islands has been widely observed in human colorectal tumors and is associated with gene silencing

64 rized by the development of mixed-morphology colorectal tumors and is caused by a 40-kb genetic dupli

65 a(2+)/Li(+) exchanger NCLX (SLC8B1) in human colorectal tumors and its association with advanced-stag

66 ls with colorectal cancer, including primary colorectal tumors and matched adjacent non-tumor tissues

67 thylation within these domains in 25 diverse colorectal tumors and matched adjacent tissue.

68 ts using single-cell RNA-seq from 11 primary colorectal tumors and matched normal mucosa.

69 s of urine and tissue samples from mice with colorectal tumors and of colorectal tumor samples from p

70 c significance of Ras pathway alterations in colorectal tumors and other solid tumor malignancies.

71 nship among markers of different subtypes of colorectal tumors and patient survival.

72 new oncogenes we sequenced the exomes of 25 colorectal tumors and respective healthy colon tissue.

73 expression profiles of 17 lines aligning to colorectal tumors and selected based on their similarity

74 biology: the basis of Wnt activation in non-colorectal tumors and the identity of a 4q35 tumor suppr

75 ls significant heterogeneity between primary colorectal tumors and their liver metastases.

76 analysis of transcriptional heterogeneity in colorectal tumors and their microenvironments using sing

77 n to be abnormally expressed and modified in colorectal tumors and to function as an important transc

78 e was sequenced in a collection of 134 human colorectal tumors and was found to contain coding region

79 , but not deletion, is associated with human colorectal tumors, and colorectal cancer patients with l

80 hat Ahr null mice showed increased number of colorectal tumors, and mice treated with I3C exhibited f

81 Pol beta is mutated in a large number of colorectal tumors, and these mutations may drive carcino

82 ight be used to identify a specific group of colorectal tumors, and to select treatment or determine

83 g channel of the endoscope after biopsies of colorectal tumors, and whether these cells maintain viab

84 The majority of colorectal tumors are aneuploid because of the underlyin

85 monstrated that the 2 APC mutations in human colorectal tumors are coselected, because tumorigenesis

86 sults support the hypothesis that APC-mutant colorectal tumors are transcriptionally distinct from AP

87 SI) and mismatch-repair deficiency (dMMR) in colorectal tumors are used to select treatment for patie

88 methylation, and KRAS and BRAF mutations in colorectal tumors) are becoming routine clinical practic

89 1b(+)Jag2(+) cells, which infiltrate primary colorectal tumors, are sufficient to induce EMT in tumor

90 miR-34a feedback loop was present in primary colorectal tumors as well as CRC, breast, and prostate c

91 Analyses of transcriptomes of human colorectal tumors associated lower levels of RNase H2 wi

92 emical and immunofluorescent analyses of 116 colorectal tumor biopsies to determine levels of EGFR in

93 a from pancreatic tissue, mononuclear cells, colorectal tumor biopsies, and circulating dendritic cel

94 ns are the most prevalent genetic changes in colorectal tumors, but it is unknown whether these mutat

95 s in CC cells and in metastases derived from colorectal tumors, but not in normal human cells.

96 Ps) are precursors to 20% to 30% of cases of colorectal tumors, but patients' long-term risk after re

97 of ZAP inhibits the malignant phenotypes of colorectal tumor by cell cycle arrest.

98 suppresses the growth of tRXRalpha-mediated colorectal tumor by inhibiting the NF-kappaB-IL-6-STAT3

99 ation patterns of a specific CpG region in 9 colorectal tumors by bisulfite sequencing and apply a tu

100 ancer cells and is frequently inactivated in colorectal tumors by genetic and epigenetic mechanisms.

101 ollowed up in 6 studies; these included 3056 colorectal tumor cases (2098 cancer, 958 adenoma) and 66

102 we genotyped 550,163 tagSNPs in 940 familial colorectal tumor cases (627 CRC, 313 high-risk adenoma)

103 on study of 550,000 tag SNPs in 930 familial colorectal tumor cases and 960 controls.

104 he Wnt/beta-catenin pathway may also control colorectal tumor cell fate during the maintenance phase

105 NA) mutations in the COXI and ND5 genes in a colorectal tumor cell line.

106 Accordingly, treatment of the colorectal tumor cell lines with the DNA methyltransfera

107 body was raised by immunization of mice with colorectal tumor cell lines.

108 does not introduce new clonal mutations into colorectal tumor cell populations; and (iv) the rates at

109 ive response to hypoxia with implication for colorectal tumor cell survival and angiogenesis.

110 egulation of PGC-1alpha and PGC-1beta in the colorectal tumor cells can be part of an adaptation mech

111 dition, elevated levels of PGE(2) in hypoxic colorectal tumor cells enhance vascular endothelial grow

112 rther, we exploited the device for isolating colorectal tumor cells from unprocessed whole blood; as

113 -164 cells but also heterologous C51 or CT26 colorectal tumor cells in a CD8(+) T-cell-dependent proc

114 ibition of glycogen synthase kinase-3beta in colorectal tumor cells markedly induced the activity of

115 Tumorigenicity and metastatic potential of colorectal tumor cells over and underexpressing PHD3 wer

116 a mouse xenograft model using HCT-116 human colorectal tumor cells, CC-5079 significantly inhibits t

117 ted the effect of platelet interactions with colorectal tumor cells.

118 ition (EMT) and found no evidence for EMT of colorectal tumor cells.

119 tifies COX-2 as a direct target for HIF-1 in colorectal tumor cells.

120 in the majority of a panel of primary human colorectal tumors compared with its expression in uninvo

121 showed an increase in the number and size of colorectal tumors compared with wild-type mice.

122 re found over-expressed in almost 80% of the colorectal tumors, compared to paired adjacent normal co

123 Levels of SIGIRR are lower in human colorectal tumors, compared with nontumor tissues; tumor

124 Recent reports show that colorectal tumors contain microbiota that are distinct f

125 A high percentage of colorectal tumors contain mutations that disrupt TGF-bet

126 The stroma of human colorectal tumors contains TWIST1-positive cancer cells

127 TWIST1-positive cells in the stroma of human colorectal tumors correlated with microsatellite stabili

128 tant metastasis from primary stage II or III colorectal tumors (Cox proportional hazard analysis: haz

129 e (LS) have high lifetime risk of developing colorectal tumors (CRTs) because of a germline mutation

130 We conclude that MSI colorectal tumors deficient in DSB repair secondary to m

131 of small intestine tumors seemed to inhibit colorectal tumor development in the mouse, and gender-sp

132 ational analysis of PRR5 in human breast and colorectal tumors did not reveal somatic mutations.

133 ifferentiation offers a valid model to study colorectal tumor differentiation and differentiation of

134 Human colorectal tumors display increased levels of reactive o

135 e, we show that more than one-third of human colorectal tumors exhibit aberrant DNA demethylation of

136 colon progenitor cells; however, only 39% of colorectal tumors express EphB2 and expression levels de

137 in expression was likewise enhanced in human colorectal tumors expressing low levels of PHD3.

138 In human colorectal tumors, expression of EMT markers was signifi

139 passing the region of putative linkage in 57 colorectal tumor families from the United Kingdom.

140 We screened human colorectal tumors for EGFR-positive myeloid cells and in

141 Prostaglandin E(2) (PGE(2)) promotes colorectal tumor formation and progression by unknown me

142 Identifying the genetic loci associated with colorectal tumor formation could elucidate the mechanism

143 However, its role in colorectal tumor formation remains unclear.

144 of RP-MDM2 binding significantly accelerated colorectal tumor formation while having no discernable e

145 Contrary to expectations, Bcl-3 suppressed colorectal tumor formation: Bcl-3-deficient mice were re

146 was observed in the primary and metachronous colorectal tumors from all 3 patients.

147 IL-8 was increased in colorectal tumors from patients and IL-8Tg mice compared

148 Colorectal tumors from patients had increased levels of

149 In colorectal tumors from patients, loss of SPDEF was obser

150 on of the ribonuclease H2 subunit B gene and colorectal tumors from patients, we provide evidence tha

151 We collected data on colorectal tumors from The Cancer Genome Atlas.

152 We performed DNA sequence analyses of 48 colorectal tumors (from 16 patients with mutations in ML

153 s were phenotypically indistinguishable from colorectal tumor glandular structures used by pathologis

154 It also provides details on analysis of colorectal tumor growth and metastasis, including analys

155 tors such as prostaglandin E2 (PGE2) promote colorectal tumor growth by stimulating angiogenesis, cel

156 EMAST-positive colorectal tumors had significantly higher levels of IL6

157 Colorectal tumors had significantly less methylation at

158 Patients with type 2 colorectal tumors had significantly shorter time of DSS

159 significantly up-regulated in primary human colorectal tumors harboring PI3K pathway activation.

160 A subset of colorectal tumors has an exceptionally high frequency of

161 Loss of SMAD4 from colorectal tumors has been associated with reduced survi

162 Discovery of MSI in colorectal tumors has increased awareness of the diversi

163 Colorectal tumors have a large degree of molecular heter

164 Colorectal tumors have been classified based on histolog

165 nfected human glioma U-87 MG cells and human colorectal tumor HCT-8 cells.

166 n CT measurements may measure vascularity of colorectal tumors, however, correlation with MVD, which

167 human head and neck tumors (FaDu) and human colorectal tumors (HT29) after administration of either

168 BACKGROUND & AIMS: In colorectal tumors, hypoxia causes resistance to therapy

169 gest targeting PCs as an adjunct approach to colorectal tumor immunotherapy.

170 ound in urine associated with development of colorectal tumors in Apc(Min/+) mice.

171 mphangiogenesis and metastasis by orthotopic colorectal tumors in mice and reduces lymphatic endothel

172 noncanonical WNT signaling in development of colorectal tumors in patients with IBD.

173 ere compared with that published for patient colorectal tumors in The Cancer Genome Atlas.

174 neither obstructed nor hemorrhaging primary colorectal tumors in the setting of metastatic disease.

175 h Study (n = 41,836) to associate markers of colorectal tumors, integrated pathways, and clinical and

176 tic Pol beta variant identified in a stage 3 colorectal tumor is a driver of carcinogenesis.

177 tients, the development de novo head/neck or colorectal tumors is linked to an aberrant expansion of

178 The heterogeneity among colorectal tumors is probably due to differences in deve

179 tor c-MYC is misregulated in the majority of colorectal tumors, it is difficult to target directly.

180 ained Wnt pathway activation is required for colorectal tumor maintenance.

181 These findings indicate that interval colorectal tumors may arise as the result of distinct bi

182 the establishment of inflammation-associated colorectal tumors mediated by control of IL-6 expression

183 is the most commonly observed species in the colorectal tumor microenvironment and reportedly influen

184 teria are found to be overrepresented in the colorectal tumor microenvironment.

185 trategies to reactivate TGFbeta signaling in colorectal tumors might not be warranted, and the functi

186 itoneal chemotherapy (HIPEC)-like treated 3D colorectal tumor mimics.

187 hed 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-ac

188 th primary and distant tumors on a bilateral colorectal tumor model.

189 s sensitive to tumor glucose accumulation in colorectal tumor models and can distinguish tumor types

190 essed the functional activity of CAIX in two colorectal tumor models, expressing different levels of

191 EGFR in myeloid cells in the stroma of human colorectal tumors; myeloid cell expression of EGFR assoc

192 re concordantly expressed with PTTG in human colorectal tumors (n=97 and n=95, respectively, P<0.001)

193 s the genetic and molecular heterogeneity of colorectal tumors not only among patients, but also with

194 of the mtDNA mutations was prevented by the colorectal tumor nuclear background.

195 Colorectal tumor number and bromodeoxyuridine labeling w

196 ed in liver metastases as well as in primary colorectal tumors of patients with metastatic disease.

197 olecular analyses for MSI and dMMR from 8836 colorectal tumors (of all stages) included in the MSIDET

198 entified as undergoing major resection for a colorectal tumor, of whom 7423 (4.7%) underwent >=1 live

199 investigated the impact of cachexia-inducing colorectal tumor on BAT in mice.

200 AF mutations in patients with double somatic colorectal tumors or Lynch syndrome.

201 Notably, colorectal tumors previously assigned to a single subtyp

202 7], our findings may shed light on how human colorectal tumors progress.

203 xpression are significantly increased during colorectal tumor progression.

204 ed mutations in genes specific to breast and colorectal tumors, providing insight into organ-specific

205 In human lung and colorectal tumors, RAS pathway activation is associated

206 Through an antigen-screening approach using colorectal tumor-reactive T cells, we identified an HLA-

207 od in three cancer cell lines and 15 primary colorectal tumors, resulting in the discovery of hundred

208 ection of CD133+ and CD133- areas in primary colorectal tumors revealed genetic differences in 7 of 1

209 provided evidence for an association between colorectal tumor risk and polymorphisms in laminin gamma

210 Dietary magnesium might be related to colorectal tumor risk through the pivotal roles of magne

211 binding protein involved in DNA repair) with colorectal tumor risk.

212 magnesium intake is associated with reduced colorectal tumor risk.

213 d 128.54 Mb were found to be associated with colorectal tumor risk.

214 Preliminary studies using 96 colorectal tumor samples and 73 matched normal tissues i

215 We searched the stroma of human colorectal tumor samples for TWIST1-positive cells with

216 Based on an analysis of blood and colorectal tumor samples from 2 large studies, high plas

217 ate levels of Smad4 and beta-catenin mRNA in colorectal tumor samples from 250 patients.

218 We analyzed levels of SPDEF in colorectal tumor samples from patients and its tumor-sup

219 We analyzed colorectal tumor samples from patients before and after

220 ples from mice with colorectal tumors and of colorectal tumor samples from patients revealed pathways

221 IGF2 DMR0 hypomethylation in colorectal tumor samples is associated with shorter surv

222 f Jag-1 and Notch correlate in human HCC and colorectal tumor samples with patient survival times, su

223 d/or chromosome 20 were detected in 17 of 20 colorectal tumor samples, each of which contained TWIST1

224 chemistry to measure levels of TWIST1 in 201 colorectal tumor samples.

225 split-sample (portion fresh/portion FFPE) of colorectal tumor samples.

226 Colorectal tumor senescence and p21 level correlate with

227 Subsequent analysis on primary disaggregated colorectal tumors show that the antibody recognizes a ce

228 c profiling of 349 individual glands from 15 colorectal tumors showed an absence of selective sweeps,

229 e was no correlation between postcolonoscopy colorectal tumor size and time to diagnosis after index

230 l-time polymerase chain reaction analyses of colorectal tumor specimens collected from patients; heal

231 We collected colorectal tumor specimens from 467 patients, measured l

232 of Polepsilon in a collection of 52 sporadic colorectal tumor specimens.

233 -cell RNA-Seq analyses of human melanoma and colorectal tumor specimens.

234 expression of EGFR in myeloid cells from the colorectal tumor stroma associates with tumor progressio

235 We review the features of the colorectal tumor stroma that are associated with patient

236 t expression of EGFR by myeloid cells of the colorectal tumor stroma, rather than the cancer cells th

237 Colorectal tumor subtypes might therefore be used in det

238 cells present at the invasive front of human colorectal tumors, suggesting a coordinated role for the

239 f human hepatic metastasis and their primary colorectal tumors, suggesting that it might be possible

240 CDH3, and VIM at the leading edge of a human colorectal tumor, supporting a role for PLAC8 in cancer

241 covered four new potential cell polarity and colorectal tumor suppressor genes (RASA3, NUPL1, DENND5A

242 In contrast to its described role as a colorectal tumor suppressor, CDX2 when amplified is requ

243 rovide evidence that RNase H2 functions as a colorectal tumor suppressor.

244 Widespread colorectal tumor testing to identify families with the L

245 onal repressor expressed in human and murine colorectal tumors that can bind to methylated clusters o

246 cyclase 2C (GUCY2C) is a marker expressed by colorectal tumors that could reveal occult metastases in

247 limited numbers of genes has indicated that colorectal tumors that develop in patients with IBD diff

248 Colorectal tumors that develop in patients with IBD have

249 ts into the different molecular subgroups of colorectal tumors that develop via each of these differe

250 Colorectal tumors that express a high level of miR-21 di

251 of 473 families, including 488 patients with colorectal tumors that had normal expression of mismatch

252 tected in poorly differentiated and invasive colorectal tumors that have lost epithelial characterist

253 low cell culture densities and human primary colorectal tumors that manifested a poor clinical outcom

254 ct BMPR1a, BMPR1b, BMPR2, and SMAD4 in human colorectal tumors; these were related to patient surviva

255 levels are low in a significant fraction of colorectal tumors, they are predicted to be particularly

256 ranscription-PCR confirmed overexpression in colorectal tumor tissue compared with adjacent nonmalign

257 ity measured with this assay, we distinguish colorectal tumor tissue from healthy adjacent tissue, il

258 y enzyme activity in eight cell lines and in colorectal tumor tissue.

259 ly up-regulated ( approximately 70 times) in colorectal tumor tissues compared with their normal pair

260 Moreover, HEF1 levels in human colorectal tumor tissues increased with the tumor grade.

261 owed that reduction of MGL expression in the colorectal tumor tissues predominantly occurred in the c

262 re over-expressed in 80%, 70% and 40% of the colorectal tumor tissues, as compared to the paired adja

263 essels), VEGFC, and VEGFR3 were increased in colorectal tumor tissues, compared with controls.

264 ing were also detected in FBXW7 mutant human colorectal tumor tissues.

265 lost or had lower levels of HES1 than other colorectal tumor types or nontumor tissues.

266 ; high levels of VEGFC have been measured in colorectal tumors undergoing lymphangiogenesis and corre

267 nalysis of copy number changes in breast and colorectal tumors using approaches that can reliably det

268 Fusobacteria were also visualized within colorectal tumors using FISH.

269 mpared CD133+ and CD133- cells of 12 primary colorectal tumors using laser capture microdissection an

270 lar profiles of the primary and metachronous colorectal tumors using next-generation sequencing.

271 ly showed that the truncated APC proteins in colorectal tumors usually retain a total of 1-2 beta-cat

272 D4 and normal expression of BMP receptors in colorectal tumors was associated with reduced survival t

273 sue collected from 29 carriers with multiple colorectal tumors was directly sequenced between codons

274 t reduction in the development and growth of colorectal tumors was found in Villin-Cre Foxm1-/- mice

275 The prevalence of mutations in sporadic colorectal tumors was obtained from previously published

276 In an analysis of 79 colorectal tumors, we found significant heterogeneity in

277 Data from a set of breast and colorectal tumors were analyzed.

278 Colorectal tumors were found in 88% of mice fed the West

279 ase in the expression of phospholipase D1 in colorectal tumors when compared with adjacent normal muc

280 ranscriptionally distinct from APC-wild-type colorectal tumors with canonical WNT signaling activated

281 a therapeutic strategy for the treatment of colorectal tumors with defects in mitochondrial-regulate

282 es with the development of human right-sided colorectal tumors with epigenetic loss of MLH1.

283 an sessile serrated adenomas and right-sided colorectal tumors with epigenetic loss of MutL homolog 1

284 r, immunohistochemistry was performed on 566 colorectal tumors with known clinical outcome.

285 In study I, stool samples from patients with colorectal tumors with known mutations (KRAS, APC, BRAF,

286 Patients with colorectal tumors with microsatellite instability (MSI)

287 ions were observed in 32% (37 of 116) of the colorectal tumors with microsatellite instability analyz

288 About 25% of patients with stages II-III colorectal tumors with MSI have an excellent response to

289 Colorectal tumors with MSI have distinctive features, in

290 d 329 consecutive patients with stage II-III colorectal tumors with MSI who underwent surgical resect

291 Colorectal tumors with reduced accumulation of T(eff) ex

292 ere expressed in vivo in well-differentiated colorectal tumors with retained epithelial characteristi

293 a loxP-targeted Apc allele developed mainly colorectal tumors, with carcinomas seen in 6 of 36 (17%)

294 They have a slightly better prognosis than colorectal tumors without MSI and do not have the same r

295 st-line therapy for patients with metastatic colorectal tumors without RAS mutations.

296 ificant in vivo efficacy in the HCT116 human colorectal tumor xenograft model in nude mice with up to

297 luciferase and to retarget virus to hepatic colorectal tumor xenografts and non-small cell lung tumo

298 nin signaling is required for maintenance of colorectal tumor xenografts harboring APC mutations.

299 ll carcinomas, caused complete regression of colorectal tumor xenografts in mice treated with CPT-11,

300 otype for gastrointestinal, endometrial, and colorectal tumors, yet the landscape of instability even