ライフサイエンスコーパス: colorectal tumor

1 from Wilms' tumor, head and neck tumor, and colorectal tumor.

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

3 several cancers including hepatocellular and colorectal tumors.

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

5 hibit the progression of neoantigen-specific colorectal tumors.

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

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

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

9 magnesium are associated with lower risk of colorectal tumors.

10 t in gastric/esophageal adenocarcinomas than colorectal tumors.

11 accelerated the incidence and progression of colorectal tumors.

12 cancer-prone mice accelerates development of colorectal tumors.

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

14 -2 common molecular events observed in human colorectal tumors.

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

16 re effective in suppressing the formation of colorectal tumors.

17 previously uncharacterized gene (ZKSCAN3) in colorectal tumors.

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

19 uppressor is inactivated by mutation in most colorectal tumors.

20 surface antigen expressed by the majority of colorectal tumors.

21 immunohistochemistry for binding to primary colorectal tumors.

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

23 50% of pancreatic tumors and in about 15% of colorectal tumors.

24 veral cancer types and are best described in colorectal tumors.

25 ociated with reduced CES2 mRNA expression in colorectal tumors.

26 e earliest events in the development of most colorectal tumors.

27 in most melanomas and a small proportion of colorectal tumors.

28 ecal DNA from patients with relatively early colorectal tumors.

29 h the progression of microsatellite-unstable colorectal tumors.

30 ally provide an optimal marker for detecting colorectal tumors.

31 cently proposed role in the establishment of colorectal tumors.

32 oral activity in some chemotherapy-resistant colorectal tumors.

33 imilar disparity is likely to exist in human colorectal tumors.

34 gene mutation is an early alteration in most colorectal tumors.

35 of G to A mutations in the K-ras oncogene in colorectal tumors.

36 ation of microsatellite instability (MSI) in colorectal tumors.

37 have distinct genetic features from sporadic colorectal tumors.

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

39 t-villus axis and compartmentalize incipient colorectal tumors.

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

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

42 effectors may lead to selective toxicity in colorectal tumors.

43 human tumor tissues and mice with orthotopic colorectal tumors.

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

45 ines closely resembled those seen in primary colorectal tumors.

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

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

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

49 63 tag SNPs in 940 individuals with familial colorectal tumor (627 CRC, 313 advanced adenomas) and 96

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

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

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

53 was up-regulated in the majority of primary colorectal tumors analyzed.

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

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

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

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

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

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

60 ain reaction (TaqMan RT-PCR) on RNAs from 13 colorectal tumors and 13 normal tissues (seven of which

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

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

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

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

65 sor gene are present in approximately 85% of colorectal tumors and are thought to contribute early in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 xamined the sequence of this region in human colorectal tumors and the surrounding normal tissue.

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

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

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

84 s, comprising 13 colon cancer cell lines, 61 colorectal tumors, and 87 gastric tumors.

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

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

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

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

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

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

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

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

93 1b(+)Jag2(+) cells, which infiltrate primary colorectal tumors, are sufficient to induce EMT in tumor

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

95 s isolated encoded a protein that was termed colorectal tumor-associated antigen-1 (COA-1).

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

97 evealed PRR5 overexpression in a majority of colorectal tumors but substantial downregulation of PRR5

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

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

100 Calcium can reduce the risk of colorectal tumors by binding secondary bile and fatty ac

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

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

103 viral particles injected into a 0.5-cm human colorectal tumor can be detected by [(124)I]FIAU PET ima

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

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

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

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

108 Further studies in a colorectal tumor cell line lacking PLCepsilon show resto

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

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

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

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

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

114 0] showed improved cytotoxicity toward human colorectal tumor cells (H630), and 5-FU-resistant colore

115 ectal tumor cells (H630), and 5-FU-resistant colorectal tumor cells (H630-10).

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

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

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

119 -164 cells but also heterologous C51 or CT26 colorectal tumor cells in a CD8(+) T-cell-dependent proc

120 osa), which might efficiently eliminate CEA+ colorectal tumor cells in the mucosa.

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

122 pecific T cells killed CEA-expressing murine colorectal tumor cells only after pretreatment of the ta

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

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

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

126 of chromosome instability (CIN+) observed in colorectal tumor cells.

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

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

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

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

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

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

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

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

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

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

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

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

139 ation of calcium intake with early stages of colorectal tumor development.

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

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

142 Human colorectal tumors display increased levels of reactive o

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

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

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

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

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

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

149 IHC in colorectal tumors for protein products hMLH1 and hMSH2 p

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

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

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

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

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

155 Colorectal tumors from patients had increased levels of

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

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

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

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

160 Colorectal tumors had significantly less methylation at

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

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

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

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

165 Colorectal tumors have a large degree of molecular heter

166 Noninvasive methods for detecting colorectal tumors have the potential to reduce morbidity

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

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

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

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

171 s to induce CEA-specific CTLs at the site of colorectal tumors (i.e., intestinal mucosa), which might

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

173 agents with high specificity for metastatic colorectal tumors in humans.

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

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

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

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

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

179 ated hypersialylation likely plays a role in colorectal tumor invasion.

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

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

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

183 Likewise, a mismatch repair (MMR)-deficient colorectal tumor line failed to show rapid up-regulation

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

185 Colorectal tumors manifesting high-frequency microsatell

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

187 Many alterations found in colorectal tumors may reflect such occult clonal progres

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

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

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

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

192 w that expression of these chemokines in the colorectal tumor model CMT93 significantly decreases tum

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

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

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

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

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

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

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

200 Colorectal tumor number and bromodeoxyuridine labeling w

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

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

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

204 Notably, colorectal tumors previously assigned to a single subtyp

205 xpression are significantly increased during colorectal tumor progression.

206 for 15-PGDH due to loss of expression during colorectal tumor progression.

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

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

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

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

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

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

213 tionship between common genetic variants and colorectal tumor risk are being proposed.

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

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

216 magnesium intake is associated with reduced colorectal tumor risk.

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

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

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

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

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

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

223 We analyzed colorectal tumor samples from patients before and after

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

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

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

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

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

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

230 Colorectal tumor senescence and p21 level correlate with

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

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

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

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

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

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

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

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 Widespread colorectal tumor testing to identify families with the L

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

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

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

247 Colorectal tumors that develop in patients with IBD have

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

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

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

251 tous polyposis coli (APC) gene that initiate colorectal tumors theoretically provide an optimal marke

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 Fusobacteria were also visualized within colorectal tumors using FISH.

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

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

269 ated antigen targeted for the development of colorectal tumor vaccines.

270 No colorectal tumor was found to carry two CDC4 mutations p

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

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

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

274 The CDC4 mutation spectrum in colorectal tumors was heavily biased towards C:G > T:A c

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

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

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

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

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

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

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

285 Patients with colorectal tumors with microsatellite instability (MSI)

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

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

288 Colorectal tumors with MSI have distinctive features, in

289 The biological behavior of colorectal tumors with MSI is distinctive; the most intr

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