ライフサイエンスコーパス: colon cancer cell line

1 ppresses anchorage-independent growth of the colon cancer cell line.

2 te rapid cell migration in a AQP1-expressing colon cancer cell line.

3 fied as curcumin binding targets from HCT116 colon cancer cell line.

4 ersistent MAPK activation in the SW620 human colon cancer cell line.

5 soft agar growth in the CDX2-negative HT-29 colon cancer cell line.

6 ntiation and limiting survival of this human colon cancer cell line.

7 uced apoptosis in the DLD-1 (COX-2-negative) colon cancer cell line.

8 JH-2 (Thy4), derived previously from a human colon cancer cell line.

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

10 nsport and biosynthesis of terpenoids in the colon cancer cell line.

11 ty and induced apoptosis in the HCT116 human colon cancer cell line.

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

13 iency were assessed in vitro in a polarizing colon cancer cell line.

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

15 anistic basis for EGFR overexpression in MSI colon cancer cell lines.

16 use model of intestinal/colon cancer, and in colon cancer cell lines.

17 ted with beta-catenin levels in a variety of colon cancer cell lines.

18 , inhibited claudin-1 expression in multiple colon cancer cell lines.

19 HDAC inhibitors and resistance in vitro used colon cancer cell lines.

20 compounds active against two drug-resistant colon cancer cell lines.

21 uces Akt activation in the FET, CBS, and GEO colon cancer cell lines.

22 tion-dependent manner to the CDKN2A in human colon cancer cell lines.

23 prostate, breast, glioblastoma, sarcoma, and colon cancer cell lines.

24 llular proliferation and colony formation in colon cancer cell lines.

25 molar inhibitory activity against breast and colon cancer cell lines.

26 t are potent against multiple drug-resistant colon cancer cell lines.

27 d increase in MAT2A expression and growth in colon cancer cell lines.

28 orectal carcinoma tumor samples and in human colon cancer cell lines.

29 ways were examined in colon, cultured IEC or colon cancer cell lines.

30 ng and colon tumors and in a subset of human colon cancer cell lines.

31 TR1) and TRAIL-R2 (lexatumumab, HGS-ETR2) in colon cancer cell lines.

32 induced Smad3 in RIE-1 cells and in 4 human colon cancer cell lines.

33 A-resistant (HCT-116, SW620, and WiDR) human colon cancer cell lines.

34 in kidney epithelial cells and in breast and colon cancer cell lines.

35 these increases were also observed in other colon cancer cell lines.

36 n invasive phenotype was identified in human colon cancer cell lines.

37 n in human colon cancer tissues and in human colon cancer cell lines.

38 on cancers, as well as in colon adenomas and colon cancer cell lines.

39 suppressing anchorage-independent growth of colon cancer cell lines.

40 in >85% of microsatellite instability (MSI)+ colon cancer cell lines.

41 sactivation in HT-29, HCT-15, RKO, and SW480 colon cancer cell lines.

42 ly down-regulated in colon tumor samples and colon cancer cell lines.

43 as negatively correlated with cell growth in colon cancer cell lines.

44 II mRNA and protein in HT29 and HCT116 human colon cancer cell lines.

45 topors protein is not detectable in several colon cancer cell lines.

46 RF3, a representative Ad E4 protein, only in colon cancer cell lines.

47 d coincides with experimental measures using colon cancer cell lines.

48 d in 59% of primary colon cancers and 52% of colon cancer cell lines.

49 inhibition and differentiation in resistant colon cancer cell lines.

50 p21(KRAS) steady-state levels in mutant KRAS colon cancer cell lines.

51 product of CEA-cDNA and cDNA from different colon cancer cell lines.

52 of the TRAIL by inhibition of PI 3-kinase in colon cancer cell lines.

53 were reported in some noncoding SMTs in MMP colon cancer cell lines.

54 vity of the Cdx-2 gene was analyzed in human colon cancer cell lines.

55 compared using simulations and real data on colon cancer cell lines.

56 d adenocarcinomas of the colon as well as in colon cancer cell lines.

57 on Src-transformed rat fibroblasts and human colon cancer cell lines.

58 promoter methylation was noted in nine of 34 colon cancer cell lines.

59 results were observed in the SW480 and SW620 colon cancer cell lines.

60 in colon tumors, normal colonic mucosa, and colon cancer cell lines.

61 oproliferative role for LRH-1 in established colon cancer cell lines.

62 ompared with clones of the HCT-116 and HT-29 colon cancer cell lines.

63 o induce differentiation in human breast and colon cancer cell lines.

64 affected Notch1 signaling in the breast and colon cancer cell lines.

65 eloma cell lines and was also active against colon cancer cell lines.

66 colonic epithelial cells, tumor tissues, and colon cancer cell lines.

67 a panel of colon tumors and patient-derived colon cancer cell lines.

68 ia, Dbait induced cytotoxicity in all tested colon cancer cell lines.

69 ice with colitis-associated cancer and human colon cancer cell lines.

70 d the effect of LPA on HIF-1alpha in several colon cancer cell lines.

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

72 combination, against the SW480 and RKO human colon cancer cell lines.

73 1 in YAMC mouse colonocytes and Caco-2 human colon cancer cell lines.

74 ortalized colonic epithelial cells and human colon cancer cell lines.

75 y targeted homologous recombination in human colon cancer cell lines.

76 old higher in CCIC compared with widely used colon cancer cell lines.

77 identify genes that are regulated by Cdx2 in colon cancer cells lines.

78 three independent sample sets, comprising 13 colon cancer cell lines, 61 colorectal tumors, and 87 ga

79 erlotinib synergistically inhibits growth of colon cancer cell lines, achieves promising efficacy in

80 in primary colon cancers and up-regulated in colon cancer cell lines after global DNA demethylation b

81 with MMR deficiency is seen both in a human colon cancer cell line and in normal mouse fibroblast ce

82 lification of cDNA ends with the S1 parental colon cancer cell line and its drug-resistant ABCG2-over

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

84 rine T cells and the Il2 target locus, and a colon cancer cell line and the Cdx2 target locus, we sho

85 d transfection experiments in the MC38 mouse colon cancer cell line and the effects on growth tested

86 nt of the wild-type HCT116 (wt HCT116) human colon cancer cell line and the isogenic p53(-/-) HCT116

87 tational signatures were identified for each colon cancer cell line and tumor specimen.

88 isplayed significant synergy in a metastatic colon cancer cell line and was effective in a MTX-transp

89 STAT3 activation was examined in the HCT116 colon cancer cell line and young adult mouse colon cells

90 FAM120A was overexpressed in human colon cancer cell lines and 55% of human colon cancer sp

91 imes more potent in inhibiting the growth of colon cancer cell lines and also quite effective in prev

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

93 oxylates were evaluated in the HeLa and HT29 colon cancer cell lines and compared to the clinically a

94 d exerted antiproliferative effects in human colon cancer cell lines and CRC cells isolated by surgic

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

96 Knockdown of KIT decreased proliferation of colon cancer cell lines and growth of xenograft tumors i

97 We measured D3 expression in 6 colon cancer cell lines and human tumors and correlated

98 MAP1D is overexpressed in colon cancer cell lines and in colon tumors as compared

99 ssion was associated with Jagged1 in various colon cancer cell lines and in tissues from colon cancer

100 intracellular Ca2+ levels in pancreatic and colon cancer cell lines and led to loss of lysosome inte

101 o bisabolane derivatives were active against colon cancer cell lines and may be interesting as lead s

102 e that NF-kappaB is constitutively active in colon cancer cell lines and NF-kappaB, and its downstrea

103 rase p300, whose levels are also elevated in colon cancer cell lines and patient samples.

104 adult glioma, IDH1 G97, which is mutated in colon cancer cell lines and pediatric glioblastoma, and

105 Colon cancer cell lines and primary cancers were examine

106 tional status of Cables were investigated in colon cancer cell lines and primary colon tumors.

107 was observed in a significant proportion of colon cancer cell lines and primary colorectal tumors.

108 erase chain reaction identified JAK3 mRNA in colon cancer cell lines and primary tumors.

109 lasm and nuclei of several established human colon cancer cell lines and this localization pattern is

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

111 In addition, Poldelta variants were found in colon-cancer cell lines and in sporadic colorectal carci

112 nhibition of cell proliferation of the DLD-1 colon cancer cell line, and similar results were observe

113 ectors in DLD1, HT29, LS174T, and COLO320 DM colon cancer cell lines, and in UM-COLON#8 and POP77 xen

114 Evi1 is overexpressed in some human colon cancer cell lines, and overexpression is associate

115 ione synthesis impaired survival of multiple colon cancer cell lines, and pharmacological targeting o

116 dose-dependent and is observed in different colon cancer cell lines, and the degree of inhibition co

117 Statins inhibit the growth of colon-cancer cell lines, and secondary analyses of some,

118 mutations, yet only a subset of KRAS mutant colon cancer cell lines are dependent upon KRAS signalin

119 Colon cancer cell lines are most similar to their respec

120 Studying the HT-29 colon cancer cell line as a model, we found that Cox-2 m

121 ermore, VRX-009 replicates preferentially in colon cancer cell lines as evidenced by virus productivi

122 ce as active towards pancreatic, breast, and colon cancer cell lines as its (R,R) enantiomer at 24 h.

123 Human lung cancer, pancreatic cancer, and colon cancer cell lines as well as a murine melanoma cel

124 ukemia (AML), immortalized keratinocyte, and colon cancer cell lines, as well as normal human bone ma

125 ified and validated in a panel of additional colon cancer cell lines, as well as the kinetics of syne

126 n, with LC(50) activity in the HCT 116 human colon cancer cell line below 10 nM.

127 rlotinib cotreatment on growth inhibition of colon cancer cell lines both as a result of enhanced inh

128 an up-regulate NKG2DL expression in multiple colon cancer cell lines by activating the ATM-Chk2-media

129 pression and function of VGSCs in a panel of colon cancer cell lines by electrophysiologic recordings

130 rearrangements in 48 breast, pancreatic and colon cancer cell lines by fluorescence in situ hybridiz

131 er, we disrupted CDX2 in LOVO and SW48 human colon cancer cell lines by targeted homologous recombina

132 ell culturing, we validated the results from colon cancer cell lines by using clinical colon cancer s

133 ther this shift occurs in vitro in the human colon cancer cell line Caco-2 in association with the lo

134 Cells of the polarized human colon cancer cell line, CaCo-2, take up phenylalanine by

135 proliferation to differentiation of a human colon cancer cell line, CaCo2.

136 ting wild-type ACVR2 (wt-ACVR2) into a MSI-H colon cancer cell line carrying an ACVR2 frameshift muta

137 tisense inhibition of SIM2-s expression in a colon cancer cell line caused inhibition of gene express

138 In colon cancer cell lines, Cdx2 directly regulated the tra

139 een the theory and experiments using a human colon cancer cell line (COLO205) as the capture targets.

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

141 In a human colon cancer cell line, cysmethynil treatment blocks anc

142 icity studies toward HT-29 and HCT-116 human colon cancer cell lines demonstrated that ent-DCA had si

143 endogenous Wnt/beta-catenin target gene in a colon cancer cell line depends on the presence of beta-c

144 nergistic interaction of this combination in colon cancer cell lines depends on the effect exerted by

145 ntitation platforms to analyze a panel of 10 colon cancer cell lines differing by mutations in DNA mi

146 ntrapment and subsequent growth of two human colon cancer cell lines differing in their propensity to

147 that transient transfection of clusterin to colon cancer cell lines directly enhanced basal and chem

148 esent study, we found that a series of human colon cancer cell lines displayed various levels of expr

149 pression of LMNB1 by RNA interference in the colon cancer cell line DLD-1 and showed a dramatic redis

150 P) expression vector was introduced into the colon cancer cell line DLD-1, and a blue fluorescent pro

151 ficient but claudin-1-positive SW480 or HT29 colon cancer cell lines down-regulates claudin-1 express

152 Some human colon cancer cell lines (e.g., H508 cells) express M3 su

153 pen reading frames in a human KRAS-dependent colon cancer cell line engineered to express an inducibl

154 these compounds were evaluated against HT-29 colon cancer cell lines ex vivo.

155 was tested by confocal microscopy in a human colon cancer cell line exclusively expressing Nox1 (HT-2

156 Using a panel of human colon cancer cell lines exhibiting differential Src-spec

157 We further showed that the colon cancer cell line expressing the wild-type APC gene

158 s hypothesis, we generated stable HT29 human colon cancer cell lines expressing either bCD (HT29/bCD)

159 3kinase inhibitor), retinol, and sulindac in colon cancer cell lines expressing the poor prognostic p

160 n vitro using human epidermoid, ovarian, and colon cancer cell lines expressing various levels of P-g

161 We screened a panel of 30 colon cancer cell lines for sensitivity to HDACi-induced

162 of oncogenic Ki-ras(G12V) converts the HD6-4 colon cancer cell line from insensitive to TGF-beta1 to

163 Genes containing frameshift mutations in colon cancer cell line have been identified using a modi

164 In the human colon cancer cell line HCT-116, both compounds potently

165 Exposure of the colon cancer cell lines HCT-116 and Caco-2 to purified r

166 ability to inhibit the proliferation of the colon cancer cell line, HCT-116, in vitro, DNA damage an

167 Four colon cancer cell lines, HCT-116 and LoVo expressing wil

168 report that SAHA induced polyploidy in human colon cancer cell line HCT116 and human breast cancer ce

169 Finally, experiments done with human colon cancer cell line HCT116 and its isogenic CHK2 knoc

170 ibroblast cultures enhanced proliferation of colon cancer cell line HCT116 to a greater extent than c

171 In this study, using the human colon cancer cell line HCT116, we find that established

172 The colon cancer cell line HCT116, which contains wild-type

173 ze the genome-wide hnRNPK-DNA interaction in colon cancer cell line HCT116.

174 his finding was confirmed in two independent colon cancer cell lines HCT116 (KRAS mutant) and HKe3 (K

175 h was investigated using the paired isogenic colon cancer cell lines HCT116 p53(+/+) and HCT116 p53(-

176 unds were active against a transformed human colon cancer cell line (HCT116) while maintaining an acc

177 -proficient and p53-deficient pairs of human colon cancer cell lines (HCT116 versus HCT116 p53-/- and

178 e beta-catenin signaling pathway using human colon cancer cell lines (HCT116, Colo201).

179 many cancers and, upon 5-FU treatment of the colon cancer cell line, HCT116, evidence of allelic swit

180 We show that the G(1) population of a colon cancer cell line, HCT116, that is null for the p53

181 ct with the DNA methyltransferase DNMT1 in a colon cancer cell line, HCT116.

182 cer cell line, H1299, and two isogenic human colon cancer cell lines, HCT116 p53(+/+) and HCT116 p53(

183 poptosis in human epithelial cells using two colon cancer cell lines, HCT116Bax (Bax(+/-)) and HCT116

184 ncluding breast cancer cell line MDA-MB-231, colon cancer cell line HT-29, hepatocellular carcinoma c

185 Here, we show that treatment of the colon cancer cell line HT29 with the differentiating age

186 Colon cancer cell lines HT29 (human) and MC26 (murine) w

187 duced the phosphorylation of ERK1/2 in human colon cancer cell lines HT29 and Caco-2.

188 lation of apoptotic gene expression in human colon cancer cell lines HT29, HCT-116, and Caco-2.

189 red the transcriptional responses of a model colon cancer cell line, HT29, to TNF-alpha and anti-Fas

190 cally) similar but genetically altered human colon cancer cell lines, HT29 cells and Csk shRNA-transf

191 Screening of a panel of 33 colon cancer cell lines identified cell lines sensitive

192 and protein expression levels in a panel of colon cancer cell lines identified strong expression of

193 ted decay pathway in microsatellite unstable colon cancer cell lines identified the p300 gene as a po

194 ZKSCAN3 knockdown in two independent colon cancer cell lines impaired anchorage-independent g

195 xpression profiles were analyzed in SW620, a colon cancer cell line in which beta-catenin levels are

196 of compounds are toxic in HT-29 and BE human colon cancer cell lines in a clonogenic assay.

197 s is sphingosine, and treatment of two human colon cancer cell lines in culture (SW480 and T84) with

198 th arrest, differentiation, and apoptosis of colon cancer cell lines in vitro and have demonstrated a

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

200 resent study, we have generated stable human colon cancer cell lines, in which the function of KILLER

201 ot detected in several poorly differentiated colon cancer cell lines including DLD-1.

202 l 12-myristate 13-acetate (PMA) treatment of colon cancer cell lines increases MUC2 expression, so we

203 We show that knockdown of c-Myc in human colon cancer cell lines increases the expression of matu

204 Evidence from knockout mice as well as colon cancer cell lines indicated that CDK2 is dispensab

205 tic manipulations of claudin-1 expression in colon cancer cell lines induced changes in cellular phen

206 APEX1 overexpression or knockdown in human colon cancer cell lines induced profound changes in mali

207 on of the mutant Ki-ras allele in the HCT116 colon cancer cell line is sufficient to restore the expr

208 nt with this, LCT13 expression in breast and colon cancer cell lines is associated with silencing and

209 In the colon cancer cell lines, JNK1 expression was up-regulate

210 ckdown of Ron kinase in a highly tumorigenic colon cancer cell line led to reduced proliferation as c

211 Unlike what has been reported in T cells and colon cancer cell lines, Lef1DeltaN activated gene trans

212 iability assay showed that IC(50)s for human colon cancer cell lines LoVo and DLD-1, for human lung c

213 CDX2 has tumorigenic potential in the human colon cancer cell lines LOVO and SW48.

214 a time- and dose-dependent manner in a human colon cancer cell line (LoVo).

215 mouse tumor xenograft models using the human colon cancer cell line LS174T, while measuring the bioma

216 ished by intrasplenic injection of the human colon cancer cell line LS174t.

217 lved in MUC2 up-regulation by PMA in the HM3 colon cancer cell line may serve as a model for the effe

218 growth using two different aggressive human colon cancer cell lines metastatic to the liver.

219 re, we describe the establishment and use of colon cancer cell line model systems to dissect the func

220 al drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116

221 ust as the gene expression profiles from six colon cancer cell lines obtained by this method were sim

222 antiproliferative activity against different colon cancer cell lines, opening the route to a new clas

223 er, Imm-H did not inhibit malignant B cells, colon cancer cell lines, or normal human nonstimulated T

224 optosis in both HCT-116 and metastatic SW480 colon cancer cell lines, our study suggests that curcumi

225 d demonstrate selectivity for drug-resistant colon cancer cell lines over noncancerous cell lines.

226 d demonstrate selectivity for drug-resistant colon cancer cell lines over noncancerous cell lines.

227 d DNA damage-induced cell death in the human colon cancer cell line, p53 null HCT 116.

228 lencing of claudin-2 expression in Caco-2, a colon cancer cell line, prevents the EGF-induced increas

229 etion of the mutant Ras allele in the HCT116 colon cancer cell line protected cells from 5-FU-induced

230 iated through KLF5 and identifies subsets of colon cancer cell lines responsive and refractory to thi

231 Silencing of HDAC3 expression in colon cancer cell lines resulted in growth inhibition, a

232 erexpression of Hath1 in HT29, an aggressive colon cancer cell line, resulted in a significant inhibi

233 knockout cell lines and the wild-type HCT116 colon cancer cell line revealed a significant decrease i

234 -183 knockdown in synovial sarcoma, RMS, and colon cancer cell lines revealed deregulation of a miRNA

235 to identify interacting proteins from human colon cancer cell line RKO cell lysates.

236 ssion and that silencing HSF1 sensitizes the colon cancer cell line RKO to HNE-induced apoptosis.

237 t of liver cancer cell lines HepG2 and Huh7, colon cancer cell line RKO, and breast cancer cell line

238 r specimens, polyps from Min mice, and human colon cancer cell lines RKO and HT-29.

239 Nur77 is expressed in several colon cancer cell lines (RKO, SW480, HCT-116, HT-29, and

240 ate of proliferation of a stably transfected colon cancer cell line, RKO, was significantly decreased

241 Moreover, Foxm1-depleted colon cancer cell lines showed reduced DNA replication a

242 ved efficiency of this approach, we analysed colon cancer cell lines showing microsatellite instabili

243 tutive expression of RV-cyclin in the HCT116 colon cancer cell line significantly increases the level

244 Induction of DACOR1 in colon cancer cell lines significantly reduced their abil

245 rease of cells in the G(0)-G(1) phase in all colon cancer cell lines studied after treatment with PC-

246 t V2) knockdown also leads to apoptosis in a colon cancer cell line, suggesting these variants play s

247 mediated genome editing in a patient-derived colon cancer cell line suppressed anchorage-independent

248 However, among several human colon cancer cell lines surveyed, expression of GKLF is

249 tion and cell cycle progression in two human colon cancer cell lines, SW-480 and HT-29.

250 mucosa from these patients, and in the human colon cancer cell line SW480.

251 tion, ubiquitination, and degradation in the colon cancer cell lines SW480, DLD-1, and HT29, each of

252 estigated the effects of PC-SPES in vitro in colon cancer cell lines SW480, SW620, and DLD-1 and in v

253 ced the invasiveness of the MMP-9 expressing colon cancer cell line, SW480, through Matrigel in a dos

254 (pJAK3) are expressed constitutively in two colon cancer cell lines, SW480 and HT29.

255 ls involving CT26 and MC38, which are murine colon cancer cell lines syngeneic to BALB/c and C57BL/6

256 aluated by gene transfer experiments using a colon cancer cell line that lacks functional APC.

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

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

259 evaluate this possibility, we treated three colon cancer cell lines that are either proficient in mi

260 axin2 and hnkd were expressed only in human colon cancer cell lines that are known to have activatin

261 rmed a large-scale screen in isogenic paired colon cancer cell lines that differ by a single allele o

262 Using isogenic colon cancer cell lines that differ only by the presence

263 l cancer progression, we used three isogenic colon cancer cell lines that differ only in KRAS mutatio

264 By using pairs of isogenic colon cancer cell lines that differ only in p53 expressi

265 We have identified four human colon cancer cell lines that do no undergo growth inhibi

266 human colon tumor biopsy cultures as well as colon cancer cell lines that exhibit deregulated Wnt sig

267 Among colon cancer cell lines, those with KRAS mutations were

268 Animals injected intravenously with a human colon cancer cell line to establish microdisseminated co

269 cell line system (YB5) derived from the SW48 colon cancer cell line to study DAC-induced reactivation

270 Because Kaiso inactivation sensitized colon cancer cell lines to chemotherapy, it is possible

271 ering RNA-depleted human DLD1 and mouse CT26 colon cancer cell lines to examine DNA replication and a

272 and activation of this receptor causes most colon cancer cell lines to undergo a differentiative res

273 two synchronized isogenic MMR(+) and MMR(-) colon cancer cell lines treated with and without IUdR.

274 potential PTK6 substrates in the human SW620 colon cancer cell line using mass spectrometry, includin

275 , we profiled gene expression in a set of 18 colon cancer cell lines using cDNA microarrays represent

276 we analyzed biological triplicates of eight colon cancer cell lines using the MultiNotch MS3 method.

277 In this work, we describe a colon cancer cell line, VACO-9M, that is Smad4 null when

278 induced loss of ERBB3 in a KRAS mutant human colon cancer cell line was associated with loss of ERBB4

279 HPP1 expression in the HCT116 colon cancer cell line was restored after treatment with

280 and S-1 to inhibit cellular proliferation in colon cancer cell lines was also evaluated.

281 In RRM1 transgenic human lung and colon cancer cell lines, we observed induction of G(2) c

282 estinal epithelial (RIE-1) cells and 6 human colon cancer cell lines were examined.

283 For the in vitro studies, colon cancer cell lines were exposed to an ethanolic ext

284 -beta-secreting (CT26-TGF-beta) stable mouse colon cancer cell lines were generated using a retrovira

285 To do so, 22 colon cancer cell lines were screened for cetuximab resp

286 Human and murine colon cancer cell lines were subjected to mild hyperther

287 nding assays, and transient transfections in colon cancer cell lines were used to determine the effec

288 In addition, colon cancer cell lines were used to validate the role o

289 t p53 is inducibly knocked down in the SW480 colon cancer cell line, which contains mutant p53(R273H/

290 In the highly metastatic CT26 murine colon cancer cell line, which expresses endogenous TrkC,

291 14 against cancer cell growth in bladder and colon cancer cell lines, which provides valuable informa

292 Stable transfection of the SW620 metastatic colon cancer cell line with Drg-1 cDNA induced morpholog

293 egment encoding amino acids 2140-2421 into a colon cancer cell line with mutant APC prevents cell cyc

294 HCT116, a colon cancer cell line with wild type p53 alleles, under

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

296 Analysis of an additional two human colon cancer cell lines with and without K-ras mutation

297 Treatment of four human colon cancer cell lines with iso-effective concentration

298 We demonstrated that colon cancer cell lines with Ki-ras mutations display re

299 Consistent with our finding that colon cancer cell lines with mutant Ras have reduced exp

300 ted in migration assays using HT29 and SW480 colon cancer cell lines, with high and low levels of AQP