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1 also confirmed in mouse prostate cancer and colon carcinoma.
2 n IFN-alpha-driven tumor microenvironment in colon carcinoma.
3 xymethane and dextran sodium sulfate-induced colon carcinoma.
4 s as a suppressor of spontaneous sarcoma and colon carcinoma.
5 the colitic microenvironment and associated colon carcinoma.
6 o as a therapeutic target in models of human colon carcinoma.
7 NR) may have independent prognostic value in colon carcinoma.
8 pressed in human multiple myeloma as well as colon carcinoma.
9 mber of tumor entities such as pancreatic or colon carcinoma.
10 ls contributes to the hematogenous spread of colon carcinoma.
11 pithelial to mesenchymal transition (EMT) of colon carcinoma.
12 rall survival (OS) after primary surgery for colon carcinoma.
13 tem cell self-renewal and is dysregulated in colon carcinoma.
14 get to prevent the metastatic progression of colon carcinoma.
15 repeat genotyping to study the evolution of colon carcinoma.
16 mutations can be found in other cancers than colon carcinoma.
17 igen over 7 d using a syngeneic rat model of colon carcinoma.
18 18)F-FLT uptake in arthritic ankles and CT26 colon carcinomas.
19 ay lead to improved therapeutic regimens for colon carcinomas.
20 of tumor growth in mice with implanted CT-26 colon carcinomas.
21 of microsatellite instability (MSI) in human colon carcinomas.
22 ar matrix surrounding tumor cells, including colon carcinomas.
23 brin, but not fibrinogen, receptor on LS174T colon carcinomas.
24 nous dissemination of tumor cells, including colon carcinomas.
25 dendrimer was evaluated in mice bearing C-26 colon carcinomas.
26 f antiangiogenesis in ectopic and orthotopic colon carcinomas.
27 ely correlated with PTEN expression in human colon carcinomas.
28 spontaneously developed small intestine and colon carcinomas.
29 n several epithelial cancers, including many colon carcinomas.
30 drome, 28 for acute myeloid leukemia, 36 for colon carcinoma, 33 for osteogenic sarcoma, and 12 for f
31 MCF-7 (human breast carcinoma), HT-29 (human colon carcinoma), A2780 (human ovarian carcinoma), and A
38 sed expression of claudin-1 in human primary colon carcinoma and metastasis and in cell lines derived
39 cumulated on the lateral interfaces of human colon carcinoma and normal intestinal epithelial cells b
40 ion between MET and TNS4 expression in human colon carcinoma and ovarian carcinoma suggests TNS4 play
41 nism for how RhoC expression is regulated in colon carcinoma and substantiate its utility as a progno
42 models of human cancer, including LoVo human colon carcinoma and U87-MG human glioblastoma, when dose
44 show that USP39 is up-regulated in lung and colon carcinomas and its expression correlates with KRAS
46 p85beta expression is elevated in breast and colon carcinomas and that its increased expression corre
47 f ST6Gal-I occurs in many cancers, including colon carcinoma, and correlates with metastasis and poor
48 ciated with multiple malignancies, including colon carcinoma, and with ectodermal and mesoendodermal
49 adenomas, human FAP adenomas, human sporadic colon carcinomas, and in the intestine of apc(mcr) mutan
50 oxygenase-2 (COX-2) is up-regulated in human colon carcinomas, and its inhibition is associated with
51 man lung carcinoma, Colo205 and LS174T human colon carcinomas, and U87MG human glioblastoma multiform
53 are as effective in treating the murine C26 colon carcinoma as Doxil, a commercial liposome doxorubi
54 ranging from 0.05 to 2.45 muM against HT-29 colon carcinoma as well as MCF-7 and MDA-MB-231 mammary
55 antimetastatic activity in a murine model of colon carcinoma, as well as potent antiadhesive properti
57 We injected arthritic, healthy, and CT26 colon carcinoma-bearing mice with (18)F-FLT before stati
58 is by 10 wk post-infection, progressing into colon carcinoma by 20 wk post-infection, with pronounced
60 ity and CaSR protein expression in the human colon carcinoma CBS cells, which possessed a functional
61 Moreover, CEA and CD44v cooperate to mediate colon carcinoma cell adhesion to E- and L-selectin at el
62 ne model, leads to a significant decrease in colon carcinoma cell adhesion, migration and metastasis.
63 ves have been synthesized and evaluated in a colon carcinoma cell growth inhibition assay using HCT11
64 ncer cell cytotoxicity assays with the human colon carcinoma cell line (HT-29) showed that internaliz
65 n largazole 1 in growth inhibition of HCT116 colon carcinoma cell line and in inducing increases in g
66 isense inhibition of SIM2-s in a RKO-derived colon carcinoma cell line causes growth inhibition, apop
67 We recently demonstrated that the LS174T colon carcinoma cell line expresses the CD44 glycoform k
68 We identified LSR splice variants in the colon carcinoma cell line HCT116 and disrupted the LSR g
69 ach to a study of gene expression in the RKO colon carcinoma cell line in response to varying dosage
70 tudies, and blot rolling assays of LS174T, a colon carcinoma cell line known to interact with E-selec
72 ominant MHC class I tumor antigen of a mouse colon carcinoma cell line stimulates a tumor-specific T-
73 x1-mediated ROS generation in the HT29 human colon carcinoma cell line through a Rac-dependent mechan
75 modulates a subset of p53 target genes in a colon carcinoma cell line, consistent with the observati
76 inhibited cell growth of an aggressive human colon carcinoma cell line, FET6alphaS26X, which harbors
81 pathways controlled by p53, isogeneic human colon carcinoma cell lines (HCT116) differing only in th
82 tumorigenicity, and metastasis in Smad4-null colon carcinoma cell lines (MC38 and SW620) and in those
83 imulation were immunoprecipitated from human colon carcinoma cell lines and identified by mass spectr
87 We report MRN deficiency in three of seven colon carcinoma cell lines of the NCI Anticancer Drug Sc
88 id cells resulting from the culture of human colon carcinoma cell lines or primary mouse epithelial c
89 glycosylation profiles of the isogenic human colon carcinoma cell lines SW480 (primary tumor) and SW6
90 T61, was used to block HH signaling in human colon carcinoma cell lines that express HH signaling com
95 ve NF-kappaB activation in five of six human colon carcinoma cell lines; this activation is inhibited
97 ST6Gal-I knockdown and forced overexpression colon carcinoma cell models, we find that alpha2-6 sialy
98 so known as ArhGEF28 or p190RhoGEF) promotes colon carcinoma cell motility and tumor progression via
99 h, structure-dependent toxicity to the human colon carcinoma cell-line HCT116 p53(++), causing dramat
103 is of intracellular Ca(2+) handling in human colon carcinoma cells (HT29) versus normal human mucosa
106 esis, we genetically engineered HCT116 human colon carcinoma cells and 4T1 mouse mammary carcinoma ce
108 the expression of CD44 and/or CEA in LS174T colon carcinoma cells and analyzed their ability to meta
109 s coated with CEA immunopurified from LS174T colon carcinoma cells and selectins as substrate reveal
110 ve, i.e. autophosphorylated, ErbB2 in HCT116 colon carcinoma cells and TA3/St mammary carcinoma cells
111 been shown to be active in human breast and colon carcinoma cells and to promote their invasion thro
112 tribute to aberrant COX-2 expression in HT29 colon carcinoma cells and to reveal the role of platelet
113 romoter of the p21 gene in unstressed HCT116 colon carcinoma cells are localized within a region of r
115 lity to these viruses and observed that HT29 colon carcinoma cells are susceptible to infection by ne
116 ose findings by showing that T84 and Colo205 colon carcinoma cells bind selectins via sialidase-sensi
117 Pdcd4 suppresses tumor progression in human colon carcinoma cells by the novel mechanism of down-reg
118 Basal CXCR4 promoter activity in HCT116 colon carcinoma cells deleted of p53 [HCT116(p53KO)] was
120 pin RNA (shRNA) knockdown of fascin in human colon carcinoma cells derived from an aggressive primary
121 treated with Taxol, slippage-resistant HT29 colon carcinoma cells display robust Cdk1 activity and e
122 die in mitosis, whereas slippage-prone DLD-1 colon carcinoma cells display weak Cdk1 activity and par
124 is a key survival factor that protects human colon carcinoma cells from TNF-related apoptosis-inducin
125 ance the cytotoxicity of these drugs against colon carcinoma cells in vitro demonstrating a clear syn
126 shown that ETS1 represses tumorigenicity of colon carcinoma cells in vivo, and that the p42-ETS1 pro
128 it proliferation, migration, and invasion of colon carcinoma cells indicating tumor suppressor activi
129 e show that PTEN deletion in HCT116 and DLD1 colon carcinoma cells leads to suppression of CHK1 and C
131 t variant isoforms of CD44 (CD44v) on LS174T colon carcinoma cells possess P-/L-/E-selectin binding a
132 that CD44 variant isoforms (CD44v) on LS174T colon carcinoma cells possess selectin binding activity.
133 tion of MAP1D expression by shRNA in HCT-116 colon carcinoma cells reduces anchorage-independant grow
134 y analysis of Pdcd4-overexpressing RKO human colon carcinoma cells revealed MAP4K1 as the sole target
136 ic and metastatic profile in both breast and colon carcinoma cells than plasma from mice treated with
137 tected high levels of RhoA activity in HCA-7 colon carcinoma cells that constitutively express COX-2.
138 r, JW55 inhibited canonical Wnt signaling in colon carcinoma cells that contained mutations in either
139 formed mouse embryonic fibroblasts and HT-29 colon carcinoma cells that express a dominant negative P
140 gs, down-regulation of Hsp27 in HCT116 human colon carcinoma cells that express this heat shock prote
141 and alpha2beta1 integrins on the surface of colon carcinoma cells through the disintegrin domain.
142 S1 protein bypasses a defect in apoptosis in colon carcinoma cells through the up-regulation of caspa
143 ut enabled quiescent HD6, SW480, and colo320 colon carcinoma cells to acquire some biochemical charac
144 itro and in vivo Exposing human lymphoma and colon carcinoma cells to AZD3965 increased MCT4-dependen
151 shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related a
154 (shRNA)-mediated attenuation of ST6Gal-I in colon carcinoma cells with elevated endogenous expressio
156 N null PC3 prostate and PIK3CA mutant HCT116 colon carcinoma cells with PI-103 resulted in a concentr
158 strand breaks, activated DNA repair in human colon carcinoma cells, and effectively suppressed tumour
159 or cells, induce DNA damage and apoptosis in colon carcinoma cells, and reduce tumor size in animal m
160 ransport chain (ETC) in spermatogenic and in colon carcinoma cells, and silencing of either Fer or Fe
161 man wild-type p53- and p21-expressing HCT116 colon carcinoma cells, as well as in p53-null counterpar
162 used to deliver the doxorubicin to CT.26-WT colon carcinoma cells, eliciting a therapeutic response.
169 ith cytoplasmic extracts of untreated HCT116 colon carcinoma cells, we identified the DEAD-box RNA he
170 etion was observed in both HT1080 and HCT116 colon carcinoma cells, where p21 was induced by DNA-dama
171 with CD44 immunopurified from LS174T or T84 colon carcinoma cells, which express primarily CD44v, ef
201 interesting activity against CA-4-resistant colon-carcinoma cells and multidrug-resistant leukemia c
202 observed that both apoptotic and necroptotic colon carcinoma CT26 cells efficiently immunized mice ag
203 g and presentation assays in HeLa and murine colon carcinoma (CT26) cells showed that these inhibitor
205 Here, we demonstrate that 5-FU-generated colon carcinoma debris stimulates the growth of a subthr
207 ransfusion inhibited growth of both lung and colon carcinoma ectopic tumors, whereas blockade of miR-
208 ll lymphoma, neuroblastoma, and prostate and colon carcinomas, either as a single agent or in combina
213 esquiterpenoid content; the IC(50) values on colon carcinoma, glioblastoma, and breast adenocarcinoma
214 intestinal epithelial cell line derived from colon carcinoma grown on semipermeable tissue culture in
217 ved from extensive testing against the human colon carcinoma HCT-116 and the 60-cell-line panel at th
219 amides A-C showed cytotoxicity against human colon carcinoma (HCT-116) cells with IC(50) values betwe
222 n splicing at the genome-wide level in human colon carcinoma HCT116 and breast carcinoma MCF7 cells.
224 induced demethylation of CDKN2A promoter in colon carcinoma HCT116 cells and its reactivation after
225 n, we tested TOP1mt KO fibroblasts and human colon carcinoma HCT116 cells and measured mtDNA after 3-
226 mosome instability induced in cultured human colon carcinoma HCT116 cells by the antitumor radiomimet
229 tigate global DNA methylation changes, human colon carcinoma HCT116 cells, which were hypomorphic for
231 After a short dose of camptothecin in human colon carcinoma HT29 cells, DNA replication was inhibite
234 egrin enhances the tumorigenic properties of colon carcinoma, including activation of autocrine TGF-b
235 stable overexpression in Ras-induced murine colon carcinomas increased microvascular densities and v
238 e kinase superfamily initially identified as colon carcinoma kinase-4, is highly expressed in various
239 n two human embryonic stem cell lines, human colon carcinoma line HCT116, and mouse embryonic stem ce
242 T6Gal-I, a feature that is characteristic of colon carcinoma, may confer tumor cells with a selective
243 145 and LNCaP (prostate carcinoma), HCT-116 (colon carcinoma), MCF-7 (breast carcinoma) and NCI-H460
244 Three cell lines were employed: DLD1 (human colon carcinoma), MCF7 (human breast carcinoma) and NCI/
246 with ulcerative colitis and tumors including colon carcinoma, melanoma, hepatic carcinoma, ovarian ca
251 murine hepatocellular and colitis-associated colon carcinoma models, and this was associated with red
253 udies identify Rgnef as a novel regulator of colon carcinoma motility and invasion, and they show tha
254 ) imaging mass spectrometry (IMS) in HCT 116 colon carcinoma multicellular spheroids to assess the di
256 location were determined in stage II and III colon carcinomas (n = 160) and normal mucosa (n = 25) by
257 ermined in patients with TNM stage II or III colon carcinomas (n = 2,693) who participated in randomi
260 n HHD model in which HLA-A2(neg) tumor (MC38 colon carcinoma or B16 melanoma) cells are not recognize
261 When injected i.v. in mice bearing CT26 colon carcinoma or B16 melanoma, the 4PD nanoparticles p
265 comparatively investigated their effects on colon carcinoma proliferation, a) in vitro against colon
266 t CD44v is a functional P-selectin ligand on colon carcinoma provides a novel perspective on the enha
271 types of cancers (e.g., breast carcinoma and colon carcinoma), S664-pTSC2 seemed to be a more sensiti
272 te that expression of CD103/beta(7) in human colon carcinoma-specific CTL is synergistically enhanced
273 es, exerts growth inhibitory effects against colon carcinoma, suggesting a nutraceutical potential in
278 n of smMLCK decreased (19.5 +/- 4.7 fold) in colon carcinoma tissues compared to normal colon tissues
280 sifies the human protein encoded by immature colon carcinoma transcript-1 (ICT1) as one of a family o
281 ry tumor with SAR in patients with stage III colon carcinomas treated with adjuvant chemotherapy.
284 ith the TSA mammary adenocarcinoma and MCA38 colon carcinoma tumor models that show little response t
289 mic imbalances of chromosome 8 in 51 primary colon carcinomas using a custom-designed genomic array c
290 was measured in arthritic ankles and in CT26 colon carcinomas when the mice breathed oxygen and were
291 ls: mouse hepatocellular carcinoma and human colon carcinoma, whereby the metabolism has been profile
294 re, berberine suppresses the growth of human colon carcinoma xenograft in nude mice in an RXRalpha-de
296 ses as well as growth of subcutaneous HCT116 colon carcinoma xenograft tumors, without affecting body
297 acy studies it inhibited the growth of SW620 colon carcinoma xenografts following oral administration
298 sly that the endothelium of vessels in human colon carcinoma xenografts in mice is a mosaic structure