コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 lar, cellular, and morphologic properties of human colon.
2 f this important family of bacteria from the human colon.
3 em to be involved in the excretory system of human colon.
4 thylation patterns of cells sampled from the human colon.
5 sion assays and ex vivo using recellularized human colon.
6 etabolites of microbial communities from the human colon.
7 and peptide YY (PYY) in vitro from mouse and human colons.
8 feration, migration and viability assays and human colon adenocarcinoma (Caco-2, ATCC, Rockville, MD)
10 hat eIF3i expression was upregulated in both human colon adenocarcinoma and adenoma polyps as well as
13 eening a kinase/phosphatase shRNA library in human colon adenocarcinoma HT-29 cells, we found that kn
14 and in vivo, in a cisplatin resistant HT-29 human colon adenocarcinoma model, with and without the p
15 ion was used to analyze levels of miR-627 in human colon adenocarcinoma samples and nontumor colon mu
24 ression were inversely correlated in primary human colon and breast cancers, and in intestinal adenom
28 terleukin 6 (IL6) and its receptor (IL6R) in human colon and lung cancer cell lines by flow cytometry
31 kinase 3beta (GSK-3beta) is overexpressed in human colon and pancreatic carcinomas, contributing to c
33 ltured intestinal epithelial cells (IEC) and human colon and small intestine biopsies, RIG-I is enric
35 y expressed on the surface epithelium of the human colon and was observed to colocalize with TcdB in
37 sed interleukin 23 (IL-23) protein levels in human colon biopsy specimens positive for C. difficile t
39 roduction from (13) C-labelled fibres in the human colon by measurement of (13) C-labelled SCFA conce
40 study, we investigated EHEC adherence to the human colon by using in vitro organ culture (IVOC) of co
41 A), was implemented in different cell lines: human colon cancer (Caco-2), human hepatocarcinoma (HepG
43 f histone H3 phosphorylation at serine 10 in human colon cancer (Colo205) and tumor regression in hum
44 acrophages; its genotoxicity was assessed in human colon cancer (HCT116) and primary murine colon epi
45 s (P1 and P2), we generated Tet-On-inducible human colon cancer (HCT116) cell lines that express eith
47 ntly, treatment of mouse xenograft models of human colon cancer and multiple myeloma resulted in tumo
49 and visualized in a xenograft mouse model of human colon cancer by PET, which demonstrates that this
51 dels, including its mechanism of action with human colon cancer cell (HCCC) lines and animal tumor mo
52 s and their glutathione conjugates, prevents human colon cancer cell growth in culture as well as in
53 d between the theory and experiments using a human colon cancer cell line (COLO205) as the capture ta
54 brane was tested by confocal microscopy in a human colon cancer cell line exclusively expressing Nox1
58 tally induced loss of ERBB3 in a KRAS mutant human colon cancer cell line was associated with loss of
63 ng, and exerted antiproliferative effects in human colon cancer cell lines and CRC cells isolated by
64 cytoplasm and nuclei of several established human colon cancer cell lines and this localization patt
67 oscopically) similar but genetically altered human colon cancer cell lines, HT29 cells and Csk shRNA-
73 nhanced RIP140 expression strongly repressed human colon cancer cell proliferation in vitro and after
74 l, with an IC(50) of 24.43 microM in HCT-116 human colon cancer cells and an IC(50) of 25.82 microM i
75 effect of anthocyanin-rich plant extracts on human colon cancer cells and determine their mechanism o
77 tea catechins to suppress MET activation in human colon cancer cells and propose a mechanism by whic
78 ation of THAP11-dependent gene expression in human colon cancer cells and suggest that the THAP11-HCF
79 SAHA increase phosphocholine (PC) levels in human colon cancer cells and tumor xenografts as observe
82 of excess R2 subunits protects p53-deficient human colon cancer cells from cisplatin-induced DNA dama
84 M induced downregulation of class I HDACs in human colon cancer cells in vitro and in vivo in tumor x
86 Here, we reveal that silencing GUCY2C in human colon cancer cells increases Akt-dependent TGF-bet
90 nt setting, we carried out studies with H508 human colon cancer cells that endogenously express M3Rs
91 lopment of acquired cross-drug resistance of human colon cancer cells that harbor different genetic b
94 pounds on growth and antioxidative status in human colon cancer cells was investigated in this study.
95 rowth of primary tumors formed by murine and human colon cancer cells was reduced in mice by genetic
97 y to cause cytotoxicity to HCT-116 and HT-29 human colon cancer cells with ED50 values of 134.4 and 2
98 ng strand cleavage and growth suppression in human colon cancer cells with G12D or G12V mutations, th
99 mab synergistically reduced the viability of human colon cancer cells with wild-type but not mutant K
100 owing mechanistic inhibition of CHK2 in HT29 human colon cancer cells, a concentration dependent radi
102 ivation of beta-catenin and proliferation of human colon cancer cells, and increased tumor growth in
103 mRNA and protein abundance twofold in HCT116 human colon cancer cells, and induction was further enha
104 the nucleus of primary colorectal tumors and human colon cancer cells, and oncogenic activation of Ra
105 aused cytotoxicity to Caco-2, HT-29, HCT-116 human colon cancer cells, and reduced inflammatory respo
107 nly enhanced cancer cell killing in cultured human colon cancer cells, but also improved antitumor ac
109 best in a luciferase knockdown study in HT29 human colon cancer cells, which were found to be more di
127 formation of mouse epidermal cells JB6 Cl41, human colon cancer DLD-1, breast cancer T-47D, and melan
128 ory microenvironment and studied circulating human colon cancer HCT116 cells in response to a variety
129 owth of mouse xenograft tumours derived from human colon cancer HCT116 cells that contain wild type p
133 findings establish a new role for LIN28B in human colon cancer pathogenesis, and suggest LIN28B post
136 ohistochemical analysis of approximately 450 human colon cancer specimens (Stage III) reveals that P1
141 notypic heterogeneity between two iso-clonal human colon cancer sublines HCT116 and HCT116b on their
142 oth human colon tumor cell lines and primary human colon cancer tissue xenografted into immunodeficie
147 destruction-replenishment) was performed in human colon cancer xenografts (n = 38) by using a clinic
148 e form of matriptase in vivo was measured in human colon cancer xenografts and in a patient-derived x
149 d to nude mice inhibited the growth of SW480 human colon cancer xenografts by 58% compared with contr
150 ation on antiangiogenic treatment effects in human colon cancer xenografts compared with ex vivo refe
151 nd reproducible to assess tumor perfusion in human colon cancer xenografts in mice and allows for ass
153 Materials and Methods Twenty-three mice with human colon cancer xenografts were randomized to receive
155 e p38gamma/c-Jun/MMP9 pathway also exists in human colon cancer, and there is a coupling of increased
156 ectal cancer often differ significantly from human colon cancer, being largely restricted to the smal
158 nd Plexin D1 were found to be upregulated in human colon cancer, liver metastasis, and melanoma progr
171 multiple monkey kidney fibroblasts (MKF) and human colon cancerous (HCT-8) cells in close proximity,
172 otein, and is stabilized in both APC-mutated human colon cancers and Apc(min/+) intestinal polyps.
173 logy to conduct gene expression profiling of human colon cancers and found that loss of CHFR expressi
175 oli (APC) gene is mutated in the majority of human colon cancers and often occurs simultaneously with
176 tro, and that gene-specific 5-hmC changes in human colon cancers are directly correlated with changes
177 deletion mutation in beta-catenin present in human colon cancers both weaken tumor intercellular Ecad
179 and RIP140 protein levels were decreased in human colon cancers compared with those in normal mucosa
180 Consistent with these findings, analyses of human colon cancers demonstrated increased Dsg2 protein
183 dependency signature" is enriched in primary human colon cancers with mutations in both APC and KRAS,
184 thylated in Cancer 1 (HIC1), often occurs in human colon cancers, among others, via CpG island hyperm
185 , we investigated the expression of eIF3i in human colon cancers, tested its contribution to colon on
195 CAM accumulated on the lateral interfaces of human colon carcinoma and normal intestinal epithelial c
196 rrelation between MET and TNS4 expression in human colon carcinoma and ovarian carcinoma suggests TNS
200 olyploid cells resulting from the culture of human colon carcinoma cell lines or primary mouse epithe
201 inked glycosylation profiles of the isogenic human colon carcinoma cell lines SW480 (primary tumor) a
202 2, GANT61, was used to block HH signaling in human colon carcinoma cell lines that express HH signali
204 titutive NF-kappaB activation in five of six human colon carcinoma cell lines; this activation is inh
205 ay high, structure-dependent toxicity to the human colon carcinoma cell-line HCT116 p53(++), causing
206 ar basis of intracellular Ca(2+) handling in human colon carcinoma cells (HT29) versus normal human m
207 in effective sensitization of the metastatic human colon carcinoma cells to FasL-induced apoptosis.
208 city and potent activity in sensitization of human colon carcinoma cells to FasL-induced apoptosis.
210 ingle-strand breaks, activated DNA repair in human colon carcinoma cells, and effectively suppressed
220 tion on splicing at the genome-wide level in human colon carcinoma HCT116 and breast carcinoma MCF7 c
221 eration, we tested TOP1mt KO fibroblasts and human colon carcinoma HCT116 cells and measured mtDNA af
223 thermore, berberine suppresses the growth of human colon carcinoma xenograft in nude mice in an RXRal
225 ainst MCF-7 (human breast carcinoma), HT-29 (human colon carcinoma), A2780 (human ovarian carcinoma),
228 l models: mouse hepatocellular carcinoma and human colon carcinoma, whereby the metabolism has been p
234 L17A, IL22, and interferon-gamma by cultured human colon CD3-negative, IL7-receptor-positive cells.
235 oxicity as measured using an in vitro normal human colon cell (NCM460) assay, compared to chlorinatio
236 ion to IBD map to HNF4A binding sites in the human colon cell line CaCo2, suggesting impaired HNF4A b
237 Compounds 5c and 5j, tested in vitro on the human colon cell line HT-29, blocked the growth of cells
239 t GH suppresses p53 and reduces apoptosis in human colon cell lines as well as in induced human pluri
241 Mitochondrial dysfunction was induced in human colon-derived epithelial cell lines or colonic bio
243 RRalpha are not detectable in nontransformed human colon epithelial cells, and depletion of the AMPKg
245 RT1 was also detected in the goblet cells of human colon epithelial tissue and primary culture of col
246 rons projecting to the guinea pig rectum and human colon expressed alpha-synuclein in their axons.
248 three-stage continuous-culture model of the human colon (gut model), which represents different anat
249 t strains of Escherichia coli present in the human colon have been linked to the initiation of inflam
250 uate the activities against proliferation of human colon HCT116 and mammary adenocarcinoma MCF-7 canc
251 jected intravenously into nude mice carrying human colon HCT116 tumors efficiently suppressed tumor g
252 tempt at modelling microbial dynamics in the human colon incorporating both uncertainty and adaptatio
254 c device with the ability of detecting a few human colon invasive cancer cells (SW48) in a mixed cell
256 lose by microbes in the bovine rumen and the human colon is critical to gut health and function withi
260 gh there are many factors that determine the human colon microbiota composition, diet is an important
261 orthotopic organoid transplantation model of human colon organoids engineered to harbor different CRC
262 technology to delete key DNA repair genes in human colon organoids, followed by delayed subcloning an
264 AIL and RAc induce significant cell death in human colon polyps, providing a potentially selective ap
265 2'-deoxycytidine, was quantified in diseased human colon samples and found to be present at levels si
266 -5 mm) were stitched into 1 freshly resected human colon specimen and followed by an ex vivo molecula
268 normal and inflammatory bowel disease (IBD) human colon tissue as well as hyperplasia human tonsils.
271 Wnt inhibitors are specifically cytotoxic to human colon tumor biopsy cultures as well as colon cance
272 ll growth, invasion, and metastasis, of both human colon tumor cell lines and primary human colon can
273 or B4 (EPHB4) is aberrantly overexpressed in human colon tumor cell lines and selectively required fo
275 PXR bound to the FGF19 promoter in both human colon tumor cells and "normal" intestinal crypt ce
276 CD133-positive (CD133(+)) subpopulations of human colon tumor cells that exhibited more potent tumor
277 ly correlated with H2O2-stress signatures in human colon tumor cohorts, but positively correlated wit
278 els of NTR1, miR-21, and miR-155 increase in human colon tumor samples and correlate with tumor stage
279 R-21, and miR-155 increased significantly in human colon tumor samples, compared with normal tissues,
283 d expression of KIT in cultured cells and in human colon tumor xenografts and this contributed to the
284 ed sphere formation and viability of primary human colon tumor-initiating cells harboring mutant KRAS
285 undifferentiated colonosphere cultures from human colon tumors and used them to generate stably diff
289 vival, while elevated expression of TIGAR in human colon tumors suggested that deregulated TIGAR supp
291 se expression is elevated in both rodent and human colon tumors, collaborate to drive colon tumor for
296 systematically more than 70 pairs of primary human colon tumours by applying next-generation sequenci
299 al success in habitats such as the rumen and human colon where nitrogen is rarely limiting for growth
300 olonizes and forms stable A/E lesions on the human colon, which are likely to contribute to intestina
WebLSDに未収録の専門用語（用法）は "新規対訳" から投稿できます。