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1                      One patient developed a hepatocarcinoma.
2  the development of fibrosis, cirrhosis, and hepatocarcinoma.
3 driven metabolic stress in a murine model of hepatocarcinoma.
4  to a chronic state leading to cirrhosis and hepatocarcinoma.
5 ng adenocarcinoma and approximately 10% with hepatocarcinoma.
6 f the primary factors for liver toxicity and hepatocarcinoma.
7 lly in a malignant prostate cell line and in hepatocarcinoma.
8 tamin and OSHA inhibits the proliferation of hepatocarcinoma.
9 enhance the MRI signal in the early stage of hepatocarcinoma.
10 ing for the assessment of the early stage of hepatocarcinoma.
11 ar fingerprint that discriminates liver from hepatocarcinoma and allows sparing normal tissue while t
12 e complications of the disease which include hepatocarcinoma and liver failure.
13  tumor cell lines, including ovarian cancer, hepatocarcinoma and retinoblastoma, through the inhibiti
14 , an amino acid transporter overexpressed in hepatocarcinoma and the liver cancer cell line HepG2.
15    Moreover, NCoR is down-regulated in human hepatocarcinomas and in the more aggressive breast cance
16 or development, especially in breast cancer, hepatocarcinomas, and colorectal carcinoma.
17 liver range from steatosis to development of hepatocarcinomas, and several mechanisms for these effec
18 mRNA splicing regulator that is inhibited in hepatocarcinoma, as a pivotal gene for hepatocellular ho
19  significantly inhibited the growth of human hepatocarcinoma (BEL-7402) in nude mice by 72% in tumor
20 by which DNA hypomethylating agents suppress hepatocarcinoma cell growth.
21 e expression of UGT1A1 in human liver in the hepatocarcinoma cell line HepG2 and provided evidence of
22 n dynamics on glucose consumption by a human hepatocarcinoma cell line, HepG2.
23 both primary mouse hepatocytes and the human hepatocarcinoma cell line, HepG2.
24  virus into tumors generated by untransduced hepatocarcinoma cell line.
25 patitis C virus (HCV) replication-permissive hepatocarcinoma cell lines has provided important new vi
26                                  In hepatoma/hepatocarcinoma cell lines, FGFR3 isoforms were overexpr
27 KA97 was confirmed in other colon cancer and hepatocarcinoma cell lines.
28 xpression of SPZ1 and TWIST1 in specimens of hepatocarcinoma cells (HCCs) and non-HCCs.
29 fy proteins with altered expression in human hepatocarcinoma cells (HepG2) cells after 12 h in the pr
30 to characterize the GSH homeostasis in human hepatocarcinoma cells (HepG2) that overexpress CYP2E1.
31 ) increased DeltaPsi in HepG2 and Huh7 human hepatocarcinoma cells and HCC4006 human lung adenocarcin
32 ogen synthesis from IL-6 inhibition in HepG2 hepatocarcinoma cells as well as in mouse primary hepato
33 ly expressing FLAG-tagged human D3 or monkey hepatocarcinoma cells expressing endogenous D3, we ident
34 ived HCV particles were produced from Huh7.5 hepatocarcinoma cells in presence of daclatasvir for sho
35 ation of their lymphocytes with HEV-infected hepatocarcinoma cells led to an HEV-specific response in
36 failure to use choline as a methyl source in hepatocarcinoma cells may contribute to methionine depen
37 generated from patients after coculture with hepatocarcinoma cells permissive to HEV and IL-2/12/18.
38          Expression of recombinant apoA-V in hepatocarcinoma cells results in increased lipid droplet
39 sly identified lack of PE methyltransferase, hepatocarcinoma cells were found to lack the abilities t
40  activation enhance VDAC2-dependent death of hepatocarcinoma cells with little effect on normal hepat
41 (1) and zearalenone and were tested on human hepatocarcinoma cells with no increase in cytotoxicity o
42 o the CDP-choline pathway remained intact in hepatocarcinoma cells, contribution of choline to PE met
43                                           In hepatocarcinoma cells, four of these six ionophores exhi
44                                  In hepatoma/hepatocarcinoma cells, up-regulated FGFR3-IIIb conferred
45 o the growth inhibitory effect of TGFbeta in hepatocarcinoma cells.
46 of mitochondrial membrane potential in HepG2 hepatocarcinoma cells.
47 ivity after the knockdown of 19 599 genes in hepatocarcinoma cells.
48 replicon with a luciferase reporter in human hepatocarcinoma cells.
49 r, in murine hepatocyte-like cells and human hepatocarcinoma cells.
50 se 9 (CDK9) on gamma-FBG expression in HepG2 hepatocarcinoma cells.
51 pha or lipopolysaccharide in macrophages and hepatocarcinoma cells.
52  activates ferritin H transcription in HepG2 hepatocarcinoma cells.
53 ble of stimulating the 2D5 promoter in HepG2 hepatocarcinoma cells.
54 nt manner, suggesting a silencer function in hepatocarcinoma cells.
55 ing the uptake of fluorescent LDL into Huh-7 hepatocarcinoma cells.
56 n (HBx) plays a critical role in HBV-related hepatocarcinoma development.
57 t created by an in vivo PMC implant inhibits hepatocarcinoma growth and metastasis and has synergisti
58 n retained in certain human cancers, such as hepatocarcinoma (HCC).
59 hIP assays in breast SkBr3, colorectal LoVo, hepatocarcinoma HepG2 cancer cells, and breast cancer-as
60 ouse primary hepatocytes as well as in human hepatocarcinoma HepG2 cells.
61 NA expression and protein synthesis in human hepatocarcinoma HepG2 cells.
62 when tested at the cellular level with human hepatocarcinoma (HepG2) cells as target cells.
63 mployed to study phenolic antioxidants using hepatocarcinoma (HepG2) cells, quercetin showed antioxid
64  into LMH, normal rat kidney (NRK) and human hepatocarcinoma (HepG2) cells.
65 issive Chinese hamster ovary (CHO), in human hepatocarcinoma (HepG2), and to a lesser extent in human
66 ll lines: human colon cancer (Caco-2), human hepatocarcinoma (HepG2), human endothelial (EA.hy926) an
67 iferation of fibroblast cells (Balb/3T3) and hepatocarcinoma (HepG2).
68 siRNA into cancer cell lines including human hepatocarcinoma (Huh-7), human lung adenocarcinoma (A549
69 for oxidizing palmitate was limited to human hepatocarcinoma Huh7 cells and to C2C12 mouse myoblasts
70  in patients treated with platinum salts, or hepatocarcinoma in cirrhotic patients are examples of le
71 Treatment with TAM has been known to promote hepatocarcinoma in rats, but toremifene (TOR), a chlorin
72          Antimicrobial lectins, particularly hepatocarcinoma-intestine-pancreas/pancreatic-associated
73 fied a type 1 diabetes-related cDNA encoding hepatocarcinoma-intestine-pancreas/pancreatic-associated
74 ied this differentially expressed protein as hepatocarcinoma-intestine-pancreas/pancreatitis-associat
75 s of prostate carcinoma cell line DU 145 and hepatocarcinoma LCI-D35 were orthotopically implanted in
76 transferase (cat) gene activation in chicken hepatocarcinoma (LMH) cells.
77 rential susceptibility to the development of hepatocarcinomas observed after treatment with fibrates.
78 for myeloma and lymphoma cell lines than for hepatocarcinoma or non-activated lymphocytes.
79 ough the only effective drug against primary hepatocarcinoma, the multikinase inhibitor Sorafenib (SF
80  oxidation enzyme knockdown mutants of human hepatocarcinoma to demonstrate its utility for analyzing
81 some proliferation, and after chronic dosing hepatocarcinoma, whereas epidemiological studies suggest