ライフサイエンスコーパス: hepatocarcinoma

1 f the primary factors for liver toxicity and hepatocarcinoma.

2 One patient developed a hepatocarcinoma.

3 the development of fibrosis, cirrhosis, and hepatocarcinoma.

4 driven metabolic stress in a murine model of hepatocarcinoma.

5 to a chronic state leading to cirrhosis and hepatocarcinoma.

6 ng adenocarcinoma and approximately 10% with hepatocarcinoma.

7 lly in a malignant prostate cell line and in hepatocarcinoma.

8 e complications of the disease which include hepatocarcinoma and liver failure.

9 tumor cell lines, including ovarian cancer, hepatocarcinoma and retinoblastoma, through the inhibiti

10 , an amino acid transporter overexpressed in hepatocarcinoma and the liver cancer cell line HepG2.

11 Moreover, NCoR is down-regulated in human hepatocarcinomas and in the more aggressive breast cance

12 or development, especially in breast cancer, hepatocarcinomas, and colorectal carcinoma.

13 liver range from steatosis to development of hepatocarcinomas, and several mechanisms for these effec

14 mRNA splicing regulator that is inhibited in hepatocarcinoma, as a pivotal gene for hepatocellular ho

15 significantly inhibited the growth of human hepatocarcinoma (BEL-7402) in nude mice by 72% in tumor

16 by which DNA hypomethylating agents suppress hepatocarcinoma cell growth.

17 e expression of UGT1A1 in human liver in the hepatocarcinoma cell line HepG2 and provided evidence of

18 both primary mouse hepatocytes and the human hepatocarcinoma cell line, HepG2.

19 virus into tumors generated by untransduced hepatocarcinoma cell line.

20 patitis C virus (HCV) replication-permissive hepatocarcinoma cell lines has provided important new vi

21 In hepatoma/hepatocarcinoma cell lines, FGFR3 isoforms were overexpr

22 KA97 was confirmed in other colon cancer and hepatocarcinoma cell lines.

23 xpression of SPZ1 and TWIST1 in specimens of hepatocarcinoma cells (HCCs) and non-HCCs.

24 fy proteins with altered expression in human hepatocarcinoma cells (HepG2) cells after 12 h in the pr

25 to characterize the GSH homeostasis in human hepatocarcinoma cells (HepG2) that overexpress CYP2E1.

26 ogen synthesis from IL-6 inhibition in HepG2 hepatocarcinoma cells as well as in mouse primary hepato

27 ly expressing FLAG-tagged human D3 or monkey hepatocarcinoma cells expressing endogenous D3, we ident

28 ived HCV particles were produced from Huh7.5 hepatocarcinoma cells in presence of daclatasvir for sho

29 failure to use choline as a methyl source in hepatocarcinoma cells may contribute to methionine depen

30 Expression of recombinant apoA-V in hepatocarcinoma cells results in increased lipid droplet

31 sly identified lack of PE methyltransferase, hepatocarcinoma cells were found to lack the abilities t

32 o the CDP-choline pathway remained intact in hepatocarcinoma cells, contribution of choline to PE met

33 In hepatoma/hepatocarcinoma cells, up-regulated FGFR3-IIIb conferred

34 of mitochondrial membrane potential in HepG2 hepatocarcinoma cells.

35 ivity after the knockdown of 19 599 genes in hepatocarcinoma cells.

36 replicon with a luciferase reporter in human hepatocarcinoma cells.

37 r, in murine hepatocyte-like cells and human hepatocarcinoma cells.

38 se 9 (CDK9) on gamma-FBG expression in HepG2 hepatocarcinoma cells.

39 pha or lipopolysaccharide in macrophages and hepatocarcinoma cells.

40 activates ferritin H transcription in HepG2 hepatocarcinoma cells.

41 ble of stimulating the 2D5 promoter in HepG2 hepatocarcinoma cells.

42 nt manner, suggesting a silencer function in hepatocarcinoma cells.

43 o the growth inhibitory effect of TGFbeta in hepatocarcinoma cells.

44 n (HBx) plays a critical role in HBV-related hepatocarcinoma development.

45 hIP assays in breast SkBr3, colorectal LoVo, hepatocarcinoma HepG2 cancer cells, and breast cancer-as

46 ouse primary hepatocytes as well as in human hepatocarcinoma HepG2 cells.

47 NA expression and protein synthesis in human hepatocarcinoma HepG2 cells.

48 when tested at the cellular level with human hepatocarcinoma (HepG2) cells as target cells.

49 mployed to study phenolic antioxidants using hepatocarcinoma (HepG2) cells, quercetin showed antioxid

50 into LMH, normal rat kidney (NRK) and human hepatocarcinoma (HepG2) cells.

51 issive Chinese hamster ovary (CHO), in human hepatocarcinoma (HepG2), and to a lesser extent in human

52 ll lines: human colon cancer (Caco-2), human hepatocarcinoma (HepG2), human endothelial (EA.hy926) an

53 siRNA into cancer cell lines including human hepatocarcinoma (Huh-7), human lung adenocarcinoma (A549

54 for oxidizing palmitate was limited to human hepatocarcinoma Huh7 cells and to C2C12 mouse myoblasts

55 Treatment with TAM has been known to promote hepatocarcinoma in rats, but toremifene (TOR), a chlorin

56 Antimicrobial lectins, particularly hepatocarcinoma-intestine-pancreas/pancreatic-associated

57 fied a type 1 diabetes-related cDNA encoding hepatocarcinoma-intestine-pancreas/pancreatic-associated

58 ied this differentially expressed protein as hepatocarcinoma-intestine-pancreas/pancreatitis-associat

59 s of prostate carcinoma cell line DU 145 and hepatocarcinoma LCI-D35 were orthotopically implanted in

60 transferase (cat) gene activation in chicken hepatocarcinoma (LMH) cells.

61 rential susceptibility to the development of hepatocarcinomas observed after treatment with fibrates.

62 for myeloma and lymphoma cell lines than for hepatocarcinoma or non-activated lymphocytes.

63 ough the only effective drug against primary hepatocarcinoma, the multikinase inhibitor Sorafenib (SF

64 oxidation enzyme knockdown mutants of human hepatocarcinoma to demonstrate its utility for analyzing

65 some proliferation, and after chronic dosing hepatocarcinoma, whereas epidemiological studies suggest