ライフサイエンスコーパス: hepatic tumor

1 N represent effective strategies in reducing hepatic tumor.

2 tumors and eradicated the untreated existing hepatic tumor.

3 liver were examined prior to development of hepatic tumors.

4 .4% of fish were positive for both virus and hepatic tumors.

5 increased the number and size of DEN-induced hepatic tumors.

6 ar of age, 64% of Bhmt(-/-) mice had visible hepatic tumors.

7 N injection and followed for 6-12 months for hepatic tumors.

8 f spontaneous and diethylnitrosamine-induced hepatic tumors.

9 (90)Y microspheres is a novel treatment for hepatic tumors.

10 hepatectomy enabling resection of extensive hepatic tumors.

11 ients undergoing percutaneous RF ablation of hepatic tumors.

12 all models that included mammary, s.c., and hepatic tumors.

13 ce to place the RF needle electrode into the hepatic tumors.

14 ent after radio-frequency ablation in rabbit hepatic tumors.

15 substantially improves the detectability of hepatic tumors.

16 Of 29 patients who had ablation of hepatic tumors adjacent to the diaphragm, five (17%) had

17 infected) woodchucks, 10 with WHV-associated hepatic tumors and 10 without tumors, were cultured by m

18 c biliary mucinous cystic neoplasms are rare hepatic tumors and account for less than 5% of intrahepa

19 es a better prognosis than for other primary hepatic tumors and for secondary hepatic carcinoids.

20 icate that local expression of GM-CSF in the hepatic tumors and prolonged mIL-2 expression are necess

21 TS levels in hepatic tumors and resection margin are independent pred

22 ry, the majority of patients presenting with hepatic tumors are unfortunately not candidates for rese

23 Biliary cystadenoma, a benign hepatic tumor arising from Von Meyenberg complexes, usua

24 Acoustic emission enabled detection of hepatic tumors as small as 3 mm in diameter.

25 y determination of the numbers of high-grade hepatic tumors at 13 months of age.

26 GCIP has little inhibition on the number of hepatic tumors at later stages (40 weeks), hepatocellula

27 Measurements of hepatic tumor attenuation at multidetector CT are reprod

28 lly invasive procedure for the management of hepatic tumors between January 2001 and April 2008.

29 High hepatic tumor burden and liver transaminase levels at ba

30 atment resulted in significant reductions in hepatic tumor burden compared with untreated controls.

31 Liver fibrosis, portal pressure, and hepatic tumor burden in BALB/c.Mdr2(-/-) mice were studi

32 mouse model, and STO-609 treatment regresses hepatic tumor burden in this model.

33 rmance score of less than or equal to 70%, a hepatic tumor burden of greater than or equal to 25%, an

34 The hepatic tumor burden was less and the interval from brea

35 of primary tumor, age at radioembolization, hepatic tumor burden, presence of extrahepatic disease,

36 d RNA and chromatin from insulin-treated rat hepatic tumor cell line expressing human insulin recepto

37 In hepatic tumor cells derived from Tet-O-MYC mice, the exp

38 s detected in a lymph node initially and the hepatic tumor cells subsequently.

39 vation led to the spontaneous development of hepatic tumors composed of cells with cancer stem cell c

40 stribution in the targeted liver tissues and hepatic tumors confirmed with MRI and CT imaging.

41 ACE is an effective treatment for inoperable hepatic tumors, especially hypervascular tumors such as

42 e NK cell-dependent destruction of a primary hepatic tumor following infection with an attenuated int

43 procedure known to accelerate the growth of hepatic tumor, following tumor challenge.

44 ironment of the hepatic parenchyma regulates hepatic tumor formation from transplanted neoplastic cel

45 In contrast to the situation in the rat, hepatic tumor formation in the mouse was not accompanied

46 nal level of 22% markedly inhibited (by 75%) hepatic tumor formation in these transgenic mice.

47 whereas BAMBI and PLK1 were overexpressed in hepatic tumors from X/c-myc bitransgenics and WHV-infect

48 observations suggest that the regression of hepatic tumors from young rats was the direct result of

49 n cell culture, in s.c. tumor grafts, and in hepatic tumor grafts.

50 Hepatic tumors grew more quickly in B7-DC KO mice, assoc

51 es showed that gammaIFN decreases metastatic hepatic tumor growth by stimulating Kupffer cells (KC).

52 nd c-myc transgenes in the liver accelerated hepatic tumor growth in both the presence and absence of

53 gineered to secrete GM-CSF or IL-2 decreases hepatic tumor growth, and whether stimulation of both ma

54 r of hepatic tumors >1 (p = 0.0004), largest hepatic tumor >5 cm (p = 0.01), and carcinoembryonic ant

55 metastases <12 months (p = 0.03), number of hepatic tumors >1 (p = 0.0004), largest hepatic tumor >5

56 In vivo, the hepatic tumors had a lower percentage injected dose per

57 erformed in 65 rabbits, 38 of which had VX-2 hepatic tumor implants.

58 y, NK cell-mediated destruction of a primary hepatic tumor in infected mice led to long-lived CD4- an

59 ignaling pathways can explain the absence of hepatic tumors in AAV-NT mice.

60 n inducing surgical resectability of primary hepatic tumors in children.

61 his study from the International Registry of Hepatic Tumors in Liver Transplantation is to analyze th

62 trial, in 1992 an International Registry of Hepatic Tumors in Liver Transplantation was established

63 th, whereas the persistence and expansion of hepatic tumors in old rats was related to increased cell

64 in hepatic tumors in young rats relative to hepatic tumors in old rats.

65 The prevalence of hepatic tumors in these fish was 4.9%, and only 2.4% of

66 reased apoptotic cell death were detected in hepatic tumors in young rats relative to hepatic tumors

67 By 40 weeks, hepatic tumor incidence was 100%/75% (17%/0%) and 44%/17

68 , we used several transgenic mouse models of hepatic tumors induced by overexpression of c-myc in the

69 The Children's Hepatic tumor International Collaborative (CHIC) effort

70 we formed a global coalition, the Children's Hepatic tumors International Collaboration (CHIC), with

71 iver malignancies with no or negligible left-hepatic tumor involvement who were treated by right-loba

72 Hepatic tumor load before liver transplantation, time fr

73 , variant vasculature, tumor encasement, and hepatic tumor localization for presurgical planning.

74 irus and provided an anatomical reference of hepatic tumor localization.

75 essor region (-850) and core promoter of the hepatic tumor marker alpha-fetoprotein (AFP) gene.

76 Fifteen hepatic tumors (mean diameter, 2.9 cm) in 12 patients we

77 It is feasible to quantify reduction of hepatic tumor metabolism objectively after (90)Y treatme

78 Liver tissue was also prepared to quantitate hepatic tumor necrosis factor (TNF) mRNA and processed f

79 ely correlated with transaminase release and hepatic tumor necrosis factor alpha (TNF-alpha) expressi

80 Moreover, ethanol elevated hepatic tumor necrosis factor alpha (TNF-alpha) messenge

81 mmation, which were accompanied by increased hepatic tumor necrosis factor alpha (TNF-alpha; P < 0.00

82 is and hepatitis, characterized by increased hepatic tumor necrosis factor alpha levels and activatio

83 y glutathione depletion virtually eliminated hepatic tumor necrosis factor alpha responses to both E.

84 ydroxynonenal protein adducts, expression of hepatic tumor necrosis factor alpha, and resulted in hep

85 Levels of serum alanine aminotransferase and hepatic tumor necrosis factor alpha, indicators of hepat

86 ges, serum alanine transferase activity, and hepatic tumor necrosis factor-alpha in both metallothion

87 le electroporation (IRE) in the treatment of hepatic tumors not suitable for thermal ablation (radiof

88 Hepatic tumors often recur in the liver after surgical r

89 c coiled-coil protein 3 (TACC3), colonic and hepatic tumor overexpressed gene (ch-TOG), and clathrin

90 uction of both clathrin and ch-TOG (colonic, hepatic tumor overexpressed gene) at metaphase centrosom

91 he microtubule polymerase chTOG (colonic and hepatic tumor overexpressed gene), play a crucial functi

92 We show here that colonic-hepatic tumor-overexpressed gene (ch-TOGp) is an abundan

93 Multiple hepatic tumors (P < 0.001), regional nodal involvement (

94 ction (lobectomy or more), gender, number of hepatic tumors, primary cancer site (colon vs. rectum),

95 ic organochlorine pesticide that is a rodent hepatic tumor promoter, with inconclusive carcinogenicit

96 Twelve patients with primary and metastatic hepatic tumors received 30 treatments (mean, 2.5 per pat

97 leukin (mIL)-2 genes resulted in substantial hepatic tumor regression, induced an effective systemic

98 the treated animals eventually succumbed to hepatic tumor relapse or distant metastases.

99 Hepatic tumor RFA can be performed with low mortality an

100 ys after) complication rates associated with hepatic tumor RFA.

101 e proliferation and promotion of DEN-induced hepatic tumors secondary to aberrant c-Myc activation.

102 enograft models that do not recapitulate the hepatic tumors seen in patients.

103 Many hepatic tumors such as hepatocellular adenomas, hepatoce

104 Although DDT is known to cause rodent hepatic tumors, the marked species differences in PXR/CA

105 There is persistent uptake of [125I]IUdR in hepatic tumors, thereby making hepatic artery infusion a

106 By immunohistochemical staining of hepatic tumor tissue from 155 patients, the expression o

107 Autophagy is required for benign hepatic tumors to progress into malignant hepatocellular

108 Pre-established hepatic tumors treated with a recombinant adenoviral vec

109 The PET-based median ratio of hepatic tumor uptake to normal-liver uptake was 3.9 (ran

110 cells resulted in a significant reduction of hepatic tumor volumes (P < 0.04).

111 o 6 months before randomization, and 33% had hepatic tumor volumes greater than 25%.

112 Hepatic tumors were characterized for histology, prolife

113 Hepatic tumors were established by direct injection with

114 icide gene cytotoxicity in vitro, multifocal hepatic tumors were established in syngeneic mice with m

115 unless extrahepatic disease or unresectable hepatic tumors were found.

116 and frequent decrease in GRB14 expression in hepatic tumors when compared to adjacent nontumoral pare

117 hanced US and MR imaging in the detection of hepatic tumors, whereas contrast-enhanced US had the hig

118 However, hepatic tumors which developed in TGF-alpha/c-myc mice e

119 oved intraprocedural depiction of peripheral hepatic tumors while achieving a slight radiation exposu

120 nd typically appeared as a large symptomatic hepatic tumor with clinical, laboratory, and CT features

121 providing a growth advantage in a subset of hepatic tumors with a more differentiated phenotype.

122 ly 40% of the Txnip-deficient mice developed hepatic tumors with an increased prevalence in male mice

123 olutionized the surgical management of large hepatic tumors with insufficient future liver remnant (F

124 Past studies have identified hepatic tumors with mixed hepatocellular carcinoma (HCC)

125 es, including male-predominant steatosis and hepatic tumors with up-regulation of protein kinase B an