ライフサイエンスコーパス: hepatoblastoma

1 the majority of patients with advanced-stage hepatoblastoma.

2 egimen B) improved survival in children with hepatoblastoma.

3 ons with the growth advantage to progress to hepatoblastoma.

4 e in the development of Wilms tumor (WT) and hepatoblastoma.

5 emoembolization (TACE) in treating pediatric hepatoblastoma.

6 ent in the more complex or advanced types of hepatoblastoma.

7 plays a key role in successful treatment for hepatoblastoma.

8 local therapy for patients with unresectable hepatoblastoma.

9 is part two of a two-part state of the art--hepatoblastoma.

10 icular focus on the histological subtypes of hepatoblastoma.

11 comes when compared with other patients with hepatoblastoma.

12 ent alternative for small infants with large hepatoblastoma.

13 cisplatin was the most active agent against hepatoblastoma.

14 in children with unresectable or metastatic hepatoblastoma.

15 a sets to examine perinatal risk factors for hepatoblastoma.

16 bility to Wilms' tumor, rhabdomyosarcoma and hepatoblastoma.

17 tumors, notably fibrolamellar carcinoma and hepatoblastoma.

18 ribute to tumor development in children with hepatoblastoma.

19 , but bear a close molecular pathogenesis to hepatoblastomas.

20 to other infantile embryonal tumors such as hepatoblastomas.

21 n protein accumulation in chemically induced hepatoblastomas.

22 in the number of hepatocellular adenomas and hepatoblastomas.

23 us correlates with differentiation status in hepatoblastomas.

24 CCND1 is correlated with the age of onset of hepatoblastomas.

25 0 neuroblastomas, 12 of 16 melanomas, 3 of 4 hepatoblastomas, 7 of 8 Wilms' tumors, 3 of 3 rhabdoid t

26 examined this CCND1polymorphism in a series hepatoblastoma, a childhood liver cancer that shares oth

27 idelines for the diagnosis and management of hepatoblastoma, a rare pediatric liver tumor.

28 : For patients with hepatoblastoma, a timely and complete resection of the t

29 Among children less than 5 years of age, hepatoblastoma accounted for 91% of primary hepatic mali

30 ere low in Wilms' tumors (19%) and absent in hepatoblastomas, acute leukemias, osteosarcomas, Ewing's

31 ement of selected children with unresectable hepatoblastoma, an almost opposite strategy was proposed

32 PC) gene are at increased risk of developing hepatoblastoma, an embryonal form of liver cancer, sugge

33 orectal metastases, and one patient each for hepatoblastoma and cholangiocarcinoma.

34 ed for patients with stage I-UH and stage II hepatoblastoma and for subsets of patients with stage II

35 28B overexpression is sufficient to initiate hepatoblastoma and hepatocellular carcinoma in murine mo

36 of age, of which 184 (67%) and 83 (31%) were hepatoblastoma and hepatocellular carcinoma, respectivel

37 ects for two ongoing case-control studies of hepatoblastoma and infant leukemia.

38 Increased risks of hepatoblastoma and rhabdomyosarcoma were detected, but t

39 Overexpression of AP2 in HepG2 human hepatoblastoma and SW480 human colon adenocarcinoma cell

40 e identified in all 19 anthraquinone-induced hepatoblastomas and all 8 oxazepam-induced hepatoblastom

41 activation developed HCC and, in some cases, hepatoblastomas and lung metastases.

42 the cellular etiology and biology of HCC and hepatoblastomas and the development of improved therapeu

43 emia, 1 Hodgkin disease, 8 leiomyosarcoma, 1 hepatoblastoma, and 1 schwannoma.

44 ular carcinoma has worse survival rates than hepatoblastoma, and its incidence has not increased.

45 ukemia, infant acute lymphoblastic leukemia, hepatoblastoma, and malignant brain tumors had the highe

46 months), who were assessed with unresectable hepatoblastoma, and whose pretreatment extent-of-disease

47 detected Lin28b overexpression in MYC-driven hepatoblastomas, and liver-specific deletion of Lin28a/b

48 atocellular carcinomas, cholangiocarcinomas, hepatoblastomas, and osteogenic sarcomas), individual li

49 usly reported, MYC-expressing mice exhibited hepatoblastoma- and hepatocellular carcinoma-like tumors

50 When feasible, surgical resection of hepatoblastoma at diagnosis, without chemotherapy, can i

51 Children with completely resected PFH hepatoblastoma can achieve long-term survival without ad

52 Hepatoblastoma cases (n = 58) diagnosed between 1985 and

53 actor alpha (TNF-alpha) stimulation in human hepatoblastoma cell line (HepG2) cells and primary hepat

54 To test this idea, HepG2 2.2.15, a human hepatoblastoma cell line that constitutively produces in

55 HBV replication in HepG2 cells, a human hepatoblastoma cell line, is stimulated 5- to 10-fold by

56 wild-type HBV was observed in HepG2, a human hepatoblastoma cell line.

57 totoxicity evaluation against HepG2, a human hepatoblastoma cell line.

58 Mutant human hepatoblastoma cell lines resistant to copper toxicity w

59 ivity than a control promoter in all CRC and hepatoblastoma cell lines tested, with low activities in

60 iption varied considerably among the CRC and hepatoblastoma cell lines.

61 nce the expression of multiple genes in this hepatoblastoma cell through its actions on events that a

62 machine containing a biomass derived from a hepatoblastoma cell-line cultured as three dimensional o

63 Similarly, WRL68 and HepG2 hepatoblastoma cells expressing low DNMT1 basal levels a

64 of decellularized scaffolds were seeded with hepatoblastoma cells for cytotoxicity testing or implant

65 ection and overexpression of hIRS-1 in human hepatoblastoma cells in vitro leads to the constitutive

66 Hepatoblastoma cells transfected with HBV were subjected

67 rase-expressing cell line derived from human hepatoblastoma cells) or in vitro in rabbit reticulocyte

68 xpression library generated with HepG2 human hepatoblastoma cells, and a complete cDNA, generated by

69 y and transiently transfected cultured human hepatoblastoma cells.

70 by inhibitor (IkappaB) proteolysis in HepG2 hepatoblastoma cells.

71 HBV inhibitor, while being nontoxic to human hepatoblastoma cells.

72 ment for unresectable unifocal or multifocal hepatoblastoma confined to the liver.

73 8.82 cases per 1 million person-years), with hepatoblastoma developing in 6 children and rhabdomyosar

74 t mutations, the pattern of mutations in the hepatoblastomas did not differ from that identified in h

75 Next, 7 of 10 hepatoblastomas displayed simultaneous beta-catenin and

76 the majority of colorectal cancers (CRC) and hepatoblastomas due to either an APC or beta-catenin gen

77 d hepatoblastomas and all 8 oxazepam-induced hepatoblastomas examined.

78 xpressing full-length beta-catenin and fetal hepatoblastomas expressing beta-catenin lacking its N te

79 n and differentiation status, with embryonal hepatoblastomas expressing full-length beta-catenin and

80 gy Group CureSearch grant contributed by the Hepatoblastoma Foundation; Practical Research for Innova

81 ts assessable for response, one patient with hepatoblastoma had a complete response, with partial res

82 Although several hepatoblastomas had multiple deletion and/or point mutat

83 The outcome of treatment for advanced hepatoblastoma has recently improved after the introduct

84 International collaborative efforts in hepatoblastoma have led to a new international histopath

85 International collaborative efforts in hepatoblastoma have led to increased refinements in the

86 llular adenomas, hepatocellular cancers, and hepatoblastomas have mutations in CTNNB1 that result in

87 of lung nodules in children with metastatic hepatoblastoma (HB) correlates with outcome.

88 Hepatoblastoma (HB) is a rare malignant liver tumor whic

89 ng the most common liver cancer in children, hepatoblastoma (HB) is a rare neoplasm.

90 Hepatoblastoma (HB) is associated with aberrant activati

91 rently, preclinical testing of therapies for hepatoblastoma (HB) is limited to subcutaneous and intra

92 Hepatoblastoma (HB) is the most common primary liver can

93 To analyze the outcome of hepatoblastoma (HB) patients presenting with post treatm

94 dren with primary unresectable or metastatic hepatoblastoma (HB) to investigate possible prognostic c

95 mixed tumors with hepatocellular adenoma and hepatoblastoma (HB) were also frequently observed.

96 Six patients with hepatoblastoma (HB), three with hepatocellular carcinoma

97 opment of hepatocellular carcinoma (HCC) and hepatoblastoma (HB).

98 y has improved the survival of patients with hepatoblastoma (HB).

99 Hepatoblastoma (HBL) and hepatocellular cancer (HCC) are

100 Hepatoblastoma (HBL), the most common childhood liver ca

101 atient-derived xenografts (PLC-PDXs) from 20 hepatoblastomas (HBs), 1 transitional liver cell tumor (

102 fection/over expression experiments in human hepatoblastoma (Hep-G2) cells demonstrated that mutant N

103 The overexpression of c-Maf in human hepatoblastoma (Hep-G2) cells led to the repression of A

104 e (CAT) gene expression in transfected human hepatoblastoma (Hep-G2) cells.

105 way activation occurs during liver growth in hepatoblastomas, hepatocellular cancers, and liver regen

106 both primary mouse hepatocytes and the human hepatoblastoma HepG2 cell line by lactate dehydrogenase

107 s substantial levels of enhancer activity in hepatoblastoma HepG2 cells and that sites A and B are oc

108 In this study expression of E1A 12Sor 13S in hepatoblastoma HepG2 cells repressed apoAI enhancer acti

109 ian cancer cell lines SKOV3 and EFO21, human hepatoblastoma HepG2 cells, and rat neuroblastoma B35 ce

110 example, monkey kidney CV-1 cells and human hepatoblastoma HepG2 cells, but not mouse neuroblastoma

111 on of various transcription factors in human hepatoblastoma HepG2 cells.

112 xposure of mouse hepatoma (Hepa-1) and human hepatoblastoma (HepG2) cells to antioxidant tert-butylhy

113 thin 0.5 h of antioxidant treatment in human hepatoblastoma (HepG2) cells, Fyn exports out of the nuc

114 X2), hepatocellular carcinoma (Sk-Hep-1) and hepatoblastoma (HepG2), with excellent viability, motili

115 erations in hepatocellular carcinomas (HCC), hepatoblastomas (HPBL), tissue adjacent to HCC and norma

116 The molecular pathogenesis of hepatoblastomas in the B6C3F1 mouse is unclear but may i

117 erent types of the heterogeneous spectrum of hepatoblastoma, in terms of different chemotherapeutic p

118 Hepatoblastoma is a rare embryonal tumor with unknown et

119 Hepatoblastoma is the most common malignant liver tumor

120 ildren less than 5 years of age, also, where hepatoblastoma is the predominant primary hepatic malign

121 n Bog is continuously overexpressed and form hepatoblastoma-like tumours when transplanted into nude

122 diatric tumors--Wilms' tumor, neuroblastoma, hepatoblastoma, medulloblastoma, rhabdomyosarcoma, osteo

123 5), gastrointestinal stromal tumor (n = 2), hepatoblastoma (n = 2), and squamous cell carcinoma in 1

124 oach to risk stratification in children with hepatoblastoma on the basis of rigorous statistical inte

125 oach to risk stratification in children with hepatoblastoma on the basis of rigorous statistical inte

126 ated (one), cryptogenic cirrhosis (one), and hepatoblastoma (one).

127 One patient each with hepatoblastoma or desmoplastic small round cell tumor ac

128 As a rare pediatric tumor, hepatoblastoma presents challenges to the individual pra

129 tment failure for patients with stage III/IV hepatoblastoma randomized to either C5V or CC.

130 es, between 1973 and 1977 and 1993 and 1997, hepatoblastoma rates increased (0.6 to 1.2/1,000,000, re

131 associated with a strongly increased risk of hepatoblastoma (relative risk (RR) = 56.9, 95% confidenc

132 HCC and hepatoblastomas resembled their human counterparts histo

133 al-specific beta-catenin antibodies on human hepatoblastomas revealed a correlation between full-leng

134 One patient with hepatoblastoma showed a dramatic biomarker response.

135 In a majority of the hepatoblastomas (six of seven) examined by immunohistoch

136 International hepatoblastoma specialists were brought together to high

137 It was associated with an increased risk of hepatoblastoma (standardized incidence ratio, 3.64; 95%

138 etermined in an analysis of 84 children with hepatoblastoma that the G/A exon 4 polymorphism in CCND1

139 The survival of children with hepatoblastoma, the most common malignant tumor of the l

140 Children with pure fetal histology (PFH) hepatoblastoma treated with complete surgical resection

141 ssessment of treatment results in paediatric hepatoblastoma trials has been hampered by small patient

142 m 1605 children treated in eight multicentre hepatoblastoma trials over 25 years.

143 reatment of MYC-dependent mouse lymphoma and hepatoblastoma tumors decreased tumor growth and prolong

144 ere delivered to LAP-MYC mice, which develop hepatoblastoma, using lipid nanoparticles.

145 Five-year survival for hepatoblastoma was 52%, compared with 18% for hepatocell

146 The excess risk of hepatoblastoma was associated with low birth weight.

147 Overall, oxphos activity in KO livers and hepatoblastoma was comparable with that of control count

148 birth weight, a moderately increased risk of hepatoblastoma was found for younger maternal age (<20 y

149 aired, and growth of aggressive experimental hepatoblastomas was only modestly slowed in the face of

150 Twelve patients with initially unresectable hepatoblastoma were enrolled in the study.

151 ), stage III (n = 83), and stage IV (n = 40) hepatoblastoma were randomized to receive regimen A (n =

152 ocedure in a small infant (54 days old) with hepatoblastoma who presented with insufficient FLR.

153 tidisciplinary approach to the management of hepatoblastoma, with thoughtful collaboration between pe