ライフサイエンスコーパス: hepatoblastoma

1 ribute to tumor development in children with hepatoblastoma.

2 the majority of patients with advanced-stage hepatoblastoma.

3 egimen B) improved survival in children with hepatoblastoma.

4 ons with the growth advantage to progress to hepatoblastoma.

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

6 remains the most active single agent against hepatoblastoma.

7 ent alternative for small infants with large hepatoblastoma.

8 ng individuals with high-risk and metastatic hepatoblastoma.

9 tumors, notably fibrolamellar carcinoma and hepatoblastoma.

10 ntial therapeutic targets in human high-risk hepatoblastoma.

11 emoembolization (TACE) in treating pediatric hepatoblastoma.

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

13 plays a key role in successful treatment for hepatoblastoma.

14 local therapy for patients with unresectable hepatoblastoma.

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

16 icular focus on the histological subtypes of hepatoblastoma.

17 comes when compared with other patients with hepatoblastoma.

18 cisplatin was the most active agent against hepatoblastoma.

19 in children with unresectable or metastatic hepatoblastoma.

20 a sets to examine perinatal risk factors for hepatoblastoma.

21 bility to Wilms' tumor, rhabdomyosarcoma and hepatoblastoma.

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

23 , but bear a close molecular pathogenesis to hepatoblastomas.

24 to other infantile embryonal tumors such as hepatoblastomas.

25 n protein accumulation in chemically induced hepatoblastomas.

26 in the number of hepatocellular adenomas and hepatoblastomas.

27 us correlates with differentiation status in hepatoblastomas.

28 oblastoma (10.7%; 95% CI, 3.8% to 21.7%) and hepatoblastoma (16.2%; 95% CI, 8.6% to 26.0%) survivors.

29 0 neuroblastomas, 12 of 16 melanomas, 3 of 4 hepatoblastomas, 7 of 8 Wilms' tumors, 3 of 3 rhabdoid t

30 and spatial transcriptomics to characterize hepatoblastoma, a childhood liver cancer that exhibits s

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

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

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

34 ndation for administration in non-metastatic hepatoblastoma, a weak recommendation for administration

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

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

37 1 to <3 years; HR, 4.59; 95% CI, 2.37-8.91), hepatoblastoma (age 1 to <3 years; HR, 7.10; 95% CI, 2.7

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

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

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

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

42 28B overexpression is sufficient to initiate hepatoblastoma and hepatocellular carcinoma in murine mo

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

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

45 r tumors from FLC, hepatocellular carcinoma, hepatoblastoma and intrahepatic cholangiocarcinoma are a

46 consisted solely of patients with localised hepatoblastoma and no effects on survival were shown.

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

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

49 essential to address refractory or recurrent hepatoblastoma and to increase the overall survival of p

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

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

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

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

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

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

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

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

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

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

60 Screening protocols for hepatoblastoma are recommended for children with predisp

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

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

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

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

65 ines (Huh7, Hep3B, SNU182, and SNU449) and 1 hepatoblastoma cell line (HepG2) using Western blotting

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

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

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

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

70 Mutant human hepatoblastoma cell lines resistant to copper toxicity w

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

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

73 ) kinases, specifically PIM3, play a role in hepatoblastoma cell proliferation and tumor growth and m

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

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

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

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

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

79 with AZD1208 sensitizes cisplatin-resistant hepatoblastoma cells to cisplatin, enhances cisplatin-me

80 Hepatoblastoma cells transfected with HBV were subjected

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

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

83 Here, we review recent findings in pediatric hepatoblastoma cells, tumor-associated cell types, and g

84 y and transiently transfected cultured human hepatoblastoma cells.

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

86 e the proliferation of neighboring embryonal hepatoblastoma cells.

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

88 iptomics identify distinct subpopulations of hepatoblastoma cells.

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

90 8.82 cases per 1 million person-years), with hepatoblastoma developing in 6 children and rhabdomyosar

91 e cohort study of 96 pediatric patients with hepatoblastoma diagnosed and treated between June 1, 200

92 Medical imaging is crucial for hepatoblastoma diagnosis and staging, with abdominal ult

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

94 d received no previous chemotherapy or other hepatoblastoma-directed therapy.

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

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

97 identify druggable targets shared with human hepatoblastoma (e.g., CDK7, CDK9, PRMT1, PRMT5).

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

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

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

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

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

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

104 Despite increasing incidence, treatment for hepatoblastoma has not changed significantly over the pa

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

106 Early genomic studies revealed that hepatoblastoma has the lowest mutational burden of any h

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

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

109 out a third of newly diagnosed patients with hepatoblastoma have resectable disease at diagnosis.

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

111 Management of unresectable pediatric hepatoblastoma (HB) and hepatocellular carcinoma (HCC) r

112 n in many hepatocellular carcinoma (HCC) and hepatoblastoma (HB) cases.

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

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

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

116 Hepatoblastoma (HB) is associated with aberrant activati

117 Chemoresistant hepatoblastoma (HB) is associated with poor outcomes.

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

119 Hepatoblastoma (HB) is the most common malignant liver t

120 Hepatoblastoma (HB) is the most common pediatric liver c

121 ough rare compared with adult liver cancers, hepatoblastoma (HB) is the most common pediatric liver m

122 Hepatoblastoma (HB) is the most common pediatric liver m

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

124 Hepatoblastoma (HB) is the most common primary liver mal

125 Hepatoblastoma (HB) is the predominant form of pediatric

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

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

128 all cell undifferentiated (SCU) histology in hepatoblastoma (HB) tumors has historically been associa

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

130 ances, the 5-year survival rate for stage IV hepatoblastoma (HB), the predominant pediatric liver tum

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

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

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

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

135 Hepatoblastoma (HBL) is a devastating pediatric liver ca

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

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

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

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

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

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

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

143 C3A is a subclone of the human hepatoblastoma HepG2 cell line with strong contact inhib

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

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

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

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

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

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

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

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

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

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

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

155 ygosity (LOH) at chromosome 11p15.5 may be a hepatoblastoma-initiating event, as clonal expansion of

156 Hepatoblastoma is a rare embryonal tumor with unknown et

157 Hepatoblastoma is the most common malignant liver tumor

158 Hepatoblastoma is the most common pediatric liver cancer

159 Hepatoblastoma is the most common pediatric liver malign

160 Hepatoblastoma is the most common primary liver cancer i

161 Pediatric hepatoblastoma is the most common primary liver cancer i

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

163 while beneficial when used in standard risk hepatoblastoma, is associated with reduced survival in d

164 ollowing tissues: suspected or actual HCC or hepatoblastoma lesions, non-tumor-bearing liver, renal c

165 Here, we report an improved MYC-driven hepatoblastoma-like murine model that recapitulates the

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

167 cell lines (Huh7, Hep3B, SNU182, SNU449), 1 hepatoblastoma line (HepG2), and a CD24+ colorectal canc

168 Patients with advanced hepatoblastoma may require liver transplantation.

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

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

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

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

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

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

175 en with a primary hepatic malignancy such as hepatoblastoma or hepatocellular carcinoma.

176 In pediatric patients with sarcomas, hepatoblastomas, or other types of primary tumors, lung

177 and cell lines hampers our understanding of hepatoblastoma pathogenesis and the development of new t

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

179 oncogenic B-catenin, significantly regresses hepatoblastoma, providing in vivo data to support YAP1 a

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

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

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

183 can ensure disease control in patients with hepatoblastoma resected at diagnosis.

184 HCC and hepatoblastomas resembled their human counterparts histo

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

186 One patient with hepatoblastoma showed a dramatic biomarker response.

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

188 International hepatoblastoma specialists were brought together to high

189 chniques to analyze resected human pediatric hepatoblastoma specimens, and identify five hepatoblasto

190 Notably, patient-derived hepatoblastoma spheroid cultures predict differential re

191 of Disease (PRETEXT) system is employed for hepatoblastoma staging and for guiding treatment strateg

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

193 eals oncogenes and tumor suppressor genes in hepatoblastoma that engage multiple, druggable cancer si

194 Studies of hepatoblastoma that focus exclusively on tumor cells dem

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

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

197 etic dependencies that will serve to advance hepatoblastoma therapy.

198 y be a promising adjunct in the treatment of hepatoblastoma to effectively target SCLCCs and potentia

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

200 Hepatoblastoma treatment with curative intent requires s

201 Chemotherapy is critical for human hepatoblastoma treatment.

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

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

204 In this work, we define hepatoblastoma tumor heterogeneity with single-cell reso

205 hepatoblastoma specimens, and identify five hepatoblastoma tumor signatures that may account for the

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

207 the homogeneity these studies would suggest, hepatoblastoma tumors have a high degree of heterogeneit

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

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

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

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

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

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

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

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

216 whether event-free survival in children with hepatoblastoma who had complete resection at diagnosis c

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

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

219 e pathological features of embryonal type of hepatoblastoma, with transcriptomics resembling the high

220 had histologically confirmed, stage I or II hepatoblastoma without 100% pure fetal stage I or small-

221 ibe the development of a cisplatin-resistant hepatoblastoma xenograft model of the human HuH6 cell li