Disease relevance of Hepatoblastoma

• In this study, we show that dimethylsulfoxide (DMSO)-treated HepG2 hepatoblastoma cells are infected efficiently by serum-derived hepatitis B virus (HBV) as monitored by viral gene expression and replication markers [1].
• We have compared the expression of two of these variants (V1 and V3) in several human fetal and postnatal tissues (including liver) as well as in hepatoblastomas (HBs) and hepatocellular carcinomas (HCCs) [2].
• MDM2 amplification could not be detected in specimens from 40 Wilms' tumors, 15 neuroblastomas, 12 sarcomas, or 4 hepatoblastomas tested [3].
• The molecular pathogenesis of hepatoblastomas in the B6C3F1 mouse is unclear but may involve alterations in the beta-catenin/Wnt signaling pathway as was recently described for chemically induced hepatocellular neoplasms and human liver cancers [4].
• CYP1A1 is induced by TCDD to high levels (45-fold increase) in the human hepatoblastoma line HepG2 as compared with the human renal adenocarcinoma line ACHN [5].

High impact information on Hepatoblastoma

• In coculture experiments, HepG2 hepatoblastoma cells, expressing CD95L mRNA after treatment with cytostatic drugs, killed CD95+ Jurkat lymphocytes [6].
• This increase in plasma apo A-II was due to a direct effect on hepatic apo A-II production, since fenofibric acid induced apo A-II mRNA levels to 450 and 250% of control levels in primary cultures of human hepatocytes and in human hepatoblastoma HepG2 cells respectively [7].
• Bile acid synthesis by long-term cultured cell line established from human hepatoblastoma [8].
• Next, 7 of 10 hepatoblastomas displayed simultaneous beta-catenin and epidermal growth factor receptor up-regulation, thus suggesting a strong relationship between these 2 proteins in tumors [9].
• BACKGROUND & AIMS: Wnt/beta-catenin pathway activation occurs during liver growth in hepatoblastomas, hepatocellular cancers, and liver regeneration [10].

Chemical compound and disease context of Hepatoblastoma

• CONCLUSIONS: These findings provide evidence that FAEE are toxic for intact human hepatoblastoma cells and that they or their metabolites may be an important causative agent in ethanol-induced liver damage [11].
• Menadione metabolism to thiodione in hepatoblastoma by scanning electrochemical microscopy [12].
• Cisplatin, doxorubicin, and delayed surgery for childhood hepatoblastoma: a successful approach--results of the first prospective study of the International Society of Pediatric Oncology [13].
• Cisplatin, vincristine, and fluorouracil therapy for hepatoblastoma: a Pediatric Oncology Group study [14].
• Promotion of N-nitrosodiethylamine-initiated hepatocellular tumors and hepatoblastomas by 2,3,7,8-tetrachlorodibenzo-p-dioxin or Aroclor 1254 in C57BL/6, DBA/2, and B6D2F1 mice [15].

Biological context of Hepatoblastoma

• Overexpression of cDNA derived combinations of the nuclear proteins Jun and Fos or Jun and Fra1 repressed hARE-mediated chloramphenicol acetyltransferase (CAT) gene expression in transfected human hepatoblastoma (Hep-G2) cells [16].
• Role of NAD(P)H oxidase in the tamoxifen-induced generation of reactive oxygen species and apoptosis in HepG2 human hepatoblastoma cells [17].
• Atrial natriuretic peptide induces cell death in human hepatoblastoma (HepG2) through the involvement of NADPH oxidase [18].
• Structural analysis of the CDKN2A, CDKN2B, and CDKN2C genes in hepatoblastoma cases showed the absence of deletions and/or point mutations [19].
• We suggest that HGF promotes cell survival in hepatocyte-derived cell lines (HCC, hepatoblastoma, and embryonic hepatocyte) from Fas-mediated cell death via Fas-DISC suppression as a result of Akt activation [20].

Anatomical context of Hepatoblastoma

• Regulation of erythropoietin production in a human hepatoblastoma cell line [21].
• alpha IR-3 is a mouse monoclonal antibody that binds to an epitope on the human insulin-like growth factor I (IGF-I) receptor and inhibits [125I]IGF-I binding to this receptor on human skin fibroblasts (HSF) and Hep G2 human hepatoblastoma cells [22].
• In addition to staining of endothelium, one of the two small cell hepatoblastomas exhibited strong immunoreactivity of the tumour cells for CD34 [23].
• The diagnoses in the remaining 42 cases were hepatoblastoma (27), hepatocellular carcinoma (3), rhabdomyosarcoma (6), rhabdoid tumour (3) and yolk sac tumour (3) [24].
• Maturation of peroxisomes in differentiating human hepatoblastoma cells (HepG2): possible involvement of the peroxisome proliferator-activated receptor alpha (PPAR alpha) [25].

Gene context of Hepatoblastoma

• Messenger RNA (mRNA) analysis showed that CDKN2C is expressed in all hepatoblastoma samples studied, while both CDKN2A and CDKN2B genes are not transcribed in the cancer specimens as well as in the matched normal liver tissues [19].
• These results show that CDKN2A gene family alterations are not involved in hepatoblastoma development, whereas changes in cyclin D types might play a role in this type of tumor [19].
• p57(KIP2) is not mutated in hepatoblastoma but shows increased transcriptional activity in a comparative analysis of the three imprinted genes p57(KIP2), IGF2, and H19 [26].
• Furthermore, SHBG alleles within the general population contain at least 6-10 TAAAA repeats, and the transcriptional activity of a human SHBG promoter-luciferase reporter construct containing 6 TAAAA repeats was significantly lower than for similar reporter constructs containing 7-10 TAAAA repeats when tested in human HepG2 hepatoblastoma cells [27].
• Large variations were noticed for expression of the NQO2 and NQO1 genes among various tissues, 1336 bp of the 5'-flanking region of the NQO2 gene containing ARE and XRE was found sufficient to increase expression of the CAT gene in response to beta-naphthoflavone and tCDD in transfected human hepatoblastoma (Hep-G2) cells [28].
• In vitro, PI3K inhibition diminished hepatoblastoma cell growth being accompanied by reduced AKT and GSK-3beta phosphorylation [29].

Analytical, diagnostic and therapeutic context of Hepatoblastoma

• Effective treatment of unresectable or metastatic hepatoblastoma with cisplatin and continuous infusion doxorubicin chemotherapy: a report from the Childrens Cancer Study Group [30].
• Recurrence of hepatocellular carcinoma as a mixed hepatoblastoma after liver transplantation [31].
• Indications for LTx were oxalosis (four), congenital hepatic fibrosis (two), cystinosis (one), polycystic liver disease (one), A-1-A deficiency (one), Total Parenteral Nutrition (TPN)-related (one), cryptogenic cirrhosis (one), and hepatoblastoma (one) [32].
• Northern blot analysis shows the presence of one NQO2 mRNA of 1.2 kb in control and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treated human hepatoblastoma Hep-G2 cells and that TCDD treatment does not lead to enhanced levels of NQO2 mRNA as it does for NQO1 mRNA [33].
• Taq1 digestion of PCR products revealed that both alleles were transcribed in all samples where both were present at the genomic level, indicating that the RRM1 locus is not subjected to imprinting in Wilms' tumour or hepatoblastoma [34].

References