hepatoblastoma/tyrosine

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Tyrosine phosphorylation controls nuclear export of Fyn, allowing Nrf2 activation of cytoprotective gene expression.

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Fyn, an Src kinase family member, acts as a negative regulator of NF-E2-related factor 2 (Nrf2). Under stressful conditions, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), activating defensive gene expression. Once Nrf2 completes activation, Fyn

[Diagnostic utility of tyrosine hydroxylase in peripheral neuroblastic tumors].

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Objective: To investigation the diagnostic utility of tyrosine hydroxylase (TH) immunohistochemically as a marker of peripheral neuroblastic tumors(pNT). Methods: The study included 1 024 cases, 643 primary and metastatic pNT cases, 381 non-pNT cases, including small round cell tumors such as

Evaluation of gene expression related to hepatic cell maturation and differentiation in a chemically induced mouse hepatoblastoma cell line.

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The MHB-2 cell line, established from a mouse hepatoblastoma (HB), was subjected to the reverse transcriptase-polymerase chain reaction (RT-PCR) for evaluation of gene expression related to cell differentiation. RNAs for c-kit, CD34, thy-1, albumin, cytokeratin (CK) 8, 18 and 19 could be detected,

Systematic analysis of the molecular mechanism of microRNA-124 in hepatoblastoma cells.

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The present study aimed to identify the molecular mechanisms of microRNA-124 (miRNA-124/miR-124) in hepatoblastoma. The GSE6207 microarray dataset, obtained from the Gene Expression Omnibus database, included samples extracted from HepG2 cells transfected with miR-124 duplex (the experimental group)

Tumor-associated energy homeostasis: hepatoblastoma and neuroblastoma affect glucose and lipid metabolism as well as ghrelin, GLP-1, and PYY in nude rats.

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BACKGROUND The "metabolic competition" for nutrients between cancer cells and the patient has emerged as an important research area. For pediatric oncology, it remains unclear whether the neuroendokrine regulation of appetite by gastrointestinal hormones such as ghrelin "eat", GLP-1 (glucagon-like

FAK Inhibition Decreases Hepatoblastoma Survival Both In Vitro and In Vivo.

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Hepatoblastoma is the most frequently diagnosed liver tumor of childhood, and children with advanced, metastatic or relapsed disease have a disease-free survival rate under 50%. Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that is important in many facets of tumor development and

Blockade of IGF-1 receptor tyrosine kinase has antineoplastic effects in hepatocellular carcinoma cells.

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Hepatocellular carcinoma (HCC) is one of the most common cancer-related causes of death worldwide. Due to very poor 5-year-survival new therapeutic approaches are mandatory. Most HCCs express insulin-like growth factors and their receptors (IGF-R). As IGF-1R-mediated signaling promotes survival,

Thrombopoietin stimulates migration and activates multiple signaling pathways in hepatoblastoma cells.

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Thrombopoietin (TPO), a cytokine that participates in the differentiation and maturation of megakaryocytes, is produced in the liver, but only limited information is available on the biological response of liver-derived cells to TPO. In this study, we investigated whether HepG2 cells express c-Mpl,

Corticosteroid-binding globulin synthesis regulation by cytokines and glucocorticoids in human hepatoblastoma-derived (HepG2) cells.

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Plasma corticosteroid-binding globulin (CBG) concentrations decrease dramatically in patients with septic shock or burn injury. This decrease suggests that mediators of the acute phase response, such as cytokines and glucocorticoid hormones, might influence clearance as well as liver synthesis of

beta-Catenin and met deregulation in childhood Hepatoblastomas.

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Activation of the Wnt/beta-catenin and hepatocyte growth factor/Met signaling has been implicated in various tumors. Owing to the cross-talk between these pathways and aberrant redistribution of beta-catenin in hepatoblastomas, we examined their status in this tumor. This study examined changes in

Mechanisms of Anticancer Drug Resistance in Hepatoblastoma.

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The most frequent liver tumor in children is hepatoblastoma (HB), which derives from embryonic parenchymal liver cells or hepatoblasts. Hepatocellular carcinoma (HCC), which rarely affects young people, causes one fourth of deaths due to cancer in adults. In contrast, HB usually has better

Activation of phosphatidylinositol-3'-kinase/AKT signaling is essential in hepatoblastoma survival.

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OBJECTIVE Hepatoblastoma represents the most frequent malignant liver tumor in childhood. The phosphatidylinositol-3'-kinase (PI3K)/AKT pathway is crucial in downstream signaling of multiple receptor tyrosine kinases of pathogenic importance in hepatoblastoma. Increased PI3K/AKT signaling pathway

H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR-675/FADD and miR-138/PTK2.

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BACKGROUND The objective of this study was to clarify the molecular pathways involved in hepatitis B virus (HBV)-induced hepatoblastoma. METHODS The expression of factors in different signaling pathways (H19, miR-675, miR-138, protein tyrosine kinase 2 [PTK2], fas-associated death domain [FADD],

Activation and inhibition of cellular calcium and tyrosine kinase signaling pathways identify targets of the HBx protein involved in hepatitis B virus replication.

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Human hepatitis B virus (HBV) HBx protein is a multifunctional protein that activates cellular signaling pathways and is thought to be essential for viral infection. Woodchuck HBV mutants that lack HBx are unable to replicate in vivo or are severely impaired. HBV replication in HepG2 cells, a human

Gene expression profiles in an hepatitis B virus transfected hepatoblastoma cell line and differentially regulated gene expression by interferon-alpha.

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OBJECTIVE To study interactions between hepatitis B virus (HBV) and interferon-alpha in liver- derived cells. METHODS mRNAs were separately isolated from an HBV-transfected cell line (HepG(2)2.2.15) and its parental cell line (HepG(2)) pre- and post-interferon-alpha (IFN-alpha) treatment at 6, 24

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