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1. Chien RN: Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B. Hepatol Int; 2008 Sep;2(3):296-303
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  • Concurrent hepatitis C virus (HCV), hepatitis delta virus (HDV), or human immunodeficiency virus (HIV) infection with chronic hepatitis B virus (HBV) appears to increase the risk of progressive liver disease including liver cirrhosis and hepatocellular carcinoma.
  • In chronic HBV infection acquired perinatally or in early childhood, usually HCV is dominant and may suppress or even displace HBV and HDV.
  • Additionally, patients with concurrent infection of HBV and HDV, IFN seems to be the only effective agent.
  • In patients with concurrently infected HBV and HIV, anti-HBV therapy should be considered for all patients with evidence of liver disease, irrespective of the CD4 cell count.
  • In contrast, in patients with CD4 cell counts <350 cells/mul or those already on antiretroviral therapy, agents with double anti-HBV and anti-HIV activity are preferred.

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  • (PMID = 19669257.001).
  • [ISSN] 1936-0533
  • [Journal-full-title] Hepatology international
  • [ISO-abbreviation] Hepatol Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2716893
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2. Aston NS, Watt N, Morton IE, Tanner MS, Evans GS: Copper toxicity affects proliferation and viability of human hepatoma cells (HepG2 line). Hum Exp Toxicol; 2000 Jun;19(6):367-76
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  • [Title] Copper toxicity affects proliferation and viability of human hepatoma cells (HepG2 line).
  • In Wilson's disease and Indian childhood cirrhosis (ICC) copper accumulates in the liver resulting in poor hepatocyte regeneration and fibrosis.
  • An inhibition of hepatocyte proliferation and an increase in cell death could account for these outcomes.
  • This study suggests that when liver cells sequester large amounts of copper, the toxic effects include delayed cell-cycle progression, a gradual loss of replicative capacity, and an increased incidence of cell death.
  • [MeSH-major] Cell Division / drug effects. Cell Survival / drug effects. Copper / toxicity
  • [MeSH-minor] Apoptosis / drug effects. Carcinoma, Hepatocellular / metabolism. Child. Child, Preschool. Flow Cytometry. Fluorescein-5-isothiocyanate / metabolism. G2 Phase / drug effects. Hepatolenticular Degeneration / blood. Humans. Immunochemistry. Liver Cirrhosis / blood. Liver Neoplasms / metabolism. Lysosomes / drug effects. Necrosis. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Time Factors. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Tumor Stem Cell Assay

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  • (PMID = 10962511.001).
  • [ISSN] 0960-3271
  • [Journal-full-title] Human & experimental toxicology
  • [ISO-abbreviation] Hum Exp Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 789U1901C5 / Copper; I223NX31W9 / Fluorescein-5-isothiocyanate
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3. Liu Y, Fuchs J, Li C, Lin J: IL-6, a risk factor for hepatocellular carcinoma: FLLL32 inhibits IL-6-induced STAT3 phosphorylation in human hepatocellular cancer cells. Cell Cycle; 2010 Sep 1;9(17):3423-7
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  • [Title] IL-6, a risk factor for hepatocellular carcinoma: FLLL32 inhibits IL-6-induced STAT3 phosphorylation in human hepatocellular cancer cells.
  • Hepatocellular carcinoma (HCC) is one of the most common human cancers and the patients' five-year survival rate is very low.
  • We previous reported that IL-6 induces cell survival upon drug treatment in HCC cells and inhibition of IL-6/STAT3 pathway using anti-IL-6 antibody or STAT3 small-molecule inhibitor LLL12 reduces this effect.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Curcumin / analogs & derivatives. Interleukin-6 / antagonists & inhibitors. Liver Neoplasms / metabolism. STAT3 Transcription Factor / antagonists & inhibitors
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / metabolism. Humans. Phosphorylation. Risk Factors

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  • (PMID = 20818158.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FLLL 32; 0 / Interleukin-6; 0 / STAT3 Transcription Factor; IT942ZTH98 / Curcumin
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4. Abdullaev Jafarova F, Caballero-Ortega H, Riverón-Negrete L, Pereda-Miranda R, Rivera-Luna R, Manuel Hernández J, Pérez-López I, Espinosa-Aguirre JJ: [In vitro evaluation of the chemopreventive potential of saffron]. Rev Invest Clin; 2002 Sep-Oct;54(5):430-6
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  • Cancer is a very important national health problem in Mexico, while a significant increase in the total and childhood cancer mortality has been recorded during the last decades.
  • Chemoprevention, defined as the use of natural or synthetic agents to prevent or to block the development of cancer in human beings, is a new and promising strategy in the battle against cancer.
  • Saffron, obtained from the dried red-dark stigmas of Crocus sativus L., an important spice rich in carotenoids, is commonly consumed in different parts of the world and used as a medical drug to treat numerous diseases.
  • CONCLUSIONS: Taken together, our results and literature data indicate that saffron could be used as a potential cancer chemopreventive agent in clinical trials.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Crocus / chemistry. Plant Extracts / pharmacology
  • [MeSH-minor] Adenocarcinoma / pathology. Administration, Oral. Animals. Antimutagenic Agents / pharmacology. Carcinoma, Hepatocellular / pathology. Chromatography, High Pressure Liquid. Colonic Neoplasms / pathology. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Female. HeLa Cells / drug effects. Humans. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred BALB C. Mutagenicity Tests. Rhabdomyosarcoma / pathology. Salmonella typhimurium / drug effects. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay

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  • (PMID = 12587418.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antimutagenic Agents; 0 / Plant Extracts
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5. Feitelson MA, Pan J, Lian Z: Early molecular and genetic determinants of primary liver malignancy. Surg Clin North Am; 2004 Apr;84(2):339-54
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  • [Title] Early molecular and genetic determinants of primary liver malignancy.
  • Although the overview above provides a partial molecular picture of the early stages of stepwise hepatocarcinogenesis. it should be emphasized that tumor and nontumor liver contain multiple changes, and that there is variability in their profile among different patients even within single studies.
  • These observations need to be exploited in future drug discovery and in the development of new therapeutics.
  • This suggests that there are multiple pathways to HCC, and that there is redundancy in the pathways that regulate cell growth and survival.
  • Overall, the consequences of these changes suggest that the pathogenesis of HCC is accompanied by a progressive loss of differentiation, loss of normal cell adhesion, loss of the ECM, and constitutive activation of selected signal transduction pathways that promote cell growth and survival.
  • For example, it will be important to try to identify germline mutations in HBV-infected patients that are passed on to their children, resulting in the development of HCC in childhood.
  • Clinical materials will also be important for the validation of new markers with diagnostic or prognostic potential.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Hepatitis B, Chronic / complications. Liver Neoplasms / genetics
  • [MeSH-minor] Animals. DNA Damage / physiology. DNA, Viral / genetics. Gene Expression Regulation, Neoplastic / physiology. Genetic Predisposition to Disease. Hepatitis B Antigens / physiology. Hepatitis B virus / genetics. Humans. Loss of Heterozygosity. Matrix Metalloproteinases / metabolism. Mice. Oligonucleotide Array Sequence Analysis. Up-Regulation

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  • (PMID = 15062649.001).
  • [ISSN] 0039-6109
  • [Journal-full-title] The Surgical clinics of North America
  • [ISO-abbreviation] Surg. Clin. North Am.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA48656; United States / NCI NIH HHS / CA / CA66971
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Hepatitis B Antigens; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 118
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6. Dzieran J, Beck JF, Sonnemann J: Differential responsiveness of human hepatoma cells versus normal hepatocytes to TRAIL in combination with either histone deacetylase inhibitors or conventional cytostatics. Cancer Sci; 2008 Aug;99(8):1685-92
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  • [Title] Differential responsiveness of human hepatoma cells versus normal hepatocytes to TRAIL in combination with either histone deacetylase inhibitors or conventional cytostatics.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising candidate for the treatment of cancer because it elicits cell death in many tumor cells while sparing most normal cells.
  • Liver cancer, however, is largely resistant to TRAIL and, thus, requires sensitization for TRAIL-mediated cytotoxicity.
  • Sensitization may be achieved by cotreatment with chemotherapeutic agents.
  • In this study, we comparatively investigated the treatment efficacy of TRAIL in combination with histone deacetylase inhibitors (HDI) versus TRAIL in combination with conventional cytostatics in the hepatocellular carcinoma cell line HepG2 and in the childhood hepatoblastoma cell line Huh6.
  • In searching for the determinants of HDI-mediated TRAIL sensitization in hepatoma cells, we observed that HDI treatment did not increase cell-surface expression of proapoptotic TRAIL receptors.
  • In conclusion, our data suggest that HDI are potent sensitizers to TRAIL in hepatoma cells and that the combination of HDI and TRAIL is selectively active in hepatoma cells without affecting normal hepatocytes, indicating that the combination of HDI and TRAIL may be an effective approach for the treatment of advanced liver cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols. Apoptosis / drug effects. Histone Deacetylases / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / drug therapy. Cell Line, Tumor. Drug Resistance, Neoplasm. Hepatoblastoma / drug therapy. Hepatocytes / drug effects. Histone Deacetylase Inhibitors. Humans. Liver Neoplasms / drug therapy. Rats

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  • (PMID = 18754884.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 3.5.1.98 / Histone Deacetylases
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7. Rajasekaran SA, Huynh TP, Wolle DG, Espineda CE, Inge LJ, Skay A, Lassman C, Nicholas SB, Harper JF, Reeves AE, Ahmed MM, Leatherman JM, Mullin JM, Rajasekaran AK: Na,K-ATPase subunits as markers for epithelial-mesenchymal transition in cancer and fibrosis. Mol Cancer Ther; 2010 Jun;9(6):1515-24
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  • We have shown earlier that Na,K-ATPase beta(1)-subunit levels are highly reduced in poorly differentiated kidney carcinoma cells in culture and in patients' tumor samples.

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  • (PMID = 20501797.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK056216-09; United States / NIDDK NIH HHS / DK / R01 DK056216; United States / NIDDK NIH HHS / DK / R01 DK056216-09; United States / NIDDK NIH HHS / DK / R01-DK56216
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Protein Subunits; 0 / Transforming Growth Factor beta; 9NEZ333N27 / Sodium; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase
  • [Other-IDs] NLM/ NIHMS194853; NLM/ PMC2884047
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8. Seitz G, Krause R, Fuchs J, Heitmann H, Armeanu S, Ruck P, Warmann SW: In vitro photodynamic therapy in pediatric epithelial liver tumors promoted by hypericin. Oncol Rep; 2008 Nov;20(5):1277-82
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  • [Title] In vitro photodynamic therapy in pediatric epithelial liver tumors promoted by hypericin.
  • Limited treatment results in advanced pediatric liver tumors have emphasised the need for alternative treatment approaches in these malignancies.
  • Hypericin, a naturally occurring substance found in the St. John's Wort, has regularly and successfully been used for visualisation and as photosensitizer in various tumor models.
  • However, there exist no data on the effects of hypericin as photodynamic agent in pediatric malignant epithelial liver tumors.
  • In this study, we investigated the potential role of hypericin for visualization and treatment in hepatoblastoma (HB) and pediatric hepatocellular carcinoma (HCC) cells.
  • Two HB cell lines (HUH6, HepT1) and one HCC cell line (HepG2) were incubated with ascending concentrations of hypericin.
  • Cell viability, cell proliferation and apoptotic rates were assessed using MTT assay, Ki-67 immunocytochemisty and TUNEL test, respectively.
  • Relevant hypericin uptake was observed in all cell lines according to the applied concentrations.
  • Histological analysis revealed no alterations of cell structure in HB and HCC cells after solely hypericin uptake, but severe alterations were found after PDT.
  • Enhancement of the hypericin concentration (up to 12.5 microM) and illumination time of up to 40 min resulted in a decrease of tumor cell viability (HUH6 99.8+/-2.4%, HepT1 99+/-2%, HepG2 98.4+/-1.6%, p<0.05), proliferative activity and complete apoptosis of all cells in all investigated cell lines.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Hepatoblastoma / drug therapy. Liver Neoplasms / drug therapy. Perylene / analogs & derivatives. Photochemotherapy / methods. Photosensitizing Agents / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Child. Flow Cytometry. Humans. In Situ Nick-End Labeling. In Vitro Techniques. Microscopy, Fluorescence

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  • (PMID = 18949433.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin
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9. Turner PC, Sylla A, Kuang SY, Marchant CL, Diallo MS, Hall AJ, Groopman JD, Wild CP: Absence of TP53 codon 249 mutations in young Guinean children with high aflatoxin exposure. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):2053-5
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  • Infection with hepatitis viruses and chronic exposure to high levels of dietary aflatoxins are the major etiologic agents for hepatocellular carcinoma in west Africa.
  • A challenge for the prevention of hepatocellular carcinoma in this region is that both hepatitis B virus and aflatoxin exposures start early in life; indeed, aflatoxin exposures can start in utero and continue unabated throughout childhood.
  • A mutation in the TP53 tumor suppressor gene at codon 249 (TP53 Ser249 mutation) has been reported previously for hepatocellular carcinoma tumors and matched plasma DNA samples in individuals from areas with high aflatoxin exposure.
  • Because approximately 50% of the hepatocellular carcinomas in adults in west Africa have this specific TP53 Ser249 mutation, a lack of detection in samples from children ages <5 years may indicate that a window of opportunity for intervention exists that could be exploited to lower hepatocellular carcinoma risk.
  • [MeSH-major] Adenoma, Liver Cell / chemically induced. Aflatoxins / adverse effects. DNA, Neoplasm / blood. Genes, p53 / genetics. Liver Neoplasms / chemically induced

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  • (PMID = 16103461.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES06052
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aflatoxins; 0 / DNA, Neoplasm
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10. Liu Y, Li PK, Li C, Lin J: Inhibition of STAT3 signaling blocks the anti-apoptotic activity of IL-6 in human liver cancer cells. J Biol Chem; 2010 Aug 27;285(35):27429-39
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  • [Title] Inhibition of STAT3 signaling blocks the anti-apoptotic activity of IL-6 in human liver cancer cells.
  • Recent studies demonstrate that high levels of IL-6 are associated with hepatocellular carcinoma, the most common type of liver cancer.
  • Here we reported that IL-6 promoted survival of human liver cancer cells through activating STAT3 in response to doxorubicin treatment.
  • To elucidate the mechanism of the anti-apoptotic function of IL-6, we investigated if STAT3 mediated this drug resistance.
  • Therefore, our results demonstrated that targeting STAT3 signaling could interrupt the anti-apoptotic function of IL-6 in human liver cancer cells.

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  • (PMID = 20562100.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA133652; United States / NCI NIH HHS / CA / R21CA133652-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthraquinones; 0 / Antibiotics, Antineoplastic; 0 / Antibodies; 0 / IL6 protein, human; 0 / Interleukin-6; 0 / LLL12 compound; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Sulfonamides; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2930741
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11. Eichenmüller M, Gruner I, Hagl B, Häberle B, Müller-Höcker J, von Schweinitz D, Kappler R: Blocking the hedgehog pathway inhibits hepatoblastoma growth. Hepatology; 2009 Feb;49(2):482-90
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  • Recent evidence has indicated that Hedgehog (Hh) signaling significantly contributes to liver development and regeneration and that activation of the pathway may contribute to growth of hepatocellular carcinoma (HCC) in adults.
  • However, the role of Hh signaling in pediatric liver tumors remains to be elucidated.
  • In this study, we show that Hh signaling is activated in hepatoblastoma (HB), the most common liver tumor in childhood, with most occurrences before the age of 3 years.
  • The Hh target genes glioma-associated oncogene homolog 1 (GLI1) and Patched (PTCH1) showed increased transcript levels in 65% and 30% of HB samples, respectively, compared with normal liver tissues.
  • Most interestingly, the gene encoding the hedgehog interacting protein (HHIP) is transcriptionally silenced by cytosine-phospho-guanosine (CpG) island promoter hypermethylation in 26% of HB cases and treatment with the DNA-demethylating agent 5-aza-2'-deoxycytidine partially restored HHIP expression.
  • Blocking Hh signaling with the antagonist cyclopamine had a strong inhibitory effect on cell proliferation of HB cell lines with an activated pathway.
  • We further demonstrate that this decrease in cell viability is caused by a massive induction of apoptosis, as shown by morphological changes and phosphatidylserine membrane asymmetry.
  • In cyclopamine-exposed HB cells, caspase 3 and poly(adenosine diphosphate-ribose) polymerase proteins were specifically activated by their proteolytic cleavage.
  • CONCLUSION: This study demonstrates, for the first time, the frequent occurrence of GLI1 and PTCH1 overexpression and HHIP promoter methylation in early childhood HB, thus indicating a key role for Hh signaling activation in the malignant transformation of embryonal liver cells.
  • [MeSH-major] Hedgehog Proteins / antagonists & inhibitors. Hedgehog Proteins / genetics. Hepatoblastoma / genetics. Hepatoblastoma / pathology. Liver Neoplasms / genetics. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Cell Division. Child. Child, Preschool. DNA Methylation. Female. Genes, Reporter. Humans. Infant. Male. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction


12. Warmann SW, Frank H, Heitmann H, Ruck P, Herberts T, Seitz G, Fuchs J: Bcl-2 gene silencing in pediatric epithelial liver tumors. J Surg Res; 2008 Jan;144(1):43-8
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  • [Title] Bcl-2 gene silencing in pediatric epithelial liver tumors.
  • BACKGROUND: Proteins of the Bcl-2 family prevent cells of various tumor types from undergoing apoptosis and thus contribute to their chemotherapy resistance.
  • The phenotype of multidrug resistance is a major factor for poor treatment results of advanced epithelial liver tumors in children.
  • The role of Bcl-2 proteins in these tumors is yet unclear.
  • The purpose of this study was to analyze the influence of Bcl-2 on the chemotherapy resistance of hepatoblastoma (HB) and pediatric hepatocellular carcinoma (HCC).
  • MATERIALS AND METHODS: Bcl-2 expression was analyzed in the HB cell lines HUH6 and HepT1 as well as in the HCC cell line HepG2 before and after treatment with cisplatin, doxorubicin, taxol, and etoposid.
  • Treatment efficiencies of cytotoxic agents were assessed against original and Bcl-2 siRNA transfected tumor cells.
  • RESULTS: The mixed HB cell line HUH6 showed a relevant amount of Bcl-2 expression, which increased after chemotherapy.
  • Treatment with all cytotoxic agents was significantly improved through Bcl-2 siRNA (P < 0.001-0.0054) in this cell line.
  • Further studies seem necessary to clear the susceptibility of pediatric epithelial liver tumors toward the described approach.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Drug Resistance, Neoplasm / genetics. Gene Silencing. Liver Neoplasms / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Child. Cisplatin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Multiple / genetics. Epithelium. Etoposide / pharmacology. Genetic Therapy / methods. Humans. Paclitaxel / pharmacology. Transfection

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  • (PMID = 17574594.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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13. Dokmak S, Cabral C, Couvelard A, Aussilhou B, Belghiti J, Sauvanet A: Pancreatic metastasis from nephroblastoma: an unusual entity. JOP; 2009;10(4):396-9
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  • CONTEXT: Pancreatic metastasis from renal cell carcinoma is a well-known entity.
  • A nephroblastoma is a frequent childhood cancer but can also occur in adults.
  • A metastatic nephroblastoma mainly affects the lung and the liver.
  • CASE REPORT: We report an extremely rare case of pancreatic metastases in a 20-year-old man who had a right nephroblastoma resected at 9 years of age and liver metastases treated by right hepatectomy at 18 years of age.
  • Imaging studies revealed no other localization except a 1.5 cm liver nodule.
  • The patient underwent pancreaticoduodenectomy and limited liver resection with an uneventful postoperative course.
  • Pathological examination confirmed pancreatic and liver metastases from a nephroblastoma composed of blastematous cells mixed with embryonic tubular structures without lymph node metastases.
  • After resection, the patient received adjuvant high dose chemotherapy with autologous hematopoietic stem-cell support.
  • After a 21-month follow-up, the patient was in good general condition but had liver recurrence without intra-pancreatic recurrence.
  • A nephroblastoma, like clear cell renal carcinoma, can be considered a possible etiology of pancreatic metastasis from a primary renal tumor.
  • [MeSH-minor] Combined Modality Therapy. Drug Therapy / methods. Humans. Male. Pancreaticoduodenectomy / methods. Treatment Outcome. Young Adult


14. Reingruber B, Boettcher MI, Klein P, Hohenberger W, Pelz JO: Hyperthermic intraperitoneal chemoperfusion is an option for treatment of peritoneal carcinomatosis in children. J Pediatr Surg; 2007 Sep;42(9):E17-21
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  • BACKGROUND: Gastrointestinal carcinomas in childhood are rare and frequently present at an advanced stage.
  • METHODS: After treating a series of adult patients, HIPEC for peritoneal carcinomatosis from a signet cell carcinoma of the colon was performed intraoperatively in a 12-year-old boy.
  • We performed intraoperative drug level monitoring and daily postoperative liver and kidney function tests and differential blood counts.
  • Perfusate and venous drug levels were similar to those in an adult case.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Carcinoma, Signet Ring Cell / drug therapy. Carcinoma, Signet Ring Cell / secondary. Chemotherapy, Cancer, Regional Perfusion. Hyperthermia, Induced. Mitomycin / administration & dosage. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary

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  • (PMID = 17848227.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
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15. Mitchell JD, Maguire JJ, Davenport AP: Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin S. Br J Pharmacol; 2009 Sep;158(1):87-103
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  • The NMU knockout mouse has an obese phenotype and, in agreement, the Arg165Trp amino acid variant of NMU-25 in humans, which is functionally inactive, co-segregated with childhood-onset obesity.
  • The NMU system has also been implicated in the pathogenesis of septic shock and cancers including bladder carcinoma and acute myeloid leukaemia.

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  • (PMID = 19519756.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] ENG
  • [Grant] United Kingdom / British Heart Foundation / / FS/05/020/18408; United Kingdom / British Heart Foundation / / PG/05/127/19872; United Kingdom / British Heart Foundation / / PS/02/001
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0 / Neuropeptides; 0 / neuromedin S; 117505-80-3 / neuromedin U
  • [Number-of-references] 152
  • [Other-IDs] NLM/ PMC2795236
  •  go-up   go-down


16. Davit-Spraul A, Gonzales E, Baussan C, Jacquemin E: Progressive familial intrahepatic cholestasis. Orphanet J Rare Dis; 2009;4:1
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  • Progressive familial intrahepatic cholestasis (PFIC) refers to heterogeneous group of autosomal recessive disorders of childhood that disrupt bile formation and present with cholestasis of hepatocellular origin.
  • Three types of PFIC have been identified and related to mutations in hepatocellular transport system genes involved in bile formation.
  • PFIC1 and PFIC2 usually appear in the first months of life, whereas onset of PFIC3 may also occur later in infancy, in childhood or even during young adulthood.
  • PFIC patients usually develop fibrosis and end-stage liver disease before adulthood.
  • Defects in ABCB4, encoding the multi-drug resistant 3 protein (MDR3), impair biliary phospholipid secretion resulting in PFIC3.
  • Diagnosis is based on clinical manifestations, liver ultrasonography, cholangiography and liver histology, as well as on specific tests for excluding other causes of childhood cholestasis.
  • MDR3 and BSEP liver immunostaining, and analysis of biliary lipid composition should help to select PFIC candidates in whom genotyping could be proposed to confirm the diagnosis.
  • Ursodeoxycholic acid (UDCA) therapy should be initiated in all patients to prevent liver damage.
  • However, most PFIC patients are ultimately candidates for liver transplantation.
  • Monitoring of hepatocellular carcinoma, especially in PFIC2 patients, should be offered from the first year of life.
  • [MeSH-minor] Adenosine Triphosphatases / genetics. Adult. Child. Child, Preschool. Disease Progression. Humans. Liver / pathology. Liver / physiopathology. Liver Cirrhosis / pathology. Liver Cirrhosis / physiopathology. Liver Failure / pathology. Liver Transplantation

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  • (PMID = 19133130.001).
  • [ISSN] 1750-1172
  • [Journal-full-title] Orphanet journal of rare diseases
  • [ISO-abbreviation] Orphanet J Rare Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.6.1.- / Adenosine Triphosphatases
  • [Number-of-references] 88
  • [Other-IDs] NLM/ PMC2647530
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17. von Schweinitz D, Faundez A, Teichmann B, Birnbaum T, Koch A, Hecker H, Glüer S, Fuchs J, Pietsch T: Hepatocyte growth-factor-scatter factor can stimulate post-operative tumor-cell proliferation in childhood hepatoblastoma. Int J Cancer; 2000 Jan 15;85(2):151-9
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  • [Title] Hepatocyte growth-factor-scatter factor can stimulate post-operative tumor-cell proliferation in childhood hepatoblastoma.
  • Rapid growth of residual tumor after partial hepatectomy has been observed during the period of liver regeneration in children with malignant embryonal hepatoblastoma.
  • Markedly increased serum levels of HGF-SF up to 15 ng/ml were found in 13/18 patients after liver resection and in 6/16 patients with regressive tumors after chemotherapy, in comparison with 15 patients with non-pre-treated hepatoblastoma and 20 healthy children of the same age group.
  • The hepatoblastoma cell lines HepT1, HepT3 and HUH6 reacted with significantly increased proliferation to rhHGF-SF in these concentrations (1-15 ng/ml).
  • Cultured hepatoblastoma cells ceased to proliferate at 20-50 ng/ml HGF-SF, and they underwent cell death at >/=100 ng/ml.
  • In contrast, the hepatocellular-carcinoma cell line HepG2 decreased growth under HGF-SF in a dose-dependent manner.
  • We conclude that post-operatively secreted and intratumorally produced HGF-SF can function as a growth factor for hepatoblastoma, while the same agent has a cytostatic effect in unphysiologically high concentrations.
  • [MeSH-major] Hepatoblastoma / pathology. Hepatocyte Growth Factor / physiology. Liver Neoplasms / pathology
  • [MeSH-minor] Cell Division / physiology. Child, Preschool. Fibroblasts / secretion. Humans. Infant. Proto-Oncogene Proteins c-met / genetics. Proto-Oncogene Proteins c-met / metabolism. RNA, Messenger / metabolism. Tumor Cells, Cultured


18. Theve EJ, Feng Y, Taghizadeh K, Cormier KS, Bell DR, Fox JG, Rogers AB: Sex hormone influence on hepatitis in young male A/JCr mice infected with Helicobacter hepaticus. Infect Immun; 2008 Sep;76(9):4071-8
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  • Hepatitis B virus (HBV), the leading cause of human hepatocellular carcinoma, is especially virulent in males infected at an early age.
  • Likewise, the murine liver carcinogen Helicobacter hepaticus is most pathogenic in male mice infected before puberty.
  • Male A/JCr mice were infected with H. hepaticus or vehicle at 4 weeks and randomized into surgical and pharmacologic treatment groups.
  • Interruption of androgen pathways was confirmed by hormone measurements, histopathology, and liver gene and Cyp4a protein expression.
  • No effect on hepatitis was evident in males treated with the 5alpha-reductase inhibitor dutasteride, the peroxisome proliferator-activated receptor-alpha agonist bezafibrate, or the nonsteroidal anti-inflammatory drug flufenamic acid.
  • Consistent with previous observations of hepatitis-associated liver-gender disruption, transcriptional alterations involved both feminine (cytochrome P450 4a14) and masculine (cytochrome P450 4a12 and trefoil factor 3) genes, as well gender-neutral (H19 fetal liver mRNA, lipocalin 2, and ubiquitin D) genes.
  • Hepatitis was associated with increased unsaturated C(18) long-chain fatty acids (oleic acid and linoleic acid) relative to saturated stearic acid.
  • This raises the possibility of targeted hormonal therapy in young male patients with childhood-acquired HBV.

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  • (PMID = 18559427.001).
  • [ISSN] 1098-5522
  • [Journal-full-title] Infection and immunity
  • [ISO-abbreviation] Infect. Immun.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES-02109; United States / NCI NIH HHS / CA / CA-67529; United States / NCRR NIH HHS / RR / RR-07036; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCRR NIH HHS / RR / T32 RR007036; United States / NCI NIH HHS / CA / R01 CA067529
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acute-Phase Proteins; 0 / Androgen Antagonists; 0 / Lipocalins; 0 / Mucins; 0 / Oncogene Proteins; 0 / Testosterone Congeners; 0 / Tff3 protein, mouse; 0 / Ubiquitin; 126469-30-5 / Lcn2 protein, mouse; 3XMK78S47O / Testosterone; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.- / Cyp4a14 protein, mouse; EC 1.14.15.3 / Cyp4a12 protein, mouse
  • [Other-IDs] NLM/ PMC2519413
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