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| 1 | Significance of hepatitis virus infection in the oncogenicinitiation of hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is one of the most common causes of cancer-related death worldwide. Chronic infection of hepatitis B virus(HBV) and/or hepatitis C virus(HCV) is a major risk factor in the development of the HCC, independently from excessive alcohol abuse and metabolic disease. Since the biology of HBV and HCV is different, their oncogenic effect may go through different mechanisms, direct and/or indirect. Viral hepatitis infection is associated with cellular inflammation, oxidative stress, DNA damage, that may lead to subsequent hepatic injuries such as chronic hepatitis, fibrosis, cirrhosis, and finally HCC. Direct oncogenic properties of these viruses are related with their genotypic characteristics and the ability of viral proteins to interact with host proteins, thus altering the molecular pathways balance of the cells. In addition, the integration of HBV DNA, especially the gene S and X, in a particular site of the host genome can disrupt chromosomal stability and may activate various oncogenic mechanisms, including those in hematopoietic cells. Recently, several studies also had demonstrated that viral hepatitis could trigger the population of hepatic cancer stem cells. This review summarize available pre-clinical and clinical data in literature regarding oncogenic properties of HBV and HCV in the early initiation of HCC. | Caecilia HC Sukowati Korri E El-Khobar Susan I Ie Beatrice Anfuso David H Muljono Claudio Tiribelli | 2016 | World Journal of Gastroenterology2016，22，4： | 18 |
| 2 | Hepatic cancer stem cells and drug resistance: Relevance in targeted therapies for hepatocellular carcinoma显示文摘Hepatocellular carcinoma (HCC) is one of most common malignancies in the world. Systemic treatments for HCC, particularly for advanced stages, are limited by the drug resistance phenomenon which ultimately leads to therapy failure. Recent studies have indicated an association between drug resistance and the existence of the cancer stem cells (CSCs) as tumor initiating cells. The CSCs are resistant to conventional chemotherapies and might be related to the mechanisms of the ATP Binding Cassette (ABC) transporters and alterations in the CSCs signaling pathways. Therefore, to contribute to the development of new HCC treatments, further information on the characterization of CSCs, the modulation of the ABC transporters expression and function and the signaling pathway involved in the self renewal, initiation and maintenance of the cancer are required. The combination of transporters modulators/inhibitors with molecular targeted therapies may be a potent strategy to block the tumoral progression. This review summarizes the association of CSCs, drug resistance, ABC transporters activities and changes in signaling pathways as a guide for future molecular therapy for HCC. | Caecilia HC Sukowati Natalia Rosso Lory S Crocè Claudio Tiribelli | 2010 | World Journal of Hepatology2010，2，3： | 16 |
| 3 | Translational approaches: From fatty liver to non-alcoholic steatohepatitis显示文摘Over the past few decades, non-alcoholic fatty liver disease(NAFLD) has become one, if not the most common,cause of chronic liver disease affecting both adults and children. The increasing number of cases at an early age is the most worrying aspect of this pathology, since it provides more time for its evolution. The spectrum of this disease ranges from liver steatosis to steatohepatitis, fibrosis and in some cases, hepatocellular carcinoma. NAFLD may not always be considered a benign disease and hepatologists must be cautious in the presence of fatty liver. This should prompt the use of the available experimental models to understand better the pathogenesis and to develop a rational treatment of a disease that is dangerously increasing. In spite of the growing efforts, the pathogenesis of NAFLD is still poorly understood. In the present article we review the most relevant hypotheses and evidence that account for the progression of NAFLD to non-alcoholic steatohepatitis(NASH) and fibrosis. The available in vitro and in vivo experimental models of NASH are discussed and revised in terms of their validity in translational studies. These studies must be aimed at the discovery of the still unknown triggers or mediators that induce the progression of hepatic inflammation, apoptosis and fibrosis. | Natalia Rosso Norberto C Chavez-Tapia Claudio Tiribelli Stefano Bellentani | 2014 | World Journal of Gastroenterology2014，20，27： | 14 |
| 4 | Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis显示文摘The nonalcoholic fatty liver disease(NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-alcoholic steatohepatitis(NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes(Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a na?ve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies. | Carla Melisa Chackelevicius Sabrina Eliana Gambaro Claudio Tiribelli Natalia Rosso | 2016 | World Journal of Gastroenterology2016，22，41： | 10 |
| 5 | Epidemiology of fatty liver: An update显示文摘We provide a concise review of the main epidemiological literature on fatty liver(FL) published between January 2011 and October 2013. The findings from the literature will be considered in light of the already available knowledge. We discuss the limitations inherent in the categorization of FL into non-alcoholic and alcoholic FL, the potential relevance of FL as an independent predictor of cardiometabolic disease, and recent research addressing the role of FL as an independent predictor of mortality. This review is organized as a series of answers to relevant questions about the epidemiology of FL. | Giorgio Bedogni Valerio Nobili Claudio Tiribelli | 2014 | World Journal of Gastroenterology2014，20，27： | 7 |
| 6 | The many functions of APE1/Ref-1:not only a DNA repair enzyme structures显示文摘 | Tell G Quadrifoglio F Tiribelli C | | 0，，03： | 1 |
| 7 | High Prevalence of Celiac Disease in Italian General Population显示文摘 | Umberto Volta Stefano Bellentani Francesco Bianco Bianchi Giovanni Brandi Lucia De Franceschi Lucia Miglioli Alessandro Granito Fiorella Balli Claudio Tiribelli | 2001 | Digestive Diseases and Sciences2001，，7： | 1 |
| 8 | Quantitative assessment of WTl gene expression after allogeneic stem cell transplantation is a useful tool for monitoring minimal residual disease in acute myeloid leukemia显示文摘 | J Candoni A Tiribelli M Toffoletti E | 2009 | Eur J Haematol2009，82，： | 1 |
| 9 | Reassessment of the unbound concentrations of unconjugated bilirubin in relation to neurotoxicity in vitro显示文摘 | Ostrow JD Pascolo L Tiribelli C | 2003 | Pediatr Res2003，54，6： | 1 |
| 10 | Bilirubin-induced neurologic damage--mechanisms and management approaches显示文摘 | Watchko JF Tiribelli C | 2013 | N Engl J Med2013，369，21： | 1 |
| 11 | The many functions of APE1/Ref-1: not only a DNA repair enzyme 显示文摘 | Tell G Quadrifoglio F Tiribelli C | 2009 | Antioxid Redox Signal2009，11，3： | 1 |
| 12 | The preS1 domain of hepatitis virus and IgA cross-react in their binding to the hepatocyte surface显示文摘 | Pontisso P Ruvoletto MG Tiribelli C | 1992 | J Gen Virol1992，73，8： | 1 |
| 13 | Epstein-Barr virus reactivati- on in a patient treated with antithymocyte globulin for severe aplastic anemia显示文摘 | Calistri E Tiribelli M Battista M | 2006 | Am J Hematol2006，81，： | 1 |
| 14 | The prognostic value of P-glycoprotein (ABCB) and breast cancer resistance protein (ABCG2) in adults with de novo acute myeloid leukemia with normal karyotype 显示文摘 | Damiani D Tiribelli M Calistri E | 2006 | Haematologica2006，91，6： | 1 |
| 15 | Liver cirrhosis and pregnancy显示文摘 | Tiribelli C Rigato I | 2009 | Ann Hepatol2009，5，3： | 1 |
| 16 | Lack of SH3 domain does not imply a more severe clinical course in Ph+ chronic myeloid leukemia patients 显示文摘 | Tiribelli M Tonso A Ferrro D | 2000 | Blood2000，95，12： | 1 |
| 17 | Epstein-Barr virus reactivation in a patient treated with anti-thymocyte globulin for severe aplastic anemia显示文摘 | Calistri E Tiribelli M Battista M | 2006 | AmJ Hematol2006，81，5： | 1 |
| 18 | Bilirubin-induced neurological damage显示文摘 | Gazzin S Tiribelli C | 2011 | J Matem Fetal Neonatal Med2011，24，： | 1 |
| 19 | The many functions of APE1/Ref-1 :not only a DNA repair enzyme 显示文摘 | Tell G Quadrifoglio F Tiribelli C | 2009 | Antioxid Redox Signal2009，11，3： | 1 |
| 20 | The prognostic value of P-glycoprotein (ABCB) and breast cancer resistance protein (ABCG2) in adults with de novo acute myeloid leukemia with normal karyotype显示文摘 | Damiani D Tiribelli M Calistri E | 2006 | Haematologica2006，91，6： | 1 |
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