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4. Liver damage and senescence increases in patients developing hepatocellular carcinoma

Author

Rey S., Quintavalle C., Burmeister K., Calabrese D., Schlageter M., Quagliata L., Cathomas G., Diebold J., Molinolo A., Heim M.H., Terracciano L.M., and Matter M.S.

Subjects
hepatocellular carcinoma, senescence, telomeres, neoplasms, digestive system diseases
Abstract

BACKGROUND AND AIM: Most patients with a hepatocellular carcinoma (HCC) have an underlying chronic liver inflammation, which causes a continuous damage leading to liver cirrhosis and eventually HCC. However, only a minority of cirrhotic patients develop HCC. To assess a possible differential impact of liver inflammation in patients developing HCC versus patients remaining tumor-free, we designed a longitudinal study and analysed liver tissue of the same patients (n = 33) at two points in time: once when no HCC was present and once several years later when an HCC was present. As a control group, we followed cirrhotic patients (n = 37) remaining tumor-free over a similar time frame. METHODS: We analysed cell damage and senescence of hepatocytes by measuring ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, nuclear size, and telomere length. RESULTS: ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, in the first liver biopsy was similar in patients developing HCC later on and cirrhotic patients remaining tumor free. In contrast, ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, was significantly higher in the second non-tumoral liver biopsy of HCC patients than in the control patients. Consequently, the individual increase in ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, from the first biopsy to the second biopsy was significantly higher in patients developing HCC than in patients remaining tumor free. In addition, changes in nuclear size and telomere length revealed a more pronounced cell aging in patients developing HCC than in patients remaining tumor free. CONCLUSIONS: Hepatocytes from patients developing HCC go through more pronounced cell damage and senescence in contrast to cirrhotic patients remaining tumor free.

Published
2017
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6. Genetic profiling using plasma-derived cell-free DNA in therapy-naïve hepatocellular carcinoma patients: A pilot study

Author

Di Costanzo, G.G., primary, Ng, C.K.Y., additional, Tosti, N., additional, Tortora, R., additional, Paradiso, V., additional, Coto-Llerena, M., additional, Roscigno, G., additional, Perrina, V., additional, Quintavalle, C., additional, Boldanova, T., additional, Wieland, S., additional, Marino-Marsilia, G., additional, Lanzafame, M., additional, Quagliata, L., additional, Condorelli, G., additional, Matter, M.S., additional, Heim, M.H., additional, Guarracino, M., additional, Terracciano, L.M., additional, and Piscuoglio, S., additional

Published
2018
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9. MIR-146A-5P, A Proviral Factor Up-Regulated by Hepatitis C Virus Infection, Deregulates Metabolic Pathways Relevant for Liver Disease Progression in Hepatocytes

Author

Pernot, S., primary, Bandiera, S., additional, El Saghire, H., additional, Durand, S.C., additional, Ye, T., additional, Thumann, C., additional, Crouchet, E., additional, Schuster, C., additional, Fofana, I., additional, Heim, M.H., additional, Baumert, T.F., additional, and Zeisel, M.B., additional

Published
2016
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10. Interferons induce degradation of HBV CccDNA

Author

Xia, Y., Lucifora, J., Zhang, K., Cheng, X., Stadler, D., Reisinger, F., Feuerherd, M., Makowska, Z., Hartmann, D., Thasler, W.E., Heim, M.H., Heikenwälder, M., and Protzer, U.

Published
2013

11. O027 : The expression of tumor suppressor PTPRD is down-regulated in the liver of patients with HCV infection and in tumor lesions of patients with hepatocellular carcinoma

Author

Van Renne, N., primary, Duong, F.H.T., additional, Gondeau, C., additional, Calabrese, D., additional, Fontaine, N., additional, Ababsa, A., additional, Durand, S.C., additional, Pessaux, P., additional, Heim, M.H., additional, Baumert, T.F., additional, and Lupberger, J., additional

Published
2015
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12. P0676 : Clearance of persistent hepatitis c virus infection using a monoclonal antibody specific for tight junction protein claudin-1

Author

Mailly, L., primary, Xiao, F., additional, Lupberger, J., additional, Wilson, G.K., additional, Aubert, P., additional, Duong, F.H., additional, Calabrese, D., additional, Leboeuf, C., additional, Fofana, I., additional, Thumann, C., additional, Bandiera, S., additional, Lütgehetmann, M., additional, Volz, T., additional, Davis, C., additional, Harris, H.J., additional, Mee, C., additional, Girardi, E., additional, Chane-Woon-Ming, B., additional, Ericsson, M., additional, Fletcher, N., additional, Bartenschlager, R., additional, Pessaux, P., additional, Vercauteren, K., additional, Meuleman, P., additional, Villa, P., additional, Kaderali, L., additional, Pfeffer, S., additional, Heim, M.H., additional, Neunlist, M., additional, Zeisel, M.B., additional, Dandri, M., additional, McKeating, J.A., additional, Robinet, E., additional, and Baumert, T.F., additional

Published
2015
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14. 2007 4 Week therapy with the non-nucleosidic polymerase inhibitor bi207127 in combination with peginterferon-alfa2a and ribavirin in treatment naive and treatment experienced chronic HCV GT1 patients

Author

Larrey, D., Lohse, A., de Ledinghen, V., Trepo, C., Gerlach, T., Zarski, J.-P., Tran, A., Mathurin, P., Thimme, R., Arastéh, K., Trautwein, C., Cerny, A., Dikopoulos, N., Schuchmann, M., Heim, M.H., Gerken, Guido, Stern, J., Wu, K., Abdallah, N., Girlich, B., Josepf, S., Wulff, Beate, Berger, F., Steffgen, J., and BI207127 Study Group

Subjects
medicine.medical_specialty, Hepatology, business.industry, Ribavirin, Medizin, Gastroenterology, Treatment experienced, Therapy naive, chemistry.chemical_compound, chemistry, Internal medicine, Medicine, Polymerase inhibitor, business
Published
2010

15. Novel approach identifies SNPs in SLC2A10 and KCNK9 with evidence for parent-of-origin effect on body mass index

Author

Hoggart, C.J., Venturini, G., Mangino, M., Gomez, F., Ascari, G., Zhao, J.H., Teumer, A., Winkler, T.W., Tsernikova, N., Luan, J., Mihailov, E., Ehret, G.B., Zhang, W., Lamparter, D., Esko, T., Mace, A., Rueger, S., Bochud, P.Y., Barcella, M., Dauvilliers, Y., Benyamin, B., Evans, D.M., Hayward, C., Lopez, M.F., Franke, L., Russo, A., Heid, I.M., Salvi, E., Vendantam, S., Arking, D.E., Boerwinkle, E., Chambers, J.C., Fiorito, G., Grallert, H., Guarrera, S., Homuth, G., Huffman, J.E., Porteous, D., Moradpour, D., Iranzo, A., Hebebrand, J., Kemp, J.P., Lammers, G.J., Aubert, V., Heim, M.H., Martin, N.G., Montgomery, G.W., Peraita-Adrados, R., Santamaria, J., Negro, F., Schmidt, C.O., Scott, R.A., Spector, T.D., Strauch, K., Volzke, H., Wareham, N.J., Yuan, W., Bell, J.T., Chakravarti, A., Kooner, J.S., Peters, A., Matullo, G., Wallaschofski, H., Whitfield, J.B., Paccaud, F., Vollenweider, P., Bergmann, S., Beckmann, J.S., Tafti, M., Hastie, N.D., Cusi, D., Bochud, M., Frayling, T.M., Metspalu, A., Jarvelin, M.R., Scherag, A., Smith, G.D., Borecki, I.B., Rousson, V., Hirschhorn, J.N., Rivolta, C., Loos, R.J., Kutalik, Z., Vermeulen, S., Kiemeney, L.A., et al., Hoggart, C.J., Venturini, G., Mangino, M., Gomez, F., Ascari, G., Zhao, J.H., Teumer, A., Winkler, T.W., Tsernikova, N., Luan, J., Mihailov, E., Ehret, G.B., Zhang, W., Lamparter, D., Esko, T., Mace, A., Rueger, S., Bochud, P.Y., Barcella, M., Dauvilliers, Y., Benyamin, B., Evans, D.M., Hayward, C., Lopez, M.F., Franke, L., Russo, A., Heid, I.M., Salvi, E., Vendantam, S., Arking, D.E., Boerwinkle, E., Chambers, J.C., Fiorito, G., Grallert, H., Guarrera, S., Homuth, G., Huffman, J.E., Porteous, D., Moradpour, D., Iranzo, A., Hebebrand, J., Kemp, J.P., Lammers, G.J., Aubert, V., Heim, M.H., Martin, N.G., Montgomery, G.W., Peraita-Adrados, R., Santamaria, J., Negro, F., Schmidt, C.O., Scott, R.A., Spector, T.D., Strauch, K., Volzke, H., Wareham, N.J., Yuan, W., Bell, J.T., Chakravarti, A., Kooner, J.S., Peters, A., Matullo, G., Wallaschofski, H., Whitfield, J.B., Paccaud, F., Vollenweider, P., Bergmann, S., Beckmann, J.S., Tafti, M., Hastie, N.D., Cusi, D., Bochud, M., Frayling, T.M., Metspalu, A., Jarvelin, M.R., Scherag, A., Smith, G.D., Borecki, I.B., Rousson, V., Hirschhorn, J.N., Rivolta, C., Loos, R.J., Kutalik, Z., Vermeulen, S., Kiemeney, L.A., and et al.

Abstract

Contains fulltext : 136406.pdf (publisher's version ) (Open Access), The phenotypic effect of some single nucleotide polymorphisms (SNPs) depends on their parental origin. We present a novel approach to detect parent-of-origin effects (POEs) in genome-wide genotype data of unrelated individuals. The method exploits increased phenotypic variance in the heterozygous genotype group relative to the homozygous groups. We applied the method to >56,000 unrelated individuals to search for POEs influencing body mass index (BMI). Six lead SNPs were carried forward for replication in five family-based studies (of approximately 4,000 trios). Two SNPs replicated: the paternal rs2471083-C allele (located near the imprinted KCNK9 gene) and the paternal rs3091869-T allele (located near the SLC2A10 gene) increased BMI equally (beta = 0.11 (SD), P<0.0027) compared to the respective maternal alleles. Real-time PCR experiments of lymphoblastoid cell lines from the CEPH families showed that expression of both genes was dependent on parental origin of the SNPs alleles (P<0.01). Our scheme opens new opportunities to exploit GWAS data of unrelated individuals to identify POEs and demonstrates that they play an important role in adult obesity.

Published
2014

16. Reduced IFNλ4 activity is associated with improved HCV clearance and reduced expression of interferon-stimulated genes

Author

Swiss Hepatitis C Cohort Study Group, Rubbia-Brandt, L., Martinetti, G., Gorgievski, M., Dufour, JF., Hirsch, H., Helbling B.<AffiliationInfo> <Affiliation>1] [2].</Affiliation></AffiliationInfo>, Regenass, S., Dollenmaier, G., Cathomas, G., Terczyńska-Dyla, E., Bibert, S., Duong, F.H., Krol, I., Jørgensen, S., Collinet, E., Kutalik, Z., Aubert, V., Cerny, A., Kaiser, L., Malinverni, R., Mangia, A., Moradpour, D., Müllhaupt, B., Negro, F., Santoro, R., Semela, D., Semmo, N., Heim, M.H., Bochud, P.Y., Hartmann, R., Swiss Hepatitis C Cohort Study Group, Rubbia-Brandt, L., Martinetti, G., Gorgievski, M., Dufour, JF., Hirsch, H., Helbling B.<AffiliationInfo> <Affiliation>1] [2].</Affiliation></AffiliationInfo>, Regenass, S., Dollenmaier, G., Cathomas, G., Terczyńska-Dyla, E., Bibert, S., Duong, F.H., Krol, I., Jørgensen, S., Collinet, E., Kutalik, Z., Aubert, V., Cerny, A., Kaiser, L., Malinverni, R., Mangia, A., Moradpour, D., Müllhaupt, B., Negro, F., Santoro, R., Semela, D., Semmo, N., Heim, M.H., Bochud, P.Y., and Hartmann, R.

Abstract

Hepatitis C virus (HCV) infections are the major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma worldwide. Both spontaneous and treatment-induced clearance of HCV depend on genetic variation within the interferon-lambda locus, but until now no clear causal relationship has been established. Here we demonstrate that an amino-acid substitution in the IFNλ4 protein changing a proline at position 70 to a serine (P70S) substantially alters its antiviral activity. Patients harbouring the impaired IFNλ4-S70 variant display lower interferon-stimulated gene (ISG) expression levels, better treatment response rates and better spontaneous clearance rates, compared with patients coding for the fully active IFNλ4-P70 variant. Altogether, these data provide evidence supporting a role for the active IFNλ4 protein as the driver of high hepatic ISG expression as well as the cause of poor HCV clearance.

Published
2014

17. Novel Approach Identifies SNPs in SLC2A10 and KCNK9 with Evidence for Parent-of-Origin Effect on Body Mass Index.

Author

Generation Scotland Consortium, LifeLines Cohort study, GIANT Consortium, Hoggart, C.J., Venturini, G., Mangino, M., Gomez, F., Ascari, G., Zhao, J.H., Teumer, A., Winkler, T.W., Ternikova, N., Luan, J., Mihailov, E., Ehret, G.B., Zhang, W., Lamparter, D., Esko, T., Macé, A., Rüeger, S., Bochud, P.Y., Barcella, M., Dauvilliers, Y., Benyamin, B., Evans, D.M., Hayward, C., Lopez, M.F., Franke, L., Russo, A., Heid, I.M., Salvi, E., Vendantam, S., Arking, D.E., Boerwinkle, E., Chambers, J.C., Fiorito, G., Grallert, H., Guarrera, S., Homuth, G., Huffman, J.E., Porteous, D., Moradpour, D., Iranzo, A., Hebebrand, J., Kemp, J.P., Lammers, G.J., Aubert, V., Heim, M.H., Martin, N.G., Montgomery, G.W., Peraita-Adrados, R., Santamaria, J., Negro, F., Schmidt, C.O., Scott, R.A., Spector, T.D., Strauch, K., Völzke, H., Wareham, N.J., Yuan, W., Bell, J.T., Chakravarti, A., Kooner, J.S., Peters, A., Matullo, G., Wallaschofski, H., Whitfield, J.B., Paccaud, F., Vollenweider, P., Bergmann, S., Beckmann, J.S., Tafti, M., Hastie, N.D., Cusi, D., Bochud, M., Frayling, T.M., Metspalu, A., Jarvelin, M.R., Scherag, A., Smith, G.D., Borecki, I.B., Rousson, V., Hirschhorn, J.N., Rivolta, C., Loos, R.J., Kutalik, Z., Generation Scotland Consortium, LifeLines Cohort study, GIANT Consortium, Hoggart, C.J., Venturini, G., Mangino, M., Gomez, F., Ascari, G., Zhao, J.H., Teumer, A., Winkler, T.W., Ternikova, N., Luan, J., Mihailov, E., Ehret, G.B., Zhang, W., Lamparter, D., Esko, T., Macé, A., Rüeger, S., Bochud, P.Y., Barcella, M., Dauvilliers, Y., Benyamin, B., Evans, D.M., Hayward, C., Lopez, M.F., Franke, L., Russo, A., Heid, I.M., Salvi, E., Vendantam, S., Arking, D.E., Boerwinkle, E., Chambers, J.C., Fiorito, G., Grallert, H., Guarrera, S., Homuth, G., Huffman, J.E., Porteous, D., Moradpour, D., Iranzo, A., Hebebrand, J., Kemp, J.P., Lammers, G.J., Aubert, V., Heim, M.H., Martin, N.G., Montgomery, G.W., Peraita-Adrados, R., Santamaria, J., Negro, F., Schmidt, C.O., Scott, R.A., Spector, T.D., Strauch, K., Völzke, H., Wareham, N.J., Yuan, W., Bell, J.T., Chakravarti, A., Kooner, J.S., Peters, A., Matullo, G., Wallaschofski, H., Whitfield, J.B., Paccaud, F., Vollenweider, P., Bergmann, S., Beckmann, J.S., Tafti, M., Hastie, N.D., Cusi, D., Bochud, M., Frayling, T.M., Metspalu, A., Jarvelin, M.R., Scherag, A., Smith, G.D., Borecki, I.B., Rousson, V., Hirschhorn, J.N., Rivolta, C., Loos, R.J., and Kutalik, Z.

Abstract

The phenotypic effect of some single nucleotide polymorphisms (SNPs) depends on their parental origin. We present a novel approach to detect parent-of-origin effects (POEs) in genome-wide genotype data of unrelated individuals. The method exploits increased phenotypic variance in the heterozygous genotype group relative to the homozygous groups. We applied the method to >56,000 unrelated individuals to search for POEs influencing body mass index (BMI). Six lead SNPs were carried forward for replication in five family-based studies (of ∼4,000 trios). Two SNPs replicated: the paternal rs2471083-C allele (located near the imprinted KCNK9 gene) and the paternal rs3091869-T allele (located near the SLC2A10 gene) increased BMI equally (beta = 0.11 (SD), P<0.0027) compared to the respective maternal alleles. Real-time PCR experiments of lymphoblastoid cell lines from the CEPH families showed that expression of both genes was dependent on parental origin of the SNPs alleles (P<0.01). Our scheme opens new opportunities to exploit GWAS data of unrelated individuals to identify POEs and demonstrates that they play an important role in adult obesity.

Published
2014

18. Long noncoding RNA HOTTIP/HOXA13 expression is associated with disease progression and predicts outcome in hepatocellular carcinoma patients

Author

Quagliata, L., Matter, M.S., Piscuoglio, S., Arabi, L., Ruiz, C., Procino, A., Kovac, M., Moretti, F., Makowska, Z., Boldanova, T., Andersen, J.B., Hämmerle, M., Tornillo, L., Heim, M.H., Diederichs, S., Cillo, C., Terracciano, L.M., Quagliata, L., Matter, M.S., Piscuoglio, S., Arabi, L., Ruiz, C., Procino, A., Kovac, M., Moretti, F., Makowska, Z., Boldanova, T., Andersen, J.B., Hämmerle, M., Tornillo, L., Heim, M.H., Diederichs, S., Cillo, C., and Terracciano, L.M.

Published
2014

19. P847 DAYTIME SLEEPINESS IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE IS LINKED TO INSULIN RESISTANCE, ELEVATED LIVER FUNCTION TESTS AND FIBROSIS

Author

Bernsmeier, C., primary, Weisskopf, D.M., additional, Mosimann, J., additional, Campana, B., additional, Meyer-Gerspach, A.C., additional, Steinert, R.E., additional, Blaser, L., additional, Jeker, L., additional, Terracciano, L., additional, Beglinger, C., additional, Heim, M.H., additional, and Cajochen, C., additional

Published
2014
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20. P196 INVESTIGATION OF HEPATITIS C VIRUS ADAPTATION TO HOST GENETIC POLYMORPHISMS

Author

Drobnik, J., primary, Lemay, J., additional, Carlson, J.M., additional, Kutalik, Z., additional, Heckerman, D., additional, Heim, M.H., additional, Dufour, J.-F., additional, Patin, E., additional, Semela, D., additional, Cerny, A., additional, Nalpas, B., additional, Malinverni, R., additional, Moradpour, D., additional, Pol, S., additional, Müllhaupt, B., additional, Negro, F., additional, Abel, L., additional, Bochud, P.-Y., additional, and Kuntzen, T., additional

Published
2014
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21. O47 PEGYLATED INTERFERON-ALPHA INDUCES SUSTAINED TRANSCRIPTIONAL RESPONSE IN LIVER INFILTRATING IMMUNE CELLS BUT NOT IN HEPATOCYTES IN THE LIVER OF PATIENTS WITH CHRONIC HEPATITIS C

Author

Dill, M.T., primary, Makowska, Z., additional, Trincucci, G., additional, Gruber, A.J., additional, Vogt, J.E., additional, Filipowicz, M., additional, Calabrese, D., additional, Krol, I., additional, Lau, D.T., additional, Terracciano, L., additional, van Nimwegen, E., additional, Roth, V., additional, and Heim, M.H., additional

Published
2014
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23. Hepatitis C: an update

Author

Moradpour, D., Cerny, A., Heim, M.H., and Blum, H.E.

Subjects
Antiviral Agents/therapeutic use, Enzyme-Linked Immunosorbent Assay, Hepacivirus/isolation & purification, Hepatitis C/diagnosis, Hepatitis C/epidemiology, Hepatitis C/therapy, Humans, Reverse Transcriptase Polymerase Chain Reaction, digestive system diseases
Abstract

Hepatitis C virus (HCV) infection is a leading cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma worldwide. While current therapeutic options for hepatitis C are limited, recent progress in the understanding of the biology of HCV led to the identification of novel targets for antiviral intervention. In addition, molecular and immunotherapeutic strategies to inhibit HCV replication or gene expression and to enhance the cellular immune response against HCV are being explored. These and other novel antiviral strategies may eventually complement existing therapeutic modalities. Here, we briefly review current concepts of the epidemiology, molecular virology, pathogenesis, natural history, diagnosis, therapy, and prevention of hepatitis C.

Published
2001

26. IFN stimulated gene expression in the liver is a better predictor of treatment response in chronic hepatitis c than the IL28b (IFN lambda 3) genotype

Author

Dill, M.T., Duong, F.H.T., Vogt, J.E., Bibert, S., Bochud, P.-Y., Terracciano, L., Papassotiropoulos, A., Roth, V., Heim, M.H., Dill, M.T., Duong, F.H.T., Vogt, J.E., Bibert, S., Bochud, P.-Y., Terracciano, L., Papassotiropoulos, A., Roth, V., and Heim, M.H.

Abstract

Background: Therapy of chronic hepatitis C (CHC) with pegIFNa/ribavirin achieves sustained virologic response (SVR) in ~55%. Pre-activation of the endogenous interferon system in the liver is associated non-response (NR). Recently, genome-wide association studies described associations of allelic variants near the IL28B (IFNλ3) gene with treatment response and with spontaneous clearance of the virus. We investigated if the IL28B genotype determines the constitutive expression of IFN stimulated genes (ISGs) in the liver of patients with CHC. Methods: We genotyped 93 patients with CHC for 3 IL28B single nucleotide polymorphisms (SNPs, rs12979860, rs8099917, rs12980275), extracted RNA from their liver biopsies and quantified the expression of IL28B and of 8 previously identified classifier genes which discriminate between SVR and NR (IFI44L, RSAD2, ISG15, IFI22, LAMP3, OAS3, LGALS3BP and HTATIP2). Decision tree ensembles in the form of a random forest classifier were used to calculate the relative predictive power of these different variables in a multivariate analysis. Results: The minor IL28B allele (bad risk for treatment response) was significantly associated with increased expression of ISGs, and, unexpectedly, with decreased expression of IL28B. Stratification of the patients into SVR and NR revealed that ISG expression was conditionally independent from the IL28B genotype, i.e. there was an increased expression of ISGs in NR compared to SVR irrespective of the IL28B genotype. The random forest feature score (RFFS) identified IFI27 (RFFS = 2.93), RSAD2 (1.88) and HTATIP2 (1.50) expression and the HCV genotype (1.62) as the strongest predictors of treatment response. ROC curves of the IL28B SNPs showed an AUC of 0.66 with an error rate (ERR) of 0.38. A classifier with the 3 best classifying genes showed an excellent test performance with an AUC of 0.94 and ERR of 0.15. The addition of IL28B genotype information did not improve the predictive power of the 3-gene cl

Published
2010

27. 1412 COMPARATIVE GENETIC ANALYSES POINT TO HCP5 AS SUSCEPTIBILITY LOCUS FOR HCV-ASSOCIATED HEPATOCELLULAR CARCINOMA

Author

Lange, C.M., primary, Bibert, S., additional, Dufour, J.-F., additional, Cellerai, C., additional, Cerny, A., additional, Heim, M.H., additional, Kaiser, L., additional, Malinverni, R., additional, Müllhaupt, B., additional, Negro, F., additional, Semela, D., additional, Moradpour, D., additional, Kutalik, Z., additional, and Bochud, P.-Y., additional

Published
2013
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29. 58 HRas SIGNAL TRANSDUCTION MEDIATES HEPATITIS C VIRUS CELL ENTRY BY TRIGGERING THE ASSEMBLY OF THE HOST TETRASPANIN RECEPTOR COMPLEX

Author

Zona, L., primary, Lupberger, J., additional, Thumann, C., additional, Ahmed-Adrar, N.S., additional, Harris, H.J., additional, Duong, F.H.T., additional, Heim, M.H., additional, Bachellier, P., additional, Zeisel, M.B., additional, Samuel, D., additional, le Naour, F., additional, McKeating, J.A., additional, and Baumert, T.F., additional

Published
2013
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33. 1401 GENOME-WIDE ASSOCIATION STUDY IDENTIFIES VARIANTS ASSOCIATED WITH LIVER FIBROSIS PROGRESSION IN HCV-INFECTED PATIENTS

Author

Patin, E., primary, Kutalik, Z., additional, Guergnon, J., additional, Bibert, S., additional, Nalpas, B., additional, Jouanguy, E., additional, Munteanu, M., additional, Bousquet, L., additional, Argiro, L., additional, Halfon, P., additional, Boland, A., additional, Mullhaupt, B., additional, Semela, D., additional, Dufour, J.-F., additional, Heim, M.H., additional, Moradpour, D., additional, Cerny, A., additional, Malmvemi, R., additional, Hirsch, H., additional, Martinetti, G., additional, Suppiah, V., additional, Stewart, G., additional, Booth, D.R., additional, George, J., additional, Casanova, J.-L., additional, Brechot, C., additional, Rice, C.M., additional, Talal, A.H., additional, Jacobson, I.M., additional, Bourliere, M., additional, Theodorou, I., additional, Poynard, T., additional, Negro, F., additional, Pol, S., additional, Abel, L., additional, and Bochud, P.-Y., additional

Published
2012
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37. 1357 A LARGE-SCALE GENETIC VALIDATION STUDY COUPLED WITH IN-VITRO ANALYSES REVEAL A ROLE OF VITAMIN D-SIGNALING IN THE PATHOGENESIS AND TREATMENT OF CHRONIC HEPATITIS C

Author

Lange, C.M., primary, Bibert, S., additional, Kutalik, Z., additional, Morikawa, K., additional, Cerny, A., additional, Dufour, J.-F., additional, Gerlach, T.J., additional, Heim, M.H., additional, Malinverni, R., additional, Müllhaupt, B., additional, Negro, F., additional, Badenhoop, K., additional, Sarrazin, C., additional, Berg, T., additional, Gouttenoire, J., additional, Bochud, P.-Y., additional, and Moradpour, D., additional

Published
2011
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39. 2007 4 WEEK THERAPY WITH THE NON-NUCLEOSIDIC POLYMERASE INHIBITOR BI207127 IN COMBINATION WITH PEGINTERFERON-ALFA2A AND RIBAVIRIN IN TREATMENT NAIVE AND TREATMENT EXPERIENCED CHRONIC HCV GT1 PATIENTS

Author

Larrey, D., primary, Lohse, A., additional, de Ledinghen, V., additional, Trepo, C., additional, Gerlach, T., additional, Zarski, J.-P., additional, Tran, A., additional, Mathurin, P., additional, Thimme, R., additional, Arastéh, K., additional, Trautwein, C., additional, Cerny, A., additional, Dikopoulos, N., additional, Schuchmann, M., additional, Heim, M.H., additional, Gerken, G., additional, Stern, J., additional, Wu, K., additional, Abdallah, N., additional, Girlich, B., additional, Josepf, S., additional, Wulf, B., additional, Berger, F., additional, and Steffgen, J., additional

Published
2010
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45. Specific activation of AP-1 but not Stat3 in regenerating liver in mice

Author

Heim, M.H., Gamboni, G., Beglinger, C., and Gyr, K.

Abstract

Liver regeneration following partial hepatectomy is regulated by hepatotrophic factors whose precise roles are still elusive. In cell culture studies, some of them have been shown to activate members of the family of the signal transducers and activators of transcription (Stat). To test this contention in vivo, nuclear extracts were isolated from livers of partially hepatectomized and sham-operated mice killed at 30 different time points between zero and 108 h after surgery. Stat3 DNA binding is rapidly induced after surgery in both partially hepatectomized and sham-operated mice. Maximum activation of Stat3 is achieved 4-6 h after resection, and elevated Stat3 activation is detected as late as 60 h after surgery in both groups. Activated Stat5 is found sporadically in both sham-operated and resected mice but appears to be absent in the first 12 h after partial hepatectomy. Neither Stat1, Stat2, Stat4 nor Stat6 is induced during the time of observation. In contrast, AP-1 DNA binding activity is specifically induced in regenerating mouse liver.

Published
1997
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