Apoptosis: A barrier against cancer no more?
Florian Baumgartner, Andreas Villunger – 2 September 2011
Glucocorticoids increase interleukin‐6–dependent gene induction by interfering with the expression of the suppressor of cytokine signaling 3 feedback inhibitor
Anna Dittrich, Christina Khouri, Sara Dutton Sackett, Christian Ehlting, Oliver Böhmer, Ute Albrecht, Johannes G. Bode, Christian Trautwein, Fred Schaper – 2 September 2011 – Glucocorticoids are known to be potent regulators of inflammation and have been used pharmacologically against inflammatory, immune, and lymphoproliferative diseases for more than 50 years. Due to their possible and well‐documented side effects, it is crucial to understand the molecular mechanisms and targets of glucocorticoid action in detail.
Comparison of eight diagnostic algorithms for liver fibrosis in hepatitis C: new algorithms are more precise and entirely noninvasive
Jérôme Boursier, Victor de Ledinghen, Jean‐Pierre Zarski, Isabelle Fouchard‐Hubert, Yves Gallois, Frédéric Oberti, Paul Calès, multicentric groups from SNIFF 32, VINDIAG 7, and ANRS/HC/EP23 FIBROSTAR studies – 2 September 2011 – The sequential algorithm for fibrosis evaluation (SAFE) and the Bordeaux algorithm (BA), which cross‐check FibroTest with the aspartate aminotransferase‐to‐platelet ratio index (APRI) or FibroScan, are very accurate but provide only a binary diagnosis of significant fibrosis (SAFE or BA for Metavir F ≥ 2) or cirrhosis (SAFE or BA for F4).
Genetic variant in PNPLA3 is associated with nonalcoholic fatty liver disease in China
Yiling Li, Chao Xing, Jonathan C. Cohen, Helen H. Hobbs – 2 September 2011
Drug therapy: Telaprevir
Michael D. Leise, W. Ray Kim, Katherine M. Canterbury, John J. Poterucha – 2 September 2011
Reply
Núria Tarrats, Anna Moles, Albert Morales, Carmen García‐Ruiz, José C. Fernández‐Checa, Montserrat Marí – 2 September 2011
Transforming growth factor‐beta signaling promotes hepatocarcinogenesis induced by p53 loss
Shelli M. Morris, Ji Yeon Baek, Amanda Koszarek, Samornmas Kanngurn, Sue E. Knoblaugh, William M. Grady – 2 September 2011 – Hepatocellular carcinoma (HCC) results from the accumulation of deregulated tumor suppressor genes and/or oncogenes in hepatocytes. Inactivation of TP53 and inhibition of transforming growth factor‐beta (TGF‐β) signaling are among the most common molecular events in human liver cancers. Thus, we assessed whether inactivation of TGF‐β signaling, by deletion of the TGF‐β receptor, type II (Tgfbr2), cooperates with Trp53 loss to drive HCC formation.
Persistent elevation of hepatocyte growth factor activator inhibitors in cholangiopathies affects liver fibrosis and differentiation
Hsiang‐Po Huang, Mei‐Hwei Chang, Yi‐Tzu Chen, Hong‐Yuan Hsu, Cheng‐Lun Chiang, Tai‐Shan Cheng, Yao‐Ming Wu, Mu Zon Wu, Yu‐Chen Hsu, Chih‐Che Shen, Chun‐Nan Lee, Ya‐Hui Chuang, Chia‐Lun Hong, Yung‐Ming Jeng, Pin‐Hsun Chen, Huey‐Ling Chen, Ming‐Shyue Lee – 2 September 2011 – Alteration of cell surface proteolysis has been proposed to play a role in liver fibrosis, a grave complication of biliary atresia (BA). In this study we investigated the roles of hepatocyte growth factor activator inhibitor (HAI)‐1 and ‐2 in the progression of BA.
An update on treatment of genotype 1 chronic hepatitis C virus infection: 2011 practice guideline by the American Association for the Study of Liver Diseases
Marc G. Ghany, David R. Nelson, Doris B. Strader, David L. Thomas, Leonard B. Seeff – 2 September 2011
MicroRNA‐194 is a target of transcription factor 1 (Tcf1, HNF1α) in adult liver and controls expression of frizzled‐6
Jan Krützfeldt, Nora Rösch, Jean Hausser, Muthiah Manoharan, Mihaela Zavolan, Markus Stoffel – 1 September 2011 – Transcription factor 1 (Tcf1; hepatocyte nuclear factor 1α [HNF1α]) is critical for hepatocyte development and function. Whether Tcf1 also regulates hepatic microRNAs (miRNAs) has not been investigated yet. Here we analyzed Tcf1‐dependent miRNA expression in adult mice in which this transcription factor had been genetically deleted (Tcf1−/−) using miRNA microarray analysis. The miR‐192/‐194 cluster was markedly down‐regulated in liver of Tcf1−/− mice.