Maxime Ronot, Stephane Bahrami, Julien Calderaro, Dominique‐Charles Valla, Pierre Bedossa, Jacques Belghti, Valérie Vilgrain, Valérie Paradis – 12 January 2011 – Hepatocellular adenomas (HCAs) are divided into genotype/phenotype subgroups associated with different evolutive profiles. Therefore, recognition of subtype is of clinical importance in patient management. Magnetic resonance imaging (MRI) is considered the most informative imaging modality and liver biopsy a key diagnostic tool whose role in HCA subtyping has never been extensively studied.

Zuzanna Makowska, Francois H. T. Duong, Gaia Trincucci, David F. Tough, Markus H. Heim – 12 January 2011 – Therapy of chronic hepatitis C with pegylated interferon α (pegIFN‐α) and ribavirin achieves sustained virological responses in approximately half of the patients. Nonresponse to treatment is associated with constitutively increased expression of IFN‐stimulated genes in the liver already before therapy.

Ersan Ozaslan – 12 January 2011

Amir Moghaddam, Espen Melum, Nils Reinton, Helmer Ring‐Larsen, Hans Verbaan, Kristian Bjøro, Olav Dalgard – 12 January 2011 – Polymorphisms near the IL28B gene, which code for interferon (IFN)‐λ3, predict response to pegylated interferon‐α (PEG‐IFN) and ribavirin treatment in hepatitis C virus (HCV) genotype 1 infected patients. Follow‐up studies of the effect of IL28B gene in HCV non–genotype 1 infected patients have almost always used predominantly HCV genotype 2–infected or mixed genotype 2/3–infected cohorts with results partly conflicting with HCV genotype 1.

Rodrigo T. Calado, Jennifer Brudno, Paulomi Mehta, Joseph J. Kovacs, Colin Wu, Marco A. Zago, Stephen J. Chanock, Thomas D. Boyer, Neal S. Young – 12 January 2011 – Some patients with liver disease progress to cirrhosis, but the risk factors for cirrhosis development are unknown. Dyskeratosis congenita, an inherited bone marrow failure syndrome associated with mucocutaneous anomalies, pulmonary fibrosis, and cirrhosis, is caused by germline mutations of genes in the telomerase complex. We examined whether telomerase mutations also occurred in sporadic cirrhosis.

Arnaud Galbois, Dominique Thabut, Richard Moreau, Didier Lebrec – 12 January 2011

Ming‐Hua Zheng, Ke‐Qing Shi, Yu‐Chen Fan, Yong‐Ping Chen – 12 January 2011

Emilio Ramos, Léon Kautz, Richard Rodriguez, Michael Hansen, Victoria Gabayan, Yelena Ginzburg, Marie‐Paule Roth, Elizabeta Nemeth, Tomas Ganz – 12 January 2011 – In response to iron loading, hepcidin synthesis is homeostatically increased to limit further absorption of dietary iron and its release from stores. Mutations in HFE, transferrin receptor 2 (Tfr2), hemojuvelin (HJV), or bone morphogenetic protein 6 (BMP6) prevent appropriate hepcidin response to iron, allowing increased absorption of dietary iron, and eventually iron overload.

Diego F. Calvisi, Maria M. Simile, Sara Ladu, Maddalena Frau, Matthias Evert, Maria L. Tomasi, Maria I. Demartis, Lucia Daino, Maria A. Seddaiu, Stefania Brozzetti, Francesco Feo, Rosa M. Pascale – 12 January 2011 – Up‐regulation of the v‐Myb avian myeloblastosis viral oncogene homolog‐like2 B‐Myb (MYBL2) gene occurs in human hepatocellular carcinoma (HCC) and is associated with faster progression of rodent hepatocarcinogenesis.

Frank Tacke, Christian Trautwein – 12 January 2011 – In the classical form of alpha1‐antitrypsin (AT) deficiency, a point mutation in AT alters the folding of a liver‐derived secretory glycoprotein and renders it aggregation‐prone. In addition to decreased serum concentrations of AT, the disorder is characterized by accumulation of the mutant alpha1‐antitrypsin Z (ATZ) variant inside cells, causing hepatic fibrosis and/or carcinogenesis by a gain‐of‐toxic function mechanism. The proteasomal and autophagic pathways are known to mediate degradation of ATZ.