Jennifer C. Lai, Jacqueline G. O'Leary, James F. Trotter, Elizabeth C. Verna, Robert S. Brown, R. Todd Stravitz, Jeffrey D. Duman, Lisa M. Forman, Norah A. Terrault, for the Consortium to Study Health Outcomes in HCV Liver Transplant Recipients (CRUSH‐C) – 23 January 2012 – Over the last decade, the use of liver grafts from hepatitis C virus antibody–positive donors [HCV(+)Ds] has tripled in the United States. Although previous studies have demonstrated no association between an HCV(+)D status and graft loss, the effects of an HCV(+)D on histological outcomes are not well known.

Donghee Kim, Su‐Yeon Choi, Eun Ha Park, Whal Lee, Jin Hwa Kang, Won Kim, Yoon Jun Kim, Jung‐Hwan Yoon, Sook Hyang Jeong, Dong Ho Lee, Hyo‐suk Lee, Joseph Larson, Terry M. Therneau, W. Ray Kim – 23 January 2012 – Nonalcoholic fatty liver disease (NAFLD) is related to risk factors of coronary artery disease, such as dyslipidemia, diabetes, and metabolic syndrome, which are closely linked with visceral adiposity.

Mina Komuta, Olivier Govaere, Vincent Vandecaveye, Jun Akiba, Werner Van Steenbergen, Chris Verslype, Wim Laleman, Jacques Pirenne, Raymond Aerts, Hirohisa Yano, Frederik Nevens, Baki Topal, Tania Roskams – 23 January 2012 – Cholangiocellular carcinoma (CC) originates from topographically heterogeneous cholangiocytes. The cylindrical mucin‐producing cholangiocytes are located in large bile ducts and the cuboidal non–mucin‐producing cholangiocytes are located in ductules containing bipotential hepatic progenitor cells (HPCs).

Karolina Rembeck, Johan Westin, Magnus Lindh, Kristoffer Hellstrand, Gunnar Norkrans, Martin Laging, For the NORDynamIC study group – 23 January 2012

Roberta D'Ambrosio, Alessio Aghemo, Maria Grazia Rumi, Guido Ronchi, Maria Francesca Donato, Valerie Paradis, Massimo Colombo, Pierre Bedossa – 23 January 2012 – Although annular fibrosis is the hallmark of cirrhosis, other microscopic changes that affect liver function such as sinusoid capillarization or loss of metabolic zonation are common. A sustained virological response (SVR) may halt fibrosis deposition in hepatitis C virus (HCV)‐infected patients, but its impact on the other cirrhosis‐associated lesions is unknown.

Keita Un, Shigeru Kawakami, Mitsuru Yoshida, Yuriko Higuchi, Ryo Suzuki, Kazuo Maruyama, Fumiyoshi Yamashita, Mitsuru Hashida – 23 January 2012 – Hepatitis is often associated with the overexpression of various adhesion molecules. In particular, intracellular adhesion molecule‐1 (ICAM‐1), which is expressed on hepatic endothelial cells (HECs) in the early stage of inflammation, is involved in serious illnesses. Therefore, ICAM‐1 suppression in HECs enables the suppression of inflammatory responses.

Piero Portincasa, David Q.‐H. Wang – 23 January 2012

David Goldberg, Benjamin French, Peter Abt, Sandy Feng, Andrew M. Cameron – 23 January 2012 – Candidates with hepatocellular carcinoma (HCC) within the Milan criteria (MC) receive standardized Model for End‐Stage LIver Disease (MELD) exception points because of the projected risk of tumor expansion beyond the MC. Exception points at listing are meant to be equivalent to a 15% rusj if 90‐day mortality, with additional points granted every 3 months, equivalent to a 10% increased morality risk.

Matthias Evert, Diego F. Calvisi, Katja Evert, Valentina De Murtas, Gioia Gasparetti, Sandra Mattu, Giulia Destefanis, Sara Ladu, Antje Zimmermann, Salvatore Delogu, Sara Thiel, Andrea Thiele, Silvia Ribback, Frank Dombrowski – 23 January 2012 – Mounting epidemiological evidence supports a role for insulin‐signaling deregulation and diabetes mellitus in human hepatocarcinogenesis. However, the underlying molecular mechanisms remain unknown.

Ming Liu, Leilei Chen, Tim Hon Man Chan, Jian Wang, Yan Li, Yan Li, Ting‐Ting Zeng, Yun‐Fei Yuan, Xin‐Yuan Guan – 19 January 2012 – Amplification of broad regions of 8q is one of the most frequent genetic alterations in hepatocellular carcinoma (HCC), suggesting the existence of oncogenes in addition to MYC at 8q24.21. In this report we examine the potential role of the candidate amplified oncogene serum and glucocorticoid kinase 3 (SGK3) at 8q13.1 in HCC pathogenesis.