Neil J. Mehta, Aygul Dogan Celik, Marion G. Peters – 19 December 2016 – While there are guidelines from all major liver societies for the screening and management of hepatocellular carcinoma (HCC), many issues remain surrounding the actual practice of screening. This review discusses how to diagnose and screen HCC and more importantly, how well we diagnose and screen for HCC. Improved survival and outcomes after HCC diagnosis depend upon accurate diagnosis of cirrhosis and the timeliness of screening.

Jennifer C. Price, Yifei Ma, Rebecca Scherzer, Natalie Korn, Kyle Tillinghast, Marion G. Peters, Susan M. Noworolski, Phyllis C. Tien – 16 December 2016 – Hepatic steatosis (HS) is common in individuals with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections, but the independent contributions of HCV and HIV to HS are unclear.

Fernando Bril, Diana Barb, Paola Portillo‐Sanchez, Diane Biernacki, Romina Lomonaco, Amitabh Suman, Michelle H. Weber, Jeffrey T. Budd, Maria E. Lupi, Kenneth Cusi – 16 December 2016 – The cut‐off point of intrahepatic triglyceride (IHTG) content to define nonalcoholic fatty liver disease (NAFLD) by proton magnetic resonance spectroscopy (1H‐MRS) was established based on the 95th percentile in a group of healthy individuals (i.e., ≥5.56%).

Marcial Sebode, Sören Weidemann, Malte Wehmeyer, Ansgar W. Lohse, Christoph Schramm – 16 December 2016 – We present a case of hepatosplenic necrotizing sarcoid granulomatosis, a variant form of “classical” sarcoidosis, that became clinically apparent in the form of multiple hepatic and splenic masses mimicking malignancy. Flow cytometry of intrahepatic T cells isolated from liver biopsy led to the targeted treatment with anti‐tumor necrosis factor‐alpha, which was highly effective in inducing remission. (Hepatology 2017;65:1410‐1412)

Peter L.M. Jansen, Ahmed Ghallab, Nachiket Vartak, Raymond Reif, Frank G. Schaap, Jochen Hampe, Jan G. Hengstler – 16 December 2016 – In this review we develop the argument that cholestatic liver diseases, particularly primary biliary cholangitis and primary sclerosing cholangitis (PSC), evolve over time with anatomically an ascending course of the disease process. The first and early lesions are in “downstream” bile ducts. This eventually leads to cholestasis, and this causes bile salt (BS)–mediated toxic injury of the “upstream” liver parenchyma. BS are toxic in high concentration.

Herbert L. Bonkovsky, David E. Kleiner, Jiezhun Gu, Joseph A. Odin, Mark W. Russo, Victor M. Navarro, Robert J. Fontana, Marwan S. Ghabril, Huiman Barnhart, Jay H. Hoofnagle, for the U.S. Drug Induced Liver Injury Network Investigators – 16 December 2016 – Bile duct loss during the course of drug‐induced liver injury is uncommon, but can be an indication of vanishing bile duct syndrome (VBDS). In this work, we assess the frequency, causes, clinical features, and outcomes of cases of drug‐induced liver injury with histologically proven bile duct loss.

Junyan Tao, Rong Zhang, Sucha Singh, Minakshi Poddar, Emily Xu, Michael Oertel, Xin Chen, Shanthi Ganesh, Marc Abrams, Satdarshan P. Monga – 16 December 2016 – Recently, we have shown that coexpression of hMet and mutant‐β‐catenin using sleeping beauty transposon/transposase leads to hepatocellular carcinoma (HCC) in mice that corresponds to around 10% of human HCC. In the current study, we investigate whether Ras activation, which can occur downstream of Met signaling, is sufficient to cause HCC in association with mutant‐β‐catenin.

Silvia Martini, Mauro Salizzoni, Ezio David, Francesco Tandoi, Paolo Fonio, Luisa Delsedime, Silvia Strona, Dominic Dell Olio, Giorgio Maria Saracco, Renato Romagnoli – 16 December 2016

Wei Fan, Heping Yang, Ting Liu, Jiaohong Wang, Tony W.H. Li, Nirmala Mavila, Yuanyuan Tang, JinWon Yang, Hui Peng, Jian Tu, Alagappan Annamalai, Mazen Noureddin, Anuradha Krishnan, Gregory J. Gores, Maria L. Martínez‐Chantar, José M. Mato, Shelly C. Lu – 16 December 2016 – Prohibitin 1 (PHB1) is best known as a mitochondrial chaperone, and its role in cancer is conflicting. Mice lacking methionine adenosyltransferase α1 (MATα1) have lower PHB1 expression, and we reported that c‐MYC interacts directly with both proteins.

16 December 2016