Yaron Rotman, Christopher Koh, Joseph M. Zmuda, David E. Kleiner, T. Jake Liang, the NASH CRN – 26 August 2010 – Genome‐wide association studies identified single‐nucleotide polymorphisms (SNPs) that are associated with increased hepatic fat or elevated liver enzymes, presumably reflecting nonalcoholic fatty liver disease (NAFLD).

Thomas Sersté, Christian Melot, Claire Francoz, François Durand, Pierre‐Emmanuel Rautou, Dominique Valla, Richard Moreau, Didier Lebrec – 26 August 2010 – Beta‐blockers may have a negative impact on survival in patients with cirrhosis and refractory ascites. The aim of this study was to evaluate the effect of the administration of beta‐blockers on long‐term survival in patients with cirrhosis and refractory ascites.

Elizabeth K. Speliotes, Johannah L. Butler, Cameron D. Palmer, Benjamin F. Voight, the GIANT Consortium the MIGen Consortium, the NASH CRN, Joel N. Hirschhorn – 26 August 2010 – Single nucleotide polymorphisms (SNPs) near 7 loci have been associated with liver function tests or with liver steatosis by magnetic resonance spectroscopy. In this study we aim to test whether these SNPs influence the risk of histologically‐confirmed nonalcoholic fatty liver disease (NAFLD).

Serif Senturk, Mine Mumcuoglu, Ozge Gursoy‐Yuzugullu, Burcu Cingoz, Kamil Can Akcali, Mehmet Ozturk – 26 August 2010 – Senescence induction could be used as an effective treatment for hepatocellular carcinoma (HCC). However, major senescence inducers (p53 and p16Ink4a) are frequently inactivated in these cancers. We tested whether transforming growth factor‐β (TGF‐β) could serve as a potential senescence inducer in HCC. First, we screened for HCC cell lines with intact TGF‐β signaling that leads to small mothers against decapentaplegic (Smad)‐targeted gene activation.

Brent A. Neuschwander‐Tetri, Jeanne M. Clark, Nathan M. Bass, Mark L. Van Natta, Aynur Unalp‐Arida, James Tonascia, Claudia O. Zein, Elizabeth M. Brunt, David E. Kleiner, Arthur J. McCullough, Arun J. Sanyal, Anna Mae Diehl, Joel E. Lavine, Naga Chalasani, Kris V. Kowdley, NASH Clinical Research Network – 26 August 2010 – The Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) was formed to conduct multicenter studies on the etiology, contributing factors, natural history, and treatment of nonalcoholic steatohepatitis (NASH).

Christina Koutsari, Konstantinos N. Lazaridis – 26 August 2010

Zichen Zhang, Regina A. Oyesanya, Deanna J. W. Campbell, Jorge A. Almenara, Jennifer L. DeWitt, Alphonse E. Sirica – 26 August 2010 – Overexpression of epidermal growth factor receptor (ErbB1) and/or ErbB2 has been implicated in the pathogenesis of cholangiocarcinoma, suggesting that combined ErbB1/ErbB2 targeting might serve as a target‐based therapeutic strategy for this highly lethal cancer.

Weiqin Chen, Benny Chang, Lan Li, Lawrence Chan – 26 August 2010 – PNPLA3 (adiponutrin), a novel patatin‐like phospholipase domain‐containing enzyme, is expressed at high level in fat, but also in other tissues including liver. Polymorphisms in PNPLA3 have been linked to obesity and insulin sensitivity. Notably, a nonsynonymous variant rs738409(G) allele of the PNPLA3 gene was found to be strongly associated with both nonalcoholic and alcoholic fatty liver disease. We have generated Pnpla3−/− mice by gene targeting.

Wei Ding, Hanning You, Hien Dang, Francis LeBlanc, Vivian Galicia, Shelly C. Lu, Bangyan Stiles, C. Bart Rountree – 26 August 2010 – Epithelial‐to‐mesenchymal transition (EMT) is predicted to play a critical role in metastatic disease in hepatocellular carcinoma. In this study, we used a novel murine model of EMT to elucidate a mechanism of tumor progression and metastasis. A total of 2 × 106 liver cells isolated from Ptenloxp/loxp/Alb‐Cre+ mice, expanded from a single CD133+CD45− cell clone, passage 0 (P0), were sequentially transplanted to obtain two passages of tumor cells, P1 and P2.

Tatsuya Tazaki, Takaaki Sasaki, Kenta Uto, Norimasa Yamasaki, Satoshi Tashiro, Ryuichi Sakai, Minoru Tanaka, Hideaki Oda, Zen‐Ichiro Honda, Hiroaki Honda – 26 August 2010 – p130Cas, Crk‐associated substrate (Cas), is an adaptor/scaffold protein that plays a central role in actin cytoskeletal reorganization. We previously showed that mice in which Cas was deleted (Cas−/−) died in utero because of early cardiovascular maldevelopment.