Genetic variation in transmembrane 6 superfamily member 2 and the risk of nonalcoholic fatty liver disease and histological disease severity

Silvia Sookoian, Gustavo O. Castaño, Romina Scian, Pablo Mallardi, Tomas Fernández Gianotti, Adriana L. Burgueño, Julio San Martino, Carlos J. Pirola – 10 October 2014 – We explored the role of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C/T nonsynonymous (p.Glu167Lys) variant in genetic susceptibility to nonalcoholic fatty liver disease (NAFLD) and disease severity. A total of 361 individuals (135 control subjects and 226 patients with histologically proven NAFLD) were included in a sample with 97% power for the additive genetic model.

Interleukin‐1β/Iinterleukin‐1 receptor‐associated kinase 1 inflammatory signaling contributes to persistent Gankyrin activation during hepatocarcinogenesis

Bo Su, Tao Luo, Junjie Zhu, Jing Fu, Xiaofang Zhao, Lei Chen, Huilu Zhang, Yibin Ren, Lexing Yu, Xiaojun Yang, Mengchao Wu, Gensheng Feng, Shao Li, Yao Chen, Hongyang Wang – 7 October 2014 – Hepatocellular carcinoma (HCC) is a prototype of inflammation‐associated cancer. Oncoprotein Gankyrin, which mostly increases in HCC, plays a critical role in HCC development and metastasis. However, the exact mechanism of Gankyrin up‐regulation in HCC remains unclear.

Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: Results of a longitudinal study

Filipe Nery, Sylvie Chevret, Bertrand Condat, Emmanuelle de Raucourt, Larbi Boudaoud, Pierre‐Emmanuel Rautou, Aurelie Plessier, Dominique Roulot, Cendrine Chaffaut, Valerie Bourcier, Jean‐Claude Trinchet, Dominique‐Charles Valla, on behalf of Groupe d'Etude et de Traitement du Carcinome Hépatocellulaire – 6 October 2014 – In cirrhosis, portal vein thrombosis (PVT) could be a cause or a consequence of the progression of liver disease.

Lineage‐dependent effects of aryl hydrocarbon receptor agonists contribute to liver tumorigenesis

Joshua A. Harrill, Bethany B Parks, Eliane Wauthier, J. Craig Rowlands, Lola M. Reid, Russell S. Thomas – 6 October 2014 – Rodent cancer bioassays indicate that the aryl hydrocarbon receptor (AHR) agonist, 2,3,7,8‐tetracholorodibenzo‐p‐dioxin (TCDD), causes increases in both hepatocytic and cholangiocytic tumors. Effects of AHR activation have been evaluated on rodent hepatic stem cells (rHpSCs) versus their descendants, hepatoblasts (rHBs), two lineage stages of multipotent, hepatic precursors with overlapping but also distinct phenotypic traits.

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