Identification of driver genes in hepatocellular carcinoma by exome sequencing

Sean P. Cleary, William R. Jeck, Xiaobei Zhao, Kui Chen, Sara R. Selitsky, Gleb L. Savich, Ting‐Xu Tan, Michael C. Wu, Gad Getz, Michael S. Lawrence, Joel S. Parker, Jinyu Li, Scott Powers, Hyeja Kim, Sandra Fischer, Maha Guindi, Anand Ghanekar, Derek Y. Chiang – 31 May 2013 – Genetic alterations in specific driver genes lead to disruption of cellular pathways and are critical events in the instigation and progression of hepatocellular carcinoma (HCC). As a prerequisite for individualized cancer treatment, we sought to characterize the landscape of recurrent somatic mutations in HCC.

Neutralization resistance of hepatitis C virus can be overcome by recombinant human monoclonal antibodies

Jannie Pedersen, Thomas H.R. Carlsen, Jannick Prentoe, Santseharay Ramirez, Tanja B. Jensen, Xavier Forns, Harvey Alter, Steven K.H. Foung, Mansun Law, Judith Gottwein, Nina Weis, Jens Bukh – 31 May 2013 – Immunotherapy and vaccine development for hepatitis C virus (HCV) will depend on broadly reactive neutralizing antibodies (NAbs). However, studies in infectious strain JFH1‐based culture systems expressing patient‐derived Core‐NS2 proteins have suggested neutralization resistance for specific HCV strains, in particular, of genotype 2.

CD73 (ecto‐5′‐nucleotidase) hepatocyte levels differ across mouse strains and contribute to mallory‐denk body formation

Natasha T. Snider, Nicholas W. Griggs, Amika Singla, David S. Moons, Sujith V.W. Weerasinghe, Anna S. Lok, Chunhai Ruan, Charles F. Burant, Hari S. Conjeevaram, M. Bishr Omary – 31 May 2013 – Formation of hepatocyte Mallory‐Denk bodies (MDBs), which are aggregates of keratins 8 and 18 (K8/K18), ubiquitin, and the ubiquitin‐binding protein, p62, has a genetic predisposition component in humans and mice. We tested the hypothesis that metabolomic profiling of MDB‐susceptible C57BL and MDB‐resistant C3H mouse strains can illuminate MDB‐associated pathways.

Retracted: Equilibrative nucleoside transporter (ENT)‐1‐dependent elevation of extracellular adenosine protects the liver during ischemia and reperfusion

Michael A. Zimmerman, Eunyoung Tak, Stefan F. Ehrentraut, Maria Kaplan, Antasia Giebler, Tingting Weng, Doo‐Sup Choi, Michael R. Blackburn, Igal Kam, Holger K. Eltzschig, Almut Grenz – 23 May 2013 – Ischemia and reperfusion‐elicited tissue injury contributes to morbidity and mortality of hepatic surgery and during liver transplantation. Previous studies implicated extracellular adenosine signaling in liver protection.

Cross‐talk between Notch and Hedgehog regulates hepatic stellate cell fate in mice

Guanhua Xie, Gamze Karaca, Marzena Swiderska‐Syn, Gregory A. Michelotti, Leandi Krüger, Yuping Chen, Richard T. Premont, Steve S. Choi, Anna Mae Diehl – 23 May 2013 – Liver repair involves phenotypic changes in hepatic stellate cells (HSCs) and reactivation of morphogenic signaling pathways that modulate epithelial‐to‐mesenchymal/mesenchymal‐to‐epithelial transitions, such as Notch and Hedgehog (Hh). Hh stimulates HSCs to become myofibroblasts (MFs).

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