The long‐term horizon: Patients who will remain untreated in the era of triple therapy
Andrew Aronsohn, Donald Jensen – 6 March 2012 – Watch the interview with the authors
A brief history of the treatment of viral hepatitis C
Doris B. Strader, Leonard B. Seeff – 6 March 2012 – Watch the interview with the authors
The new standard of HCV therapy: Retreatment in experienced patients
Naveen Gara, Marc G. Ghany – 6 March 2012 – Watch the interview with the authors
The horizon: New targets and new agents
Alison B. Jazwinski, Andrew J. Muir – 6 March 2012 – Watch the interview with the authors
Can we cure cholangiocarcinoma with neoadjuvant chemoradiation and liver transplantation? Time for a multicenter trial
Robin K. Kelley, Ryutaro Hirose, Alan P. Venook – 5 March 2012
NS5A: A new target for antiviral drugs in the treatment of hepatitis C virus infection
Jose D. Debes, Coleman I. Smith – 5 March 2012
Inhibition of natural killer cells protects the liver against acute injury in the absence of glycine N‐methyltransferase
Laura Gomez‐Santos, Zigmund Luka, Conrad Wagner, Sara Fernandez‐Alvarez, Shelly C. Lu, Jose M. Mato, Maria L. Martinez‐Chantar, Naiara Beraza – 5 March 2012 – Glycine N‐methyltransferase (GNMT) catabolizes S‐adenosylmethionine (SAMe), the main methyl donor of the body. Patients with cirrhosis show attenuated GNMT expression, which is absent in hepatocellular carcinoma (HCC) samples. GNMT−/− mice develop spontaneous steatosis that progresses to steatohepatitis, cirrhosis, and HCC.
TAT‐apoptosis repressor with caspase recruitment domain protein transduction rescues mice from fulminant liver failure
Junfeng An, Christoph Harms, Gisela Lättig‐Tünnemann, Gernot Sellge, Ana D. Mandić, Yann Malato, Arnd Heuser, Matthias Endres, Christian Trautwein, Stefan Donath – 5 March 2012 – Acute liver failure (ALF) is associated with massive hepatocyte cell death and high mortality rates. Therapeutic approaches targeting hepatocyte injury in ALF are hampered by the activation of distinct stimulus‐dependent pathways, mechanism of cell death, and a limited therapeutic window.
Frequency, clinical presentation, and outcomes of drug‐induced liver injury after liver transplantation
Stepan Sembera, Craig Lammert, Jayant A. Talwalkar, Schuyler O. Sanderson, John J. Poterucha, J. Eileen Hay, Russell H. Wiesner, Gregory J. Gores, Charles B. Rosen, Julie K. Heimbach, Michael R. Charlton – 5 March 2012 – Drug‐induced liver injury (DILI) is increasingly being recognized as a common cause of acute hepatitis. The clinical impact of DILI after liver transplantation (LT) is not known. The aim of this study was to describe the frequency, clinical presentation, and outcomes of DILI in LT recipients.
Histone deacetylase 6 functions as a tumor suppressor by activating c‐Jun NH2‐terminal kinase‐mediated beclin 1‐dependent autophagic cell death in liver cancer
Kwang Hwa Jung, Ji Heon Noh, Jeong Kyu Kim, Jung Woo Eun, Hyun Jin Bae, Young Gyoon Chang, Min Gyu Kim, Won Sang Park, Jung Young Lee, Sang‐Yeop Lee, In‐Sun Chu, Suk Woo Nam – 5 March 2012 – Ubiquitin‐binding histone deacetylase 6 (HDAC6) is uniquely endowed with tubulin deacetylase activity and plays an important role in the clearance of misfolded protein by autophagy. In cancer, HDAC6 has become a target for drug development due to its major contribution to oncogenic cell transformation.