Mixed hepatocellular cholangiocarcinoma and intrahepatic cholangiocarcinoma in patients undergoing transplantation for hepatocellular carcinoma

Gonzalo Sapisochin, Nicholas Fidelman, John P. Roberts, Francis Y. Yao – 24 March 2011 – Mixed hepatocellular cholangiocarcinoma (HCC‐CC) and intrahepatic cholangiocarcinoma (I‐CC) are increasingly being reported in patients with cirrhosis.

Heme oxygenase‐1–mediated autophagy protects against hepatocyte cell death and hepatic injury from infection/sepsis in mice

Evie H. Carchman, Jayashree Rao, Patricia A. Loughran, Matthew R. Rosengart, Brian S. Zuckerbraun – 24 March 2011 – Adaptive responses to sepsis are necessary to prevent organ failure and death. Cellular signaling responses that limit cell death and structural damage allow a cell to withstand insult from sepsis to prevent irreversible organ dysfunction. One such protective pathway to reduce hepatocellular injury is the up‐regulation of heme oxygenase‐1 (HO‐1) signaling.

Virological breakthrough and resistance in patients with chronic hepatitis B receiving nucleos(t)ide analogues in clinical practice

Chanunta Hongthanakorn, Watcharasak Chotiyaputta, Kelly Oberhelman, Robert J. Fontana, Jorge A. Marrero, Tracy Licari, Anna S. F. Lok – 24 March 2011 – Virological breakthrough (VBT) is the first manifestation of antiviral drug resistance during nucleos(t)ide analogue (NUC) treatment of chronic hepatitis B (CHB), but not all VBTs are due to drug resistance. This study sought to determine the incidence of VBT and genotypic resistance (GR) in patients with CHB who were receiving NUCs in clinical practice. Records of patients with CHB who were receiving NUCs were reviewed.

Strategies for hepatocellular carcinoma therapy and diagnostics: Lessons learned from high throughput and profiling approaches

Kai Breuhahn, Gregory Gores, Peter Schirmacher – 23 March 2011 – Over the last decade, numerous small and high‐dimensional profiling analyses have been performed in human hepatocellular carcinoma (HCC), which address different levels of regulation and modulation. Because comprehensive analyses are lacking, the following review summarizes some of the general results and compares them with insights from other tumor entities. Particular attention is given to the impact of these results on future diagnostic and therapeutic approaches. (HEPATOLOGY 2011;)

Diclofenac inhibits tumor necrosis factor‐α‐induced nuclear factor‐κB activation causing synergistic hepatocyte apoptosis

Lisa Fredriksson, Bram Herpers, Giulia Benedetti, Quraisha Matadin, Jordi C. Puigvert, Hans de Bont, Sanja Dragovic, Nico P.E. Vermeulen, Jan N.M. Commandeur, Erik Danen, Marjo de Graauw, Bob van de Water – 23 March 2011 – Drug‐induced liver injury (DILI) is an important clinical problem. It involves crosstalk between drug toxicity and the immune system, but the exact mechanism at the cellular hepatocyte level is not well understood. Here we studied the mechanism of crosstalk in hepatocyte apoptosis caused by diclofenac and the proinflammatory cytokine tumor necrosis factor α (TNF‐α).

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