Insurance status and treatment candidacy of hepatitis C patients: Analysis of population‐based data from the United States

Maria Stepanova, Fasiha Kanwal, Hashem B. El‐Serag, Zobair M. Younossi – 17 December 2010 – Successful treatment with antiviral therapy could potentially reduce morbidity and mortality in patients with hepatitis C virus (HCV) infection. However, at the population level, these benefits may be offset by a limited number of patients who have access to antiviral treatment. Using data from the National Health and Nutrition Examination Survey conducted in 2005‐2008, we analyzed the health insurance status and treatment candidacy of HCV‐positive (HCV+) individuals.

Evolution of genomic instability in diethylnitrosamine‐induced hepatocarcinogenesis in mice

Kristina Aleksic, Carolin Lackner, Jochen B. Geigl, Martina Schwarz, Martina Auer, Peter Ulz, Maria Fischer, Zlatko Trajanoski, Marcus Otte, Michael R. Speicher – 17 December 2010 – Diethylnitrosamine (DEN) is a hepatic procarcinogen which is frequently used as an inducer of hepatocellular carcinoma (HCC) in mice. Although mice after DEN exposure are among the most widely used models for liver tumorigenesis, a detailed, mechanistic characterization of the longitudinal changes in the respective tumor genomes has never been performed.

Paired box gene 5 is a novel tumor suppressor in hepatocellular carcinoma through interaction with p53 signaling pathway

Weili Liu, Xiaoxing Li, Eagle S.H. Chu, Minnie Y.Y. Go, Lixia Xu, Guijun Zhao, Lili Li, Ning Dai, Jianmin Si, Qian Tao, Joseph J.Y. Sung, Jun Yu – 17 December 2010 – The paired box 5 (PAX5) is a member of PAX transcription factors family involved in the regulation of embryonic development. However, the role of PAX5 in carcinogenesis is largely unclear. We identified that PAX5 is involved in human cancer by methylation‐sensitive representational difference analysis. We examined the biological functions and related molecular mechanisms of PAX5 in hepatocellular carcinoma (HCC).

HepaRG cells: A human model to study mechanisms of acetaminophen hepatotoxicity

Mitchell R. McGill, Hui‐Min Yan, Anup Ramachandran, Gordon J. Murray, Douglas E. Rollins, Hartmut Jaeschke – 17 December 2010 – Acetaminophen (APAP) overdose is the leading cause of acute liver failure in Western countries. In the last four decades much progress has been made in our understanding of APAP‐induced liver injury through rodent studies. However, some differences exist in the time course of injury between rodents and humans. To study the mechanism of APAP hepatotoxicity in humans, a human‐relevant in vitro system is needed.

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