Esther Unitt, Simon M. Rushbrook, Aileen Marshall, Susan Davies, Paul Gibbs, Lesley S. Morris, Nicholas Coleman, Graeme J. M. Alexander – 24 March 2005 – Hepatocellular carcinoma (HCC) has a poor prognosis with limited therapeutic options. We propose that local immune responses in patients with HCC are held in check by tumor‐infiltrating CD4+CD25+ T‐regulatory lymphocytes (Treg cells), which suppress the activity and proliferation of effector CD4+ and CD8+ T cells.

George N. Ioannou – 24 March 2005

Norman M. Kneteman, David F. Mercer – 23 March 2005

Harvey J. Alter – 23 March 2005

Kyong‐Mi Chang – 23 March 2005

Naga Chalasani – 23 March 2005

Estella M. Alonso – 23 March 2005

Salvador Benlloch, Marina Berenguer, Martín Prieto, José Miguel Rayón, Victoria Aguilera, Joaquín Berenguer – 21 March 2005 – Recurrent hepatitis C is a frequent event in liver transplantation (LT). Serial liver biopsies remain the best way of monitoring disease progression. Due to the limitations of a liver biopsy, there is an interest in developing noninvasive markers of liver fibrosis. While several models for predicting fibrosis have been constructed in patients who have not undergone transplantation, these are lacking in the transplant population.

J. Wallis Marsh, Sydney D. Finkelstein, Myron E. Schwartz, M. Isabel Fiel, Igor Dvorchik – 21 March 2005 – We analyzed global gene expression patterns of 91 human hepatocellular carcinomas (HCCs) to define the molecular characteristics of the tumors and to test the prognostic value of the expression profiles. Unsupervised classification methods revealed two distinctive subclasses of HCC that are highly associated with patient survival. This association was validated via 5 independent supervised learning methods.

Aileen Marshall, Simon Rushbrook, Lesley S. Morris, Ian S. Scott, Sarah L. Vowler, Susan E. Davies, Nicholas Coleman, Graeme Alexander – 21 March 2005 – Although graft infection with hepatitis C virus (HCV) occurs in virtually all patients transplanted for HCV‐related liver disease, the outcome ranges from minimal disease to the rapid development of cirrhosis. Induction of hepatocyte cell cycle entry followed by inhibition of cell cycle progression has been proposed as a potential mechanism whereby HCV may cause hepatocyte dysfunction and may promote fibrogenesis.