Paracrine signals from liver sinusoidal endothelium regulate hepatitis C virus replication

Ian A. Rowe, Sukhdeep K. Galsinh, Garrick K. Wilson, Richard Parker, Sarah Durant, Catalin Lazar, Norica Branza‐Nichita, Roy Bicknell, David H. Adams, Peter Balfe, Jane A. McKeating – 14 June 2013 – Hepatitis C virus (HCV) is a major cause of global morbidity, causing chronic liver injury that can progress to cirrhosis and hepatocellular carcinoma. The liver is a large and complex organ containing multiple cell types, including hepatocytes, sinusoidal endothelial cells (LSEC), Kupffer cells, and biliary epithelial cells.

Molecular profiling of stroma identifies osteopontin as an independent predictor of poor prognosis in intrahepatic cholangiocarcinoma

Laurent Sulpice, Michel Rayar, Mireille Desille, Bruno Turlin, Alain Fautrel, Eveline Boucher, Francisco Llamas‐Gutierrez, Bernard Meunier, Karim Boudjema, Bruno Clément, Cédric Coulouarn – 14 June 2013 – Intrahepatic cholangiocarcinoma (ICC) is the second most common type of primary cancer in the liver. ICC is an aggressive cancer with poor prognosis and limited therapeutic strategies. The identification of new drug targets and prognostic biomarkers is an important clinical challenge for ICC. The presence of an abundant stroma is a histological hallmark of ICC.

Molecular profiling of stroma identifies osteopontin as an independent predictor of poor prognosis in intrahepatic cholangiocarcinoma

Laurent Sulpice, Michel Rayar, Mireille Desille, Bruno Turlin, Alain Fautrel, Eveline Boucher, Francisco Llamas‐Gutierrez, Bernard Meunier, Karim Boudjema, Bruno Clément, Cédric Coulouarn – 14 June 2013 – Intrahepatic cholangiocarcinoma (ICC) is the second most common type of primary cancer in the liver. ICC is an aggressive cancer with poor prognosis and limited therapeutic strategies. The identification of new drug targets and prognostic biomarkers is an important clinical challenge for ICC. The presence of an abundant stroma is a histological hallmark of ICC.

Liver transplantation normalizes serum hepcidin level and cures iron metabolism alterations in HFE hemochromatosis

Edouard Bardou‐Jacquet, Julie Philip, Richard Lorho, Martine Ropert, Marianne Latournerie, Pauline Houssel‐Debry, Dominique Guyader, Olivier Loréal, Karim Boudjema, Pierre Brissot – 14 June 2013 – Defects in human hemochromatosis protein (HFE) cause iron overload due to reduced hepatic hepcidin secretion. Liver transplantation (LT) is a key treatment for potential complications from HFE‐related hereditary hemochromatosis (HH). This study evaluated hepcidin secretion and iron burden after LT to elucidate HH pathophysiology.

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