Immunosuppression in pediatric liver transplant recipients: Unique aspects

Tamir Miloh, Andrea Barton, Justin Wheeler, Yen Pham, Winston Hewitt, Tara Keegan, Christine Sanchez, Pinar Bulut, John Goss – 22 November 2016 – Pediatric liver transplantation has experienced improved outcomes over the last 50 years. This can be attributed in part to establishing optimal use of immunosuppressive agents to achieve a balance between minimizing the risks of allograft rejection and infection. The management of immunosuppression in children is generally more complex and can be challenging when compared with the use of these agents in adult liver transplant patients.

IL6‐mediated inflammatory loop reprograms normal to epithelial‐mesenchymal transition+ metastatic cancer stem cells in preneoplastic liver of transforming growth factor beta–deficient β2‐spectrin+/− mice

Abhisek Mitra, Jun Yan, Xueqing Xia, Shouhao Zhou, Jian Chen, Lopa Mishra, Shulin Li – 18 November 2016 – Hepatocellular carcinoma (HCC) is the second‐leading cause of cancer‐related deaths worldwide with a poor survival rate. As many as 40% of HCCs are clonal, with alteration of key tumor‐suppressor pathways in stem cells as the primary cause of HCC initiation. However, mechanisms that generate metastatic stem cells in preneoplastic liver tissue are not well understood.

Elevated FABP1 serum levels are associated with poorer survival in acetaminophen‐induced acute liver failure

Constantine J. Karvellas, Jaime L. Speiser, Mélanie Tremblay, William M. Lee, Christopher F. Rose, for the US Acute Liver Failure Study Group – 18 November 2016 – Acetaminophen (APAP)‐induced acute liver failure (ALF) is associated with significant mortality. Traditional prognostic scores lack sensitivity. Serum liver‐type fatty acid binding protein (FABP1) early (day 1) or late (day 3‐5) levels are associated with 21‐day mortality in the absence of liver transplant.

The origin of fibrogenic myofibroblasts in fibrotic liver

Tatiana Kisseleva – 18 November 2016 – Liver fibrosis results from chronic liver injury of different etiologies. It is characterized by dysregulation of physiological remodeling, activation of myofibroblasts, and formation of a fibrous scar. Myofibroblasts develop contractile functions and secrete the extracellular matrix proteins that form this fibrous scar. Myofibroblasts are not present in the normal liver but activate and proliferate in response to injury and inflammation.

Hepatitis C virus infection triggers a tumor‐like glutamine metabolism

Pierre L. Lévy, Sarah Duponchel, Hannah Eischeid, Jennifer Molle, Maud Michelet, Gaëlle Diserens, Martina Vermathen, Peter Vermathen, Jean‐Francois Dufour, Hans‐Peter Dienes, Hans‐Michael Steffen, Margarete Odenthal, Fabien Zoulim, Birke Bartosch – 18 November 2016 – Chronic infection with hepatitis C virus (HCV) is one of the main causes of hepatocellular carcinoma. However, the molecular mechanisms linking the infection to cancer development remain poorly understood.

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