Jin‐Ping Lai, Dalbir S. Sandhu, Chunrong Yu, Tao Han, Catherine D. Moser, Kenard K. Jackson, Ruben Bonilla Guerrero, Ileana Aderca, Hajime Isomoto, Megan M. Garrity‐Park, Hongzhi Zou, Abdirashid M. Shire, David M. Nagorney, Schuyler O. Sanderson, Alex A. Adjei, Ju‐Seog Lee, Snorri S. Thorgeirsson, Lewis R. Roberts – 7 January 2008 – It has been shown that the heparin‐degrading endosulfatase, sulfatase 1 (SULF1), functions as a liver tumor suppressor, but the role of the related sulfatase, sulfatase 2 (SULF2), in liver carcinogenesis remains to be elucidated.

W. Ray Kim, Steven L. Flamm, Adrian M. Di Bisceglie, Henry C. Bodenheimer – 7 January 2008

Narci C. Teoh, Yock Young Dan, Karen Swisshelm, Stacey Lehman, Jocelyn H. Wright, Jamil Haque, Yansong Gu, Nelson Fausto – 7 January 2008 – Chromosomal instability is a characteristic feature of hepatocellular carcinoma (HCC) but its origin and role in liver carcinogenesis are undefined. We tested whether a defect in the nonhomologous end‐joining (NHEJ) DNA repair gene Ku70 was associated with chromosomal abnormalities and enhanced liver carcinogenesis.

Yasuko Iwakiri, Matthew Grisham, Vijay Shah – 7 January 2008 – Portal hypertension and its complications account for the majority of morbidity and mortality that occurs in patients with cirrhosis. In addition to portal hypertension, a number of other vascular syndromes are also of great importance, especially the ischemia‐reperfusion (IR) injury. With the identification of major vascular defects that could account for many of the clinical sequelae of these syndromes, the liver vasculature field has now integrated very closely with the broader vascular biology discipline.

Piero Portincasa, Agostino Di Ciaula, Helen H. Wang, Giuseppe Palasciano, Karel J. van Erpecum, Antonio Moschetta, David Q.‐H. Wang – 7 January 2008 – Gallstones are one of the most common digestive diseases with an estimated prevalence of 10%‐15% in adults living in the western world, where cholesterol‐enriched gallstones represent 75%‐80% of all gallstones. In cholesterol gallstone disease, the gallbladder becomes the target organ of a complex metabolic disease.

Rebecca G. Wells – 7 January 2008 – Matrix stiffness (resistance to deformation), one of the many mechanical forces acting on cells, is increasingly appreciated as an important mediator of cell behavior. It regulates cell signaling broadly, with effects on growth, survival, and motility. Although the stiffness optima for different kinds of adherent cells vary widely, it is generally true that cell proliferation and differentiation increase with the stiffness of the matrix.

Kirk J. Wangensteen, Andrew Wilber, Vincent W. Keng, Zhiying He, Ilze Matise, Laura Wangensteen, Corey M. Carson, Yixin Chen, Clifford J. Steer, R. Scott McIvor, David A. Largaespada, Xin Wang, Stephen C. Ekker – 7 January 2008 – Current techniques for the alteration of gene expression in the liver have a number of limitations, including the lack of stable somatic gene transfer and the technical challenges of germline transgenesis. Rapid and stable genetic engineering of the liver would allow systematic, in vivo testing of contributions by many genes to disease.

Dominique Charles Valla – 7 January 2008

Guoli Dai, Lin He, Pengli Bu, Yu‐Jui Yvonne Wan – 31 December 2007 – Pregnane X receptor (PXR) mediates xenobiotic and endobiotic metabolism as well as hepatocyte proliferation. To determine the role of PXR in liver regeneration, 2/3 partial hepatectomy (PH) was performed on wild‐type and PXR‐null mice. Our results showed that hepatic steatosis was markedly suppressed in mice lacking PXR 36 hours after PH, concomitant with reduction of hepatocyte proliferation at the same time point.

C. Bart Rountree, Shantha Senadheera, Jose M. Mato, Gay M. Crooks, Shelly C. Lu – 31 December 2007 – Methionine adenosyltransferase (MAT) is an essential enzyme that catalyzes the biosynthesis of S‐adenosylmethionine. Hepatic MAT activity falls in chronic liver diseases, and mice lacking Mat1a are predisposed to liver injury and develop hepatocellular carcinoma (HCC) spontaneously by 18 months. The current work examined the hypothesis that liver cancer stem cells contribute to HCC in this model.