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.

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.

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

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.

Emilia Fransvea, Umberto Angelotti, Salvatore Antonaci, Gianluigi Giannelli – 7 January 2008 – Hepatocellular carcinoma (HCC) treatment is challenging because the mechanisms underlying tumor progression are still largely unknown. Transforming growth factor (TGF)–β1 is considered a crucial molecule in HCC tumorigenesis because increased levels of patients' serum and urine are associated with disease progression. The aim of the present study was to investigate the inhibition of TGF‐β signaling and its impact on HCC progression.

Yaakov Nahmias, Jonathan Goldwasser, Monica Casali, Daan van Poll, Takaji Wakita, Raymond T. Chung, Martin L. Yarmush – 7 January 2008 – Hepatitis C virus (HCV) infects over 3% of the world population and is the leading cause of chronic liver disease worldwide. HCV has long been known to associate with circulating lipoproteins, and its interactions with the cholesterol and lipid pathways have been recently described. In this work, we demonstrate that HCV is actively secreted by infected cells through a Golgi‐dependent mechanism while bound to very low density lipoprotein (vLDL).

Richard K. Sterling, Melissa J. Contos, Paula G. Smith, R. Todd Stravitz, Velimir A. Luketic, Michael Fuchs, Mitchell L. Shiffman, Arun J. Sanyal – 7 January 2008 – Hepatic steatosis has been reported in human immunodeficiency virus (HIV)/hepatitis C virus (HCV) coinfection. However, the features of steatohepatitis, including cytologic ballooning and pericellular fibrosis, its risk factors, and the impact on disease severity in such patients are unknown.

Jenny C. Ho, Ying Chi Ip, Siu Tim Cheung, Yuk Ting Lee, Kui Fat Chan, San Yu Wong, Sheung Tat Fan – 7 January 2008 – Primary liver cancer, hepatocellular carcinoma (HCC), is the fifth most common cancer and the third leading cancer killer in the world. There is no effective therapeutic option for most HCC patients. A new therapeutic strategy is essential. Granulin‐epithelin precursor (GEP, also called progranulin, acrogranin, or PC‐derived growth factor) was identified as a potential therapeutic target for HCC from our earlier genome‐wide expression profiles.

Young Joo Park, Mohammed Qatanani, Steven S. Chua, Jennifer L. LaRey, Stacy A. Johnson, Mitsuhiro Watanabe, David D. Moore, Yoon Kwang Lee – 7 January 2008 – The orphan nuclear hormone receptor small heterodimer partner (SHP) regulates the expression of several genes involved in bile acid homeostasis in the liver. Because bile acid toxicity is a major source of liver injury in cholestatic disease, we explored the role of SHP in liver damage induced by common bile duct ligation (BDL).

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.