Histological diversity in cholangiocellular carcinoma reflects the different cholangiocyte phenotypes

Mina Komuta, Olivier Govaere, Vincent Vandecaveye, Jun Akiba, Werner Van Steenbergen, Chris Verslype, Wim Laleman, Jacques Pirenne, Raymond Aerts, Hirohisa Yano, Frederik Nevens, Baki Topal, Tania Roskams – 23 January 2012 – Cholangiocellular carcinoma (CC) originates from topographically heterogeneous cholangiocytes. The cylindrical mucin‐producing cholangiocytes are located in large bile ducts and the cuboidal non–mucin‐producing cholangiocytes are located in ductules containing bipotential hepatic progenitor cells (HPCs).

A morphometric and immunohistochemical study to assess the benefit of a sustained virological response in hepatitis C virus patients with cirrhosis

Roberta D'Ambrosio, Alessio Aghemo, Maria Grazia Rumi, Guido Ronchi, Maria Francesca Donato, Valerie Paradis, Massimo Colombo, Pierre Bedossa – 23 January 2012 – Although annular fibrosis is the hallmark of cirrhosis, other microscopic changes that affect liver function such as sinusoid capillarization or loss of metabolic zonation are common. A sustained virological response (SVR) may halt fibrosis deposition in hepatitis C virus (HCV)‐infected patients, but its impact on the other cirrhosis‐associated lesions is unknown.

Efficient suppression of murine intracellular adhesion molecule‐1 using ultrasound‐responsive and mannose‐modified lipoplexes inhibits acute hepatic inflammation

Keita Un, Shigeru Kawakami, Mitsuru Yoshida, Yuriko Higuchi, Ryo Suzuki, Kazuo Maruyama, Fumiyoshi Yamashita, Mitsuru Hashida – 23 January 2012 – Hepatitis is often associated with the overexpression of various adhesion molecules. In particular, intracellular adhesion molecule‐1 (ICAM‐1), which is expressed on hepatic endothelial cells (HECs) in the early stage of inflammation, is involved in serious illnesses. Therefore, ICAM‐1 suppression in HECs enables the suppression of inflammatory responses.

Increasing disparity in waitlist mortality rates with increased model for end‐stage liver disease scores for candidates with hepatocellular carcinoma versus candidates without hepatocellular carcinoma

David Goldberg, Benjamin French, Peter Abt, Sandy Feng, Andrew M. Cameron – 23 January 2012 – Candidates with hepatocellular carcinoma (HCC) within the Milan criteria (MC) receive standardized Model for End‐Stage LIver Disease (MELD) exception points because of the projected risk of tumor expansion beyond the MC. Exception points at listing are meant to be equivalent to a 15% rusj if 90‐day mortality, with additional points granted every 3 months, equivalent to a 10% increased morality risk.

V‐AKT murine thymoma viral oncogene homolog/mammalian target of rapamycin activation induces a module of metabolic changes contributing to growth in insulin‐induced hepatocarcinogenesis

Matthias Evert, Diego F. Calvisi, Katja Evert, Valentina De Murtas, Gioia Gasparetti, Sandra Mattu, Giulia Destefanis, Sara Ladu, Antje Zimmermann, Salvatore Delogu, Sara Thiel, Andrea Thiele, Silvia Ribback, Frank Dombrowski – 23 January 2012 – Mounting epidemiological evidence supports a role for insulin‐signaling deregulation and diabetes mellitus in human hepatocarcinogenesis. However, the underlying molecular mechanisms remain unknown.

Serum and glucocorticoid kinase 3 at 8q13.1 promotes cell proliferation and survival in hepatocellular carcinoma

Ming Liu, Leilei Chen, Tim Hon Man Chan, Jian Wang, Yan Li, Yan Li, Ting‐Ting Zeng, Yun‐Fei Yuan, Xin‐Yuan Guan – 19 January 2012 – Amplification of broad regions of 8q is one of the most frequent genetic alterations in hepatocellular carcinoma (HCC), suggesting the existence of oncogenes in addition to MYC at 8q24.21. In this report we examine the potential role of the candidate amplified oncogene serum and glucocorticoid kinase 3 (SGK3) at 8q13.1 in HCC pathogenesis.

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