HNF1B deficiency causes ciliary defects in human cholangiocytes

Philip Roelandt, Aline Antoniou, Louis Libbrecht, Werner Van Steenbergen, Wim Laleman, Chris Verslype, Schalk Van der Merwe, Frederik Nevens, Rita De Vos, Evelyne Fischer, Marco Pontoglio, Frédéric Lemaigre, David Cassiman – 18 June 2012 – Heterozygous deletion or mutation in hepatocyte nuclear factor 1 homeobox B/transcription factor 2 (HNF1B/TCF2) causes renal cyst and diabetes syndrome (OMIM #137920). Mice with homozygous liver‐specific deletion of Hnf1β revealed that a complete lack of this factor leads to ductopenia and bile duct dysplasia, in addition to mild hepatocyte defects.

Long noncoding RNA associated with microvascular invasion in hepatocellular carcinoma promotes angiogenesis and serves as a predictor for hepatocellular carcinoma patients' poor recurrence‐free survival after hepatectomy

Sheng‐Xian Yuan, Fu Yang, Yuan Yang, Qi‐Fei Tao, Jin Zhang, Gang Huang, Yun Yang, Ruo‐Yu Wang, Sen Yang, Xi‐Song Huo, Ling Zhang, Fang Wang, Shu‐Han Sun, Wei‐Ping Zhou – 18 June 2012 – Survival of patients with hepatocellular carcinoma (HCC) remains poor, which is largely attributed to active angiogenesis. However, the mechanisms underlying angiogenesis in HCC remain to be discovered. In this study, we found that long noncoding RNA associated with microvascular invasion in HCC (lncRNA MVIH) (lncRNA associated with microvascular invasion in HCC) was generally overexpressed in HCC.

HNF1B deficiency causes ciliary defects in human cholangiocytes

Philip Roelandt, Aline Antoniou, Louis Libbrecht, Werner Van Steenbergen, Wim Laleman, Chris Verslype, Schalk Van der Merwe, Frederik Nevens, Rita De Vos, Evelyne Fischer, Marco Pontoglio, Frédéric Lemaigre, David Cassiman – 18 June 2012 – Heterozygous deletion or mutation in hepatocyte nuclear factor 1 homeobox B/transcription factor 2 (HNF1B/TCF2) causes renal cyst and diabetes syndrome (OMIM #137920). Mice with homozygous liver‐specific deletion of Hnf1β revealed that a complete lack of this factor leads to ductopenia and bile duct dysplasia, in addition to mild hepatocyte defects.

Transcriptomic profiling reveals hepatic stem‐like gene signatures and interplay of miR‐200c and epithelial‐mesenchymal transition in intrahepatic cholangiocarcinoma

Naoki Oishi, Mia R. Kumar, Stephanie Roessler, Junfang Ji, Marshonna Forgues, Anuradha Budhu, Xuelian Zhao, Jesper B. Andersen, Qing‐Hai Ye, Hu‐Liang Jia, Lun‐Xiu Qin, Taro Yamashita, Hyun Goo Woo, Yoon Jun Kim, Shuichi Kaneko, Zhao‐You Tang, Snorri S. Thorgeirsson, Xin Wei Wang – 18 June 2012 – Intrahepatic cholangiocellular carcinoma (ICC) is the second most common type of primary liver cancer. However, its tumor heterogeneity and molecular characteristics are largely unknown.

Hepatic enrichment and activation of myeloid dendritic cells during chronic hepatitis C virus infection

Victoria M. Velazquez, Huiming Hon, Chris Ibegbu, Stuart J. Knechtle, Allan D. Kirk, Arash Grakoui – 18 June 2012 – Chronic hepatitis C virus (HCV) infection is a serious disease that can result in numerous long‐term complications leading to liver failure or death. Approximately 80% of people fail to clear their infection, largely as the result of weak, narrowly targeting or waning antiviral T‐cell responses.

Case report of successful peginterferon, ribavirin, and daclatasvir therapy for recurrent cholestatic hepatitis C after liver retransplantation

Robert J. Fontana, Eric A. Hughes, Henry Appelman, Robert Hindes, Dessislava Dimitrova, Marc Bifano – 18 June 2012 – A recurrent hepatitis C virus (HCV) infection after liver transplantation (LT) can lead to accelerated allograft injury and fibrosis. The aim of this article is to report the first ever use of daclatasvir (DCV; also known as BMS‐790052), a potent orally administered nonstructural 5A replication complex inhibitor, in combination with peginterferon α (PEG‐IFNα) and ribavirin in an LT recipient.

Analysis of the role of hepatic PPARγ expression during mouse liver regeneration

Vered Gazit, Jiansheng Huang, Alexander Weymann, David A. Rudnick – 18 June 2012 – Mice subjected to partial hepatectomy (PH) develop hypoglycemia, followed by increased systemic lipolysis and hepatic fat accumulation, prior to onset of hepatocellular proliferation. Strategies that disrupt these metabolic events inhibit regeneration. These observations suggest that alterations in metabolism in response to hepatic insufficiency promote liver regeneration. Hepatic expression of the peroxisome proliferator‐activated receptor gamma (PPARγ) influences fat accumulation in the liver.

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