High liver fibrosis index FIB‐4 is highly predictive of hepatocellular carcinoma in chronic hepatitis B carriers

Beomseok Suh, Sehhoon Park, Dong Wook Shin, Jae Moon Yun, Hyung‐Kook Yang, Su Jong Yu, Cheong‐Il Shin, Jin‐Soo Kim, Eunmi Ahn, Hyejin Lee, Jin Ho Park, BeLong Cho – 12 December 2014 – Screening for hepatocellular carcinoma (HCC) is clinically important given that its early detection has remarkable survival benefits. We investigated the possible role of FIB‐4, a recently developed noninvasive marker for liver fibrosis based on routine laboratory tests, as a clinical indicator for predicting future HCC among hepatitis B surface antigen (HBsAg) carriers.

Vps4A functions as a tumor suppressor by regulating the secretion and uptake of exosomal microRNAs in human hepatoma cells

Jin‐xing Wei, Li‐hong Lv, Yun‐le Wan, Yang Cao, Guo‐lin Li, Hao‐ming Lin, Rui Zhou, Chang‐zhen Shang, Jun Cao, Hai He, Qing‐fang Han, Pei‐qing Liu, Gang Zhou, Jun Min – 12 December 2014 – The deregulation of microRNAs (miRNAs) plays an important role in human hepatocarcinogenesis. In this study, we highlight exosomes as mediators involved in modulating miRNA profiles in hepatocellular carcinoma (HCC) cells. First, we examined the different miRNA expression profiles in HCC cells and HCC cell–derived exosomes.

Determining the fate of hepatic cells by lineage tracing: Facts and pitfalls

Frédéric P. Lemaigre – 12 December 2014 – Slow renewal of the epithelial cells by proliferation ensures homeostasis of the liver, but extensive proliferation may occur upon injury. When proliferation is impaired, transdifferentiation of mature cells or differentiation of stem cells allows production of new hepatocytes and cholangiocytes. While lineage tracings using cyclization recombinase (Cre) recombinase–mediated cell labeling represent the gold standard for defining cell fate, there are more variables than was initially realized.

Determining the fate of hepatic cells by lineage tracing: Facts and pitfalls

Frédéric P. Lemaigre – 12 December 2014 – Slow renewal of the epithelial cells by proliferation ensures homeostasis of the liver, but extensive proliferation may occur upon injury. When proliferation is impaired, transdifferentiation of mature cells or differentiation of stem cells allows production of new hepatocytes and cholangiocytes. While lineage tracings using cyclization recombinase (Cre) recombinase–mediated cell labeling represent the gold standard for defining cell fate, there are more variables than was initially realized.

Serum sodium and survival benefit of liver transplantation

Pratima Sharma, Douglas E. Schaubel, Nathan P. Goodrich, Robert M. Merion – 11 December 2014 – Hyponatremia is associated with elevated wait‐list mortality among end‐stage liver disease candidates for liver transplantation (LT). However, the effect of low serum sodium on the survival benefit of LT has not been examined. We sought to determine whether pretransplant hyponatremia is associated with an altered LT survival benefit. Data were obtained from the Scientific Registry of Transplant Recipients.

Low‐molecular‐weight fibroblast growth factor 2 attenuates hepatic fibrosis by epigenetic down‐regulation of Delta‐like1

Ruo‐Lang Pan, Li‐Xin Xiang, Ping Wang, Xiao‐Yuan Liu, Li Nie, Wendong Huang, Jian‐Zhong Shao – 11 December 2014 – Liver fibrosis, a major cause of end‐stage liver diseases, is closely regulated by multiple growth factors and cytokines. The correlation of fibroblast growth factor 2 (FGF2) with chronic liver injury has been reported, but the exact functions of different FGF2 isoforms in liver fibrogenesis remain unclear.

Potential of human induced pluripotent stem cells in studies of liver disease

Fotios Sampaziotis, Charis‐Patricia Segeritz, Ludovic Vallier – 11 December 2014 – Liver disease is a leading cause of death in the Western world. However, our insight into the underlying disease mechanisms and the development of novel therapeutic agents has been hindered by limited availability of primary tissue, intraspecies variability associated with the use of animal models, and reduced long‐term viability of isolated and diseased liver cells.

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