Raised serum ferritin concentration in hereditary hyperferritinemia cataract syndrome is not a marker for iron overload

Dan Yin, Vasu Kulhalli, Ann P. Walker – 12 August 2013 – Hyperferritinemia and bilateral cataracts are features of the rare hereditary hyperferritinemia cataract syndrome (HHCS; OMIM #600886). HHCS is an autosomal dominant condition caused by mutations which increase expression of the ferritin light polypeptide (FTL) gene. We report a patient with HHCS who was misdiagnosed and treated as having hemochromatosis, in whom a heterozygous c.‐160A>G mutation was identified in the iron responsive element (IRE) of FTL, causing ferritin synthesis in the absence of iron overload.

No detectable resistance to tenofovir disoproxil fumarate after 6 years of therapy in patients with chronic hepatitis B

Kathryn M. Kitrinos, Amoreena Corsa, Yang Liu, John Flaherty, Andrea Snow‐Lampart, Patrick Marcellin, Katyna Borroto‐Esoda, Michael D. Miller – 12 August 2013 – One major challenge in the treatment of chronic hepatitis B is to maintain long‐term viral suppression without promoting the selection of drug‐resistant mutations. We analyzed data from 347 hepatitis B e antigen‐negative and 238 hepatitis B e antigen‐positive patients receiving tenofovir disoproxil fumarate (TDF) in an open‐label, long‐term extension of two phase 3 studies.

Hepatic oxidative stress activates the Gadd45b gene by way of degradation of the transcriptional repressor STAT3

Jung‐Hwan Kim, Aijuan Qu, Janardan K. Reddy, Bin Gao, Frank J. Gonzalez – 12 August 2013 – Growth arrest and DNA damage‐inducible beta (GADD45b) plays an important role in many intracellular events, such as cell cycle arrest, DNA repair, cell survival, apoptosis, and senescence. However, its mechanism of transcriptional regulation remains unclear. In this study the mechanism of peroxisome proliferator‐activated receptor α (PPARα) ligand induction of the Gadd45b gene in mouse liver was investigated.

Raised serum ferritin concentration in hereditary hyperferritinemia cataract syndrome is not a marker for iron overload

Dan Yin, Vasu Kulhalli, Ann P. Walker – 12 August 2013 – Hyperferritinemia and bilateral cataracts are features of the rare hereditary hyperferritinemia cataract syndrome (HHCS; OMIM #600886). HHCS is an autosomal dominant condition caused by mutations which increase expression of the ferritin light polypeptide (FTL) gene. We report a patient with HHCS who was misdiagnosed and treated as having hemochromatosis, in whom a heterozygous c.‐160A>G mutation was identified in the iron responsive element (IRE) of FTL, causing ferritin synthesis in the absence of iron overload.

Fibroblast growth factor signaling in liver carcinogenesis

Dalbir S. Sandhu, Esha Baichoo, Lewis R. Roberts – 12 August 2013 – Fibroblast growth factors, or FGFs, are a large family of polypeptide cytokines exhibiting a pleiotropy of functions, from cell growth to angiogenesis, wound healing, and tissue repair. This review broadly covers the genetics and protein expression of the FGF family members and the signaling pathways involved in FGF‐mediated growth regulation. We emphasize the role of FGFs in the pathogenesis of hepatocellular carcinoma (HCC), including their effects on regulation of the tumor microenvironment and angiogenesis.

Fibroblast growth factor signaling in liver carcinogenesis

Dalbir S. Sandhu, Esha Baichoo, Lewis R. Roberts – 12 August 2013 – Fibroblast growth factors, or FGFs, are a large family of polypeptide cytokines exhibiting a pleiotropy of functions, from cell growth to angiogenesis, wound healing, and tissue repair. This review broadly covers the genetics and protein expression of the FGF family members and the signaling pathways involved in FGF‐mediated growth regulation. We emphasize the role of FGFs in the pathogenesis of hepatocellular carcinoma (HCC), including their effects on regulation of the tumor microenvironment and angiogenesis.

Structure‐guided design affirms inhibitors of hepatitis C virus p7 as a viable class of antivirals targeting virion release

Toshana L. Foster, Gary S. Thompson, Arnout P. Kalverda, Jayakanth Kankanala, Matthew Bentham, Laura F. Wetherill, Joseph Thompson, Amy M. Barker, Dean Clarke, Marko Noerenberg, Arwen R. Pearson, David J. Rowlands, Steven W. Homans, Mark Harris, Richard Foster, Stephen Griffin – 12 August 2013 – Current interferon‐based therapy for hepatitis C virus (HCV) infection is inadequate, prompting a shift toward combinations of direct‐acting antivirals (DAA) with the first protease‐targeted drugs licensed in 2012.

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