YAP promotes proliferation, chemoresistance, and angiogenesis in human cholangiocarcinoma through TEAD transcription factors

Patricia Marti, Claudia Stein, Tanja Blumer, Yann Abraham, Michael T. Dill, Monika Pikiolek, Vanessa Orsini, Giorgia Jurisic, Philippe Megel, Zuzanna Makowska, Claudia Agarinis, Luigi Tornillo, Tewis Bouwmeester, Heinz Ruffner, Andreas Bauer, Christian N. Parker, Tobias Schmelzle, Luigi M. Terracciano, Markus H. Heim, Jan S. Tchorz – 14 July 2015 – The Yes‐associated protein (YAP)/Hippo pathway has been implicated in tissue development, regeneration, and tumorigenesis. However, its role in cholangiocarcinoma (CC) is not established.

Prediction of short‐ and long‐term outcome in patients with autoimmune hepatitis

Martha M. Kirstein, Frauke Metzler, Elena Geiger, Eyk Heinrich, Michael Hallensleben, Michael P. Manns, Arndt Vogel – 14 July 2015 – Autoimmune hepatitis (AIH) is a chronic inflammatory disease characterized by a loss of tolerance toward the hepatocellular epithelium. Liver transplantation (LT) represents the ultimate therapeutic option for a fulminant course or end‐stage liver disease. The aim of this study was to elucidate the clinical, serological, and genetic features of remission, relapse, and overall and LT‐free survival.

Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression

Young‐Kyoung Lee, Byul A. Jee, So Mee Kwon, Young‐Sil Yoon, Wei Guang Xu, Hee‐Jung Wang, Xin Wei Wang, Snorri S. Thorgeirsson, Jae‐Seon Lee, Hyun Goo Woo, Gyesoon Yoon – 14 July 2015 – Many cancer cells require more glycolytic adenosine triphosphate production due to a mitochondrial respiratory defect. However, the roles of mitochondrial defects in cancer development and progression remain unclear.

Signal transducer and activator of transcription 3‐mediated CD133 up‐regulation contributes to promotion of hepatocellular carcinoma

Cheolhee Won, Byung‐Hak Kim, Eun Hee Yi, Kyung‐Ju Choi, Eun‐Kyung Kim, Jong‐Min Jeong, Jae‐Ho Lee, Ja‐June Jang, Jung‐Hwan Yoon, Won‐Il Jeong, In‐Chul Park, Tae Woo Kim, Sun Sik Bae, Valentina M. Factor, Stephanie Ma, Snorri S. Thorgeirsson, Yun‐Han Lee, Sang‐Kyu Ye – 6 July 2015 – Enhanced expression of the cancer stem cell (CSC) marker, CD133, is closely associated with a higher rate of tumor formation and poor prognosis in hepatocellular carcinoma (HCC) patients.

World‐wide relative contribution of hepatitis B and C viruses in hepatocellular carcinoma

Catherine de Martel, Delphine Maucort‐Boulch, Martyn Plummer, Silvia Franceschi – 3 July 2015 – Hepatitis B virus (HBV) and hepatitis C virus (HCV) are major causes of hepatocellular carcinoma (HCC). In order to assess the relative contribution of HBV and HCV to HCC worldwide, and identify changes over time, we conducted a systematic review of case series published up to the year 2014. Eligible studies had to report seroprevalence of both hepatitis B surface antigen (HBsAg) and antibodies to HCV (anti‐HCV), alone and in combination, for at least 20 adult HCC cases.

Randomized phase 3 trial of ombitasvir/paritaprevir/ritonavir for hepatitis C virus genotype 1b–infected Japanese patients with or without cirrhosis

Hiromitsu Kumada, Kazuaki Chayama, Lino Rodrigues, Fumitaka Suzuki, Kenji Ikeda, Hidenori Toyoda, Ken Sato, Yoshiyasu Karino, Yasushi Matsuzaki, Kiyohide Kioka, Carolyn Setze, Tami Pilot‐Matias, Meenal Patwardhan, Regis A. Vilchez, Margaret Burroughs, Rebecca Redman – 3 July 2015 – GIFT‐I is a phase 3 trial evaluating the efficacy and safety of a 12‐week regimen of coformulated ombitasvir (OBV)/paritaprevir (PTV)/ritonavir (r) for treatment of Japanese hepatitis C virus genotype 1b–infected patients.

Temporal dynamics of inflammatory cytokines/chemokines during sofosbuvir and ribavirin therapy for genotype 2 and 3 hepatitis C infection

Aaron F. Carlin, Paula Aristizabal, Qinghua Song, Huan Wang, Matthew S. Paulson, Luisa M. Stamm, Robert T. Schooley, David L. Wyles – 3 July 2015 – The analysis of inflammatory cytokines and chemokines produced during hepatitis C virus (HCV) infection has advanced our understanding of viral‐host interactions and identified predictors of treatment response. Administration of interferons (IFNs) made it difficult to interpret biomarkers of immune activation during treatment. Direct‐acting antiviral (DAA) regimens without IFN are now being used to treat HCV with excellent efficacy.

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