Programmed cell death‐1 (PD‐1) checkpoint blockade in combination with a mammalian target of rapamycin inhibitor restrains hepatocellular carcinoma growth induced by hepatoma cell–intrinsic PD‐1

Hui Li, Xiaoqiang Li, Shuang Liu, Lei Guo, Bo Zhang, Jubo Zhang, Qinghai Ye – 21 July 2017 – Inhibitors of programmed cell death 1 (PD‐1) administered as single agents have resulted in durable tumor regression in advanced cancer patients. However, only a minority of cancer patients respond to anti‐PD‐1 immunotherapy. Here, we show that PD‐1 expression in hepatocellular carcinoma promotes tumor growth independently of adaptive immunity. Knockdown of PD‐1 suppresses tumor growth, whereas PD‐1 overexpression enhances tumorigenesis in immunodeficient xenografted mice.

Hepatocytes contribute to residual glucose production in a mouse model for glycogen storage disease type Ia

Brenda S. Hijmans, Andreas Boss, Theo H. van Dijk, Maud Soty, Henk Wolters, Elodie Mutel, Albert K. Groen, Terry G.J. Derks, Gilles Mithieux, Arend Heerschap, Dirk‐Jan Reijngoud, Fabienne Rajas, Maaike H. Oosterveer – 20 July 2017 – It is a long‐standing enigma how glycogen storage disease (GSD) type I patients retain a limited capacity for endogenous glucose production despite the loss of glucose‐6‐phosphatase activity.

TRAIL deletion prevents liver inflammation but not adipose tissue inflammation during murine diet‐induced obesity

Petra Hirsova, Peggy Weng, Warda Salim, Steven F. Bronk, Thomas S. Griffith, Samar H. Ibrahim, Gregory J. Gores – 20 July 2017 – Tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) and its cognate receptor(s) are up‐regulated in human and murine nonalcoholic steatohepatitis (NASH); however, the consequence of this enhanced expression on NASH pathogenesis remains unclear. TRAIL may either accentuate liver injury by promoting hepatic steatosis and inflammation or it may mitigate the disease process by improving systemic insulin resistance and averting hepatic fibrosis.

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