Drug‐induced allergic hepatitis develops in mice when myeloid‐derived suppressor cells are depleted prior to halothane treatment

Mala Chakraborty, Aaron M. Fullerton, Kenrick Semple, Lynette S. Chea, William R. Proctor, Mohammed Bourdi, David E. Kleiner, Xiangbin Zeng, Pauline M. Ryan, Pradeep K. Dagur, Julia D. Berkson, Timothy P. Reilly, Lance R. Pohl – 24 February 2015 – Clinical evidence suggests that many cases of serious idiosyncratic drug‐induced liver injury are mediated by the adaptive immune system in response to hepatic drug‐protein adducts, also referred to as “drug‐induced allergic hepatitis”; but detailed mechanistic proof has remained elusive due to the lack of animal models.

A novel vascular pattern promotes metastasis of hepatocellular carcinoma in an epithelial–mesenchymal transition–independent manner

Jian‐Hong Fang, Hui‐Chao Zhou, Chong Zhang, Li‐Ru Shang, Lei Zhang, Jing Xu, Limin Zheng, Yunfei Yuan, Rong‐Ping Guo, Wei‐Hua Jia, Jing‐Ping Yun, Min‐Shan Chen, Yaojun Zhang, Shi‐Mei Zhuang – 24 February 2015 – Early metastasis is responsible for frequent relapse and high mortality of hepatocellular carcinoma (HCC), but its underlying mechanisms remain unclear. Epithelial–mesenchymal transition (EMT) has been considered a key event in metastasis.

Liver fibrosis occurs through dysregulation of MyD88‐dependent innate B‐cell activity

Manoj Thapa, Raghavan Chinnadurai, Victoria M. Velazquez, Dana Tedesco, Elizabeth Elrod, Jin‐Hwan Han, Prachi Sharma, Chris Ibegbu, Andrew Gewirtz, Frank Anania, Bali Pulendran, Mehul S. Suthar, Arash Grakoui – 24 February 2015 – Chronic liver disease mediated by activation of hepatic stellate cells (HSCs) leads to liver fibrosis. Here, we postulated that the immune regulatory properties of HSCs might promote the profibrogenic activity of B cells. Fibrosis is completely attenuated in carbon tetrachloride–treated, B cell–deficient µMT mice, showing that B cells are required.

Sox12, a direct target of FoxQ1, promotes hepatocellular carcinoma metastasis through up‐regulating Twist1 and FGFBP1

Wenjie Huang, Zhangqian Chen, Xin Shang, Dean Tian, Daowen Wang, Kaichun Wu, Daiming Fan, Limin Xia – 23 February 2015 – Metastasis is the main reason for high recurrence and poor survival of hepatocellular carcinoma (HCC) after curative resection. However, the molecular mechanism underlying HCC metastasis remains unclear. Here, we report on a novel function of SRY (sex determining region Y)‐box 12 (Sox12), a member of the SYR‐related high mobility group box family proteins, in promoting HCC metastasis.

Inhibition of wild‐type p53‐induced phosphatase 1 promotes liver regeneration in mice by direct activation of mammalian target of rapamycin

Lingling Zhang, Leiming Liu, Zhiyong He, Guangbing Li, Junping Liu, Zhangfa Song, Hongchuan Jin, Karl Lenhard Rudolph, Huayu Yang, Yilei Mao, Lianfeng Zhang, Hongbing Zhang, Zhicheng Xiao, Zhenyu Ju – 23 February 2015 – The liver possesses extraordinary regenerative capacity in response to injury. However, liver regeneration (LR) is often impaired in disease conditions. Wild‐type p53‐induced phosphatase 1 (Wip1) is known as a tumor promoter and enhances cell proliferation, mainly by deactivating antioncogenes. However, in this work, we identified an unexpected role of Wip1 in LR.

Ledipasvir/sofosbuvir regimens for chronic hepatitis C infection: Insights from a work productivity economic model from the United States

Zobair M. Younossi, Yushan Jiang, Nathaniel J. Smith, Maria Stepanova, Rachel Beckerman – 23 February 2015 – Patients with chronic hepatitis C (CHC) exhibit reduced work productivity owing to their disease. Historically, most regimens indicated for CHC genotype 1 (GT1) patients were administered with pegylated interferon (Peg‐IFN) and/or ribavirin (RBV), which further compromised work productivity during treatment.

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