Efficient suppression of murine intracellular adhesion molecule‐1 using ultrasound‐responsive and mannose‐modified lipoplexes inhibits acute hepatic inflammation

Keita Un, Shigeru Kawakami, Mitsuru Yoshida, Yuriko Higuchi, Ryo Suzuki, Kazuo Maruyama, Fumiyoshi Yamashita, Mitsuru Hashida – 23 January 2012 – Hepatitis is often associated with the overexpression of various adhesion molecules. In particular, intracellular adhesion molecule‐1 (ICAM‐1), which is expressed on hepatic endothelial cells (HECs) in the early stage of inflammation, is involved in serious illnesses. Therefore, ICAM‐1 suppression in HECs enables the suppression of inflammatory responses.

Increasing disparity in waitlist mortality rates with increased model for end‐stage liver disease scores for candidates with hepatocellular carcinoma versus candidates without hepatocellular carcinoma

David Goldberg, Benjamin French, Peter Abt, Sandy Feng, Andrew M. Cameron – 23 January 2012 – Candidates with hepatocellular carcinoma (HCC) within the Milan criteria (MC) receive standardized Model for End‐Stage LIver Disease (MELD) exception points because of the projected risk of tumor expansion beyond the MC. Exception points at listing are meant to be equivalent to a 15% rusj if 90‐day mortality, with additional points granted every 3 months, equivalent to a 10% increased morality risk.

V‐AKT murine thymoma viral oncogene homolog/mammalian target of rapamycin activation induces a module of metabolic changes contributing to growth in insulin‐induced hepatocarcinogenesis

Matthias Evert, Diego F. Calvisi, Katja Evert, Valentina De Murtas, Gioia Gasparetti, Sandra Mattu, Giulia Destefanis, Sara Ladu, Antje Zimmermann, Salvatore Delogu, Sara Thiel, Andrea Thiele, Silvia Ribback, Frank Dombrowski – 23 January 2012 – Mounting epidemiological evidence supports a role for insulin‐signaling deregulation and diabetes mellitus in human hepatocarcinogenesis. However, the underlying molecular mechanisms remain unknown.

Serum and glucocorticoid kinase 3 at 8q13.1 promotes cell proliferation and survival in hepatocellular carcinoma

Ming Liu, Leilei Chen, Tim Hon Man Chan, Jian Wang, Yan Li, Yan Li, Ting‐Ting Zeng, Yun‐Fei Yuan, Xin‐Yuan Guan – 19 January 2012 – Amplification of broad regions of 8q is one of the most frequent genetic alterations in hepatocellular carcinoma (HCC), suggesting the existence of oncogenes in addition to MYC at 8q24.21. In this report we examine the potential role of the candidate amplified oncogene serum and glucocorticoid kinase 3 (SGK3) at 8q13.1 in HCC pathogenesis.

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