Guobin He

TL;DR: It is demonstrated that either dietary or genetic obesity is a potent bona fide liver tumor promoter in mice and obesity-promoted HCC development was dependent on enhanced production of the tumor-promoting cytokines IL-6 and TNF, which cause hepatic inflammation and activation of the oncogenic transcription factor STAT3.

TL;DR: This review will focus on recent studies on the roles of NF-κB and STAT3 in liver cancer and interactions between the two pathways and their potential as therapeutic targets.

TL;DR: Hepatocyte-specific p38 alpha ablation enhanced ROS accumulation and liver damage, which were prevented upon administration of an antioxidant, and IL-1 alpha release by necrotic hepatocytes is therefore an important mediator of liver tumorigenesis.

TL;DR: A transplant system that allows initiated mouse hepatocytes to form hepatocellular carcinomas (HCC) in host liver after a long latency and deletion of IKKbeta long after initiation accelerated HCC development and enhanced proliferation of tumor initiating cells.

TL;DR: In this article, the authors describe isolation and characterization of HCC progenitor cells (HcPCs) from different mouse HCC models and show that cells resembling HcPC cells reside within dysplastic lesions that appear several months before HCC nodules.