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. 2009 Nov 9;1(3):852–872. doi: 10.3390/v1030852

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© 2009 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

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Figure 3. — The proposed model of hepatocarcinogenesis. One or several types of liver cells (mature, hepatocytes, progenitor/stem cells) could support the multi-step process of accumulating genetic/epigenetic disorders leading to senescence, and subsequently bypassing senescence to reach cancer. Cirrhosis is a senescent state that could be induced by different factors such as ROS, oncogene activation and telomere shortening for instance. The senescent state is kept active by the p53/p21 and p16/pRb checkpoints. When these gatekeepers become inactive, the cell can bypass senescence, and re-enter cell cycle progression and DNA hyper-replication in a context of immortality, due to telomerase reactivation, and genetic insability. Thus, the cell is prone to acquire the last genetic/epigenetic hits necessary to get tumorigenicity and cancer stem cell capabilities.