Mouse Liver Tumorigenesis: Models, Mechanisms, and Relevance to Human Disease

Abstract excerpt

Hepatocytes have a remarkable proliferative capacity, but are quiescent in normal liver. Cell cycle activation in hepatocarcinogenesis can be directly triggered by overexpression of single and combinations of genes or be initiated indirectly by compensatory proliferation in response to liver injury. Work with transgenic and knockout mice indicate that regardless of the initiating cause, constitutive hepatocyte...

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