Abstract
Mice genetically susceptible to hepatocarcinogenesis carry a germ-line genetic alteration, which has liver-specific effects. It should be considered as an initial step in the multistage process of hepatocarcinogenesis. Any other step could add to the genetic alteration, resulting in a high susceptibility to spontaneous and carcinogen induced liver tumorigenesis. A quantitative evaluation of carcinogen-induced liver tumors showed that the genetic alteration controls liver tumor growth, but not liver tumor frequency. Our recent observations indicate that Ha-ras gene mutations at codon 61 are frequently involved in the pathogenesis of liver tumors in mice genetically susceptible to hepatocarcinogenesis, but not in genetically resistant mice. Some rare human genetic syndromes are characterized by a high predisposition to hepatocellular carcinoma development, through the prior induction of cirrhosis. However, these syndromes do not represent the human counterparts of the genetic alterations responsible for their high susceptibility to hepatocarcinogenesis of the C3H and of the CBA mouse strains.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call