HRAS (Harvey rat sarcoma virus oncogene) encodes a member of the Ras oncogene family involved in signal transduction pathways. The amino acid substitution, G12V, has the lowest GTPase activity found in patient codon 12 substitutions.H-ras 12V transgenic mice express a human HRAS gene carrying a G12V substitution (glycine to valine) under the control of the liver specific albumin (Alb) promoter. H-ras 12V is mainly expressed in the liver and, at a much lower level, in the heart. Mice that are carriers for the transgene are viable and fertile. H-ras 12V mice exhibit gender-dependent liver pathologies. H-ras 12V transcript levels in non-tumor regions are significantly higher in males than in females. Female transgenic mice exhibit reduced liver/body weight ratios, hepatocytes have higher expression of TRP53, CDKN1A (also known as p21), higher levels of hypodiploid cell formation, and enhanced cell cycle arrest than males. In addition, females have a reduced incidence of hepatocellular carcinoma as compared to males (28.6% compared to 88.2% at 9 months of age) and liver adenomas (52.4% compared to 94.1% at 9 months of age). Hepatocytes from male H-ras 12V mice develop a higher Ras activity and higher ROS (reactive oxygen species) levels than female H-ras 12V mice.

H-ras12V transgenic mice express a human HRAS gene carrying a G12V substitution (glycine to valine) under the control of the liver specific albumin (Alb) promoter. Hemizygous males develop hepatocellular carcinoma and liver adenomas with an incidence of 88.2% and 94.1%, respectively, by 9 months of age. Female H-ras12V develop hepatic cancer at a lower incidence rate.

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