Transposagen p53 TGEM™ Model Characterized in 2011 Publication

Recent paper in The American Journal of Pathology characterizes the p53 TGEM™ model and explores the p53 gene’s role in tumor suppression

November 8, 2011 - In 2011, Charles River reached an agreement with Transposagen to be the sole distributor of their p53 TGEM™ rat model. A recently published paper in The American Journal of Pathology, titled “Homozygous and heterozygous p53 knockout rats develop metastasizing sarcomas with high frequency,” characterized this p53 TGEM™ model. It also discussed the importance of the p53 gene in tumor suppression.

The following abstract summarizes the development of sarcomas in the Transposagen p53 knockout rat model:

“The p53 tumor suppressor gene is mutated in the majority of human cancers. Inactivation of p53 in a variety of animal models results in early-onset tumorigenesis, reflecting the importance of p53 as a gatekeeper tumor suppressor. We generated a mutant p53 allele in the rat using a target-selected mutagenesis approach. Here, we show that homozygosity for this allele results in complete loss of p53 function. Homozygous mutant rats predominantly develop sarcomas at 4 months of age. These sarcomas have a high occurrence of pulmonary metastases. Heterozygous rats develop sarcomas starting at 8 months of age. Molecular analysis shows that these tumors show a loss-of-heterozygosity of the wild-type p53 allele. These unique features make this rat highly complementary to other rodent p53 knockout models and a versatile tool for investigating tumorigenesis processes as well as genotoxic studies.”

Please click here for the full paper.